Nephrology

NEPHROLOGY
D r. J. B argm an
To m L e ve n ti s an d D an M o ze g, e d i to rs
C h ri sti n e B re zd e n , asso ci ate e d i to r
NORMAL RENAL FUNCTION . . . . . . . . . . . . . . . . . 2
R e n al S tru ctu re an d F u n ctio n
R e n al H e m o d yn am ics
C o n tro l o f R e n al H e m o d yn am ics
Tu b u lar R e ab so rp tio n an d S e cre tio n
E ryth ro p o ie tin
Vitam in D
M e asu re m e n t o f R e n al F u n ctio n
M e asu re m e n t o f Tu b u lar F u n ctio n
T h e K id n e y In P re gn an cy
URINE STUDIES. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
G e n e ral
U rin alysis
M icro sco p y
C rystals
U rin e E le ctro lyte s
ABNORMAL RENAL FUNCTION . . . . . . . . . . . . . . 7
P ro te in u ria
H e m atu ria
ELECTROLYTE DISORDERS. . . . . . . . . . . . . . . . . . 9
H yp o n atre m i a/H yp e rn atre m i a
H yp o n atre m ia
H yp e rn atre m ia
H yp o kale m ia
H yp e rkale m ia
ACID-BASE DISORDERS . . . . . . . . . . . . . . . . . . . . .15
R e n al C o n trib u tio n to Acid -B ase B alan ce
1 M e tab o lic Acid o sis
1 M e tab o lic Alkalo sis
1 R e sp irato ry Acid o sis H yp o ve n tilatio n )
1 R e sp irato ry Alkalo sis H yp e rve n tilatio n )
M ixe d D istu rb an ce s
RENAL FAILURE. . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
ACUTE RENAL FAILURE . . . . . . . . . . . . . . . . . . . . 18
Tre atm e n t
In d icatio n s fo r D ialysis in AR F vs. in C R F )
P ro gn o sis
CHRONIC RENAL FAILURE. . . . . . . . . . . . . . . . . . 19
C lassificatio n
C lin ical F e atu re s o f U re m ia
C o m p licatio n s
Tre atm e n t
In d icatio n s fo r D ialysis in C R F
M C C Q E 2000 R e vi e w N o te s an d L e ctu re S e ri e s N e p h ro lo gy 1
DIALYSIS AND RENAL . . . . . . . . . . . . . . . . . . 20
TRANSPLANTATION
D ialysis
R e n al Tran sp lan tatio n
GLOMERULONEPHRITIS . . . . . . . . . . . . . . . . 21
G e n e ral C o n sid e ratio n s
P rim ary G lo m e ru lo n e p h ritis
S e co n d ary G lo m e ru lo n e p h ritis
TUBULOINTERSTITIAL NEPHRITIS . . . . . 26
Acu te T IN
C h ro n ic T IN
ACUTE TUBULAR NECROSIS. . . . . . . . . . . . . 28
Isch e m ia
To xin s
NSAID NEPHROPATHY. . . . . . . . . . . . . . . . . . 29
VASCULAR DISEASES OF THE KIDNEY. . . 29
DIABETES AND THE KIDNEY. . . . . . . . . . . . 30
HYPERTENSION. . . . . . . . . . . . . . . . . . . . . . . . 31
R e n o vascu lar H yp e rte n sio n
H yp e rte n sio n C au se d b y R e n al P are n ch ym al D ise ase
PYELONEPHRITIS. . . . . . . . . . . . . . . . . . . . . . . 32
Acu te P ye lo n e p h ritis
C h ro n ic P ye lo n e p h ritis
CYSTIC DISEASES OF THE KIDNEY. . . . . . 34
Ad u lt P o lycystic K id n e y D ise ase
M e d u llary C ystic D ise ase
M e d u llary S p o n ge K id n e y
OTHER SYSTEMIC DISEASES . . . . . . . . . . . 35
AND THE KIDNEY
H yp e rte n sio n C au sin g R e n al D ise ase
M u ltip le M ye lo m a
S cle ro d e rm a
Vascu litid e s
R h e u m ato id Arth ritis
C an ce r
In fe ctio n s
H IV-Asso ciate d R e n al D ise ase
DIURETICS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
N e p h ro lo gy 2 M C C Q E 2000 R e vi e w N o te s an d L e ctu re S e ri e s
N o te s
NORMAL RENAL FUNCTION
RENAL STRUCTURE AND FUNCTION
Ne phron
J th e in d ivid u al re n al tu b u le an d its glo m e ru lu s
J glo m e ru lu s
B o wm an s cap su le - b lin d e n d o f th e re n al tu b u le
glo m e ru lar cap illarie s - filte rin g m e m b ran e wh ich co n sists o f a
th in laye r o f fe n e strate d e n d o th e lial ce lls, a b ase m e n t m e m b ran e
an d visce ral e p ith e lial ce lls o f B o wm an s cap su le i.e . p o d o cyte s)
m e san giu m - co n sists o f scatte re d ce lls with co n tractile an d
p h ago cytic fu n ctio n wh ich are cap ab le o f layin g d o wn b o th
m atrix an d co llage n an d o f se cre tin g b io lo gically active m e d iato rs
J p ro xim al co n vo lu te d tu b u le P C T )
re ab so rb s 65% o f glo m e ru lar filtrate , in clu d in g glu co se , am in o
acid s, p ro te in s, vitam in s via active tran sp o rt wate r fo llo ws p assive ly)
re asb o rb s ~ 2/3 o f filte re d N a
+
m o stly via e le ctro n e u tral N a
+
H
+
e xch an ge
im p o rtan t site o f am m o n iage n e sis
J lo o p o f H e n le
25% o f filte re d N a
+
is ab so rb e d at th e th ick asce n d in g lim b
m o stly via ch an n e l m e d iate d N a-K -2C l) re ab so rp tio n
o f N a
+
, K
+
, an d C l
1 5% o f filte re d wate r is re m o ve d in lo o p o f H e n le
J d istal co n vo lu te d tu b u le D C T )
re ab so rb s 5-1 0% filte re d N a
+
p ro b ab ly via d ire ctly co u p le d
N aC l p ath way with o u t K
+
)
re lative ly im p e rm e ab le to wate r 5% o f filte re d wate r is
re m o ve d in th is se gm e n t)
late d istal se gm e n t is a site o f AD H an d ald o ste ro n e actio n
J ju xtaglo m e ru lar J-G ) ap p aratu s
ad jace n t to glo m e ru lu s wh e re affe re n t arte rio le e n te rs
co n sists o f
m yo e p ith e lial ce lls - m o d ifie d gran u late d sm o o th m u scle
ce lls in th e m e d ia o f th e affe re n t arte rio le th at co n tain re n in
m acu la d e n sa - sp e cialize d re gio n o f th e d istal tu b u le wh ich
co n tro ls re n in re le ase
J co lle ctin g d u ct syste m
fin al re gu latio n o f flu id an d e le ctro lyte b alan ce
alo n g with late d istal se gm e n t, re sp o n d s to AD H an d ald o ste ro n e
RENAL HEMODYNAMICS
J R e n al B lo o d F lo w R B F ) = 20~ 25% o f card iac o u tp u t = 1 200 m L /m in u te
J R e n al P lasm a F lo w R P F ) = R B F x 1 - h e m ato crit) = 600 m L /m in u te
J G lo m e ru lar F iltratio n R ate G F R )
p lasm a vo lu m e filte re d acro ss glo m e ru li to B o wm an s cap su le
p e r u n it tim e
20% o f R P F = 1 20 m L /m in
m axim al in yo u n g ad u lth o o d an d d e cre ase s th e re afte r
Figure 1. Glome rular Filtration
J F iltratio n F ractio n F F )
vo lu m e o f p lasm a filte re d acro ss glo m e ru li, re lative to th e
vo lu m e o f p lasm a flo win g to th e kid n e ys p e r u n it tim e
F F = G F R /R P F
as R B F an d R P F d e cre ase , F F m u st in cre ase to p re se rve G F R ;
th is is d o n e b y An gio te n sin II AII)
NORMAL RENAL FUNCTION . . . CONT.
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20% 1 20 m l/m in u te )
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N o te s
CONTROL OF RENAL HEMODYNAMICS
J go al is m ain te n an ce o f G F R in th e face o f varyin g R B F au to re gu latio n )
J m e ch an ism : d e cre ase d R B F cau se s re n in re le ase fro m J-G ap p aratu s.
R e n in activate s AI to an gio te n sin o ge n to An gio te n sin I AI) ;
An gio te n sin C o ve rtin g E n zym e AC E ) activate s AI to AII; AII co n stricts
th e e ffe re n t re n al arte rio le s, risin g filtratio n fractio n an d m ain tain in g
G F R
J as R B F an d R P F d e cre ase , F F m u st in cre ase to p re se rve G F R ; th is is
d o n e b y An gio te n sin II AII)
TUBULAR REABSORPTION AND SECRETION
J th e u ltrafiltrate wh ich cro sse s th e glo m e ru lar cap illarie s in to
B o wm an s sp ace starts its jo u rn e y alo n g th e tu b u lar syste m
J in th e tu b u le , it is fu rth e r m o d ifie d b y re ab so rp tio n tu b u lar lu m e n
to b lo o d stre am ) o r se cre tio n b lo o d stre am to tu b u lar lu m e n )
Table 1. Proce s s e s Occurring Along the Ne phron
Site Abs orption Se cre tion
P C T N a
+
, H C O 3
o rgan ic acid s
glu co se , am in o acid s,
p h o sp h ate s, vitam in s
T h ick Asce n d in g N a
+
, K
+
, C 1
L im b o f L o o p o f H e n le
D C T N a
+
, C 1
H
+
, K
+
ERYTHROPOIETIN
J h o rm o n e p ro d u ce d b y kid n e ys an d live r to a le sse r d e gre e )
in re sp o n se to h yp o xia
J p ro d u ce d in kid n e ys b y fib ro b last-like ce lls in co rtical in te rstitiu m
J th e am o u n t o f o xyge n availab le n o t o xyge n satu ratio n o r h e m o glo b in
co n ce n tratio n d e te rm in e e ryth ro p o ie tin E p o ) re le ase
J re sp o n d s in 1 .5 to 2 h o u rs, to h yp o xia as b rie f as 1 5 m in u te s
J in re n al d ise ase an e m ia re su lts fro m d e cre ase d re n al cap acity fo r
E p o p ro d u ctio n an d re le ase , as we ll as d e cre ase d re d b lo o d ce lls life
sp an to xic h e m o lysis, h yp e rsp le n ism )
VITAMIN D
J vitam in D is co n ve rte d to th e 25-h yd ro xy-vitam in D fo rm in th e live r
J th e kid n e y co n ve rts 25-h yd ro xy-vitam in D to 1 ,25-d ih yd ro xy-vitam in D
J in re n al d ise ase th is cap acity b e co m e s im p aire d an d co n trib u te s to th e
te n d e n cy to ward s h yp o calce m ia an d su b se q u e n t se co n d ary
h yp e rp arath yro id ism sin ce 1 ,25-d ih yd ro xy-Vitam in D is n e ce ssary
fo r in te stin al calciu m ab so rp tio n )
MEASUREMENT OF RENAL FUNCTION
Se rum Cre atinine
J an in d ire ct e stim ate u sin g a p ro d u ct o f cre atin in e m e tab o lism
J valu e is d e p e n d e n t o n m u scle m ass as we ll as re n al fu n ctio n e .g. an
e ld e rly wo m an with ch ro n ic re n al failu re m ay h ave th e sam e
cre atin in e co n ce n tratio n as a 30 ye ar o ld we igh tlifte r
J ch an ge s in cre atin in e co n ce n tratio n m ay b e m o re re fle ctive o f p ath o lo gy
th an ab so lu te valu e s
J cre atin in e valu e s m ay n o t b e re fle ctive o f d e gre e o f re n al d ise ase as
cre atin in e co n ce n tratio n d o e s n o t start to rise sign ifican tly u n til G F R
is q u ite d im in ish e d
N o te s
S e ru m cre atin in e
co n ce n tratio n
0
0 G F R
Figure 2. Se rum Cre atinine Conce ntration as a Function of GFR
Cre atinine Cle arance
J e stim ate o f G F R actu ally an o ve re stim ate as so m e cre atin in e is se cre te d )
J sh o u ld b e fu ll 24 h o u r co lle ctio n
J cre atin in e cle aran ce as a re fle ctio n o f G F R can b e e stim ate d b y th e
fo llo win g fo rm u la
G F R = [U ]C r x Vu /P C r
wh e re [U ]C r is u rin e cre atin in e co n ce n tratio n , Vu is u rin e flo w rate
an d P C r is p lasm a cre atin in e co n ce n tratio n
alte rn ative ly, G F R can b e e stim ate d u sin g th e fo rm u la:
1 40 age(weight) x1.2 (men) or 0.85 (women)
PCr
age in ye ars, we igh t in kg, P C r in u m o l/L
n o rm al valu e ran ge s fro m 75-1 20 m l/m in
Clinical Pe arl
J The re is an inve rs e re lations hip be twe e n s e rum cre atinine conce ntration
and cre atinine cle arance (e .g. if s e rum double s in a give n pe rs on,
cle arance has be e n halve d)
Blood Ure a Nitroge n (BUN)
J le ss accu rate an d sh o u ld n o t b e u se d alo n e as a te st o f re n al fu n ctio n
J m o d ifie d b y E C F vo lu m e , p ro te in in take , catab o lism , re n al b lo o d flo w
J se cre te d an d re ab so rb e d in n e p h ro n
MEASUREMENT OF TUBULAR FUNCTION
J u rin ary co n ce n tratio n
a.m . u rin e o sm o lality o r sp e cific gravity s.g.)
J acid ificatio n i.e . ap p ro p riate u rin e p H give n se ru m p H )
if u rin ary p H is > 5.3 wh e n p atie n t is acid o tic co n sid e r R TA
e xce p tio n s e xist)
J p o tassiu m e xcre tio n
can calcu late th e Tran s-Tu b u lar K
+
G rad ie n t T T K G )
th e valu e asse sse s d istal tu b u lar K
+
se cre tio n an d can b e
h e lp fu l in th e se ttin g o f h yp o kale m ia o r h yp e rkale m ia se e b e lo w)
T T K G = U K /P K
U o sm /P o sm
Wh e re U K is u rin ary K
+
co n ce n tratio n , P K is p lasm a K
+
co n ce n tratio n ,
U o sm is u rin ary o sm o larity an d P o sm is p lasm a o sm o larity
J F ractio n al E xcre tio n F E ) o f vario u s so lu te s X)
F e X = U X/P X x 1 00%
U cr/P cr
THE KIDNEY IN PREGNANCY
J in cre ase d kid n e y size an d d ilatatio n o f re n al p e lvis an d u re te rs
in cre ase d U T I risk)
J 50% in cre ase in G F R alo n g with d e cre ase d cre atin in e an d B U N
J 25-50% in cre ase in re n al b lo o d flo w
J b lo o d p re ssu re falls in 1 st trim e ste r 1 00/60) , rise s slo wly to ward
n o rm al in 2n d an d 3rd trim e ste rs
J glu co su ria, sligh t p ro te in u ria < 200 m g p e r 24 h o u rs) o fte n o ccu r
N o te s
Re nal Ris k Factors for Adve rs e Pre gnancy Outcome
J p re -e xistin g h yp e rte n sio n
J co llage n -vascu lar d ise ase , e sp e cially if n o t in re m issio n o r if
asso ciate d with an tip h o sp h o lip id an tib o d ie s
J cre atin in e 1 80 u m o l/L
J n e p h ro tic-ran ge p ro te in u ria
J active U T I
URINE STUDIES
GENERAL
J fre sh ly vo id e d sp e cim e n
J u se d ip stick fo r u rin alysis sp e cific gravity, p H , glu co se , p ro te in ,
h e m o glo b in , n itrite s, le u ko cyte s)
J ce n trifu ge fo r 3-5 m in u te s
J re su sp e n d se d im e n t an d p e rfo rm m icro sco p y to lo o k fo r ce lls, casts,
crystals, an d b acte ria
URINALYSIS
Spe cific Gravity
J th e ratio o f we igh ts o f e q u al vo lu m e s o f u rin e an d H 2O
m e asu re s we igh t o f so lu te s in u rin e )
J an e stim ate o f u rin e o sm o lality an d if kid n e ys are wo rkin g, o f th e
p atie n t s state o f h yd ratio n )
J valu e s b e lo w 1 .01 0 re fle ct d ilu te u rin e , valu e s ab o ve 1 .020 re fle ct
co n ce n trate d u rin e
J m ay ge t false ly h igh valu e s if lo sin g glu co se o r p ro te in s in u rin e
pH
J u rin e p H is n o rm ally b e twe e n 4.5-7.0
J if p e rsiste n tly alkalin e , co n sid e r:
re n al tu b u lar acid o sis
U T I with u re ase p ro d u cin g b acte ria e .g. Proteus
Glucos e
J fre e ly filte re d at glo m e ru lu s an d re ab so rb e d in p ro xim al tu b u le
J m ay in d icate h yp e rglyce m ia o n ce b lo o d glu co se le ve ls e xce e d
9-1 1 m m o l/L , re n al tu b u lar cap acity fo r re ab so rp tio n o f glu co se is
o ve rwh e lm e d )
J in th e ab se n ce o f h yp e rglyce m ia, m ay in d icate p ro xim al tu b u le
d ysfu n ctio n e .g. F an co n i syn d ro m e p an P C T tran sp o rt d ysfu n ctio n
with glu co su ria, am in o acid u ria, p h o sp h atu ria, u rico su ria,
h yp o calce m ia, h yp o m agn e se m ia an d p ro xim al re n al tu b u lar acid o sis)
o r in cre ase d G F R e .g. p re gn an cy)
Prote in
J d e te ctio n b y d ip stick re ally m e asu re s alb u m in le ve ls in u rin e
J th e re fo re , o th e r p ro te in su ch as B e n ce -Jo n e s m ay b e m isse d o n
d ip b u t will b e d e te cte d b y o th e r m e an s su ch as acid p re cip itatio n
J false +ve o n d ip : p H > 7, co n ce n trate d u rin e , b lo o d co n tam in atio n ;
false ve : d ilu te u rin e d ip sticks are availab le to d e te ct
m icro alb u m in u ria i.e . ve ry sm all am o u n ts o f alb u m in ) in o rd e r to
m o n ito r th e o n se t-p ro gre ss o f d iab e tic re n al d ise ase
J go ld stan d ard is th e 24 h o u r u rin e co lle ctio n fo r to tal p ro te in
se e P ro te in u ria S e ctio n )
Clinical Pe arl
J If patie nt has clinically (dips tick) de te ctable prote inuria
it is unne s s ary to s e nd urine for microalbumin le ve ls !
He moglobin
J h igh u rin e asco rb ic acid can give false ve d ip stick re su lt
J if u rin e d ip p o sitive fo r b lo o d b u t n o R B C o n m icro sco p y, m ay
in d icate h e m o glo b in u ria e .g. h e m o lysis) o r m yo glo b in u ria
e .g. rh ab d o m yo lysis)
N o te s
URINE STUDIES . . . CONT.
MICROSCOPY
Erythrocyte s
J n o rm al is u p to 2-3 R B C s p e r h igh p o we r fie ld H P F )
J sp icu late d , p o lym o rp h ic R B C s su gge st glo m e ru lar b le e d in g
J n o n -sp icu late d , u n ifo rm R B C s su gge st e xtraglo m e ru lar b le e d in g
J se e H e m atu ria se ctio n
Le ukocyte s
J u p to 3 p e r H P F is acce p tab le
J d e te ctio n o f le u ko cyte s b y d ip stick le u ko e ste rase m e th o d in d icate s
at le ast 4 p e r H P F
J in d icate s in flam m ato ry p ro ce ss in th e u rin ary syste m e .g. U T I)
J if p e rsiste n t ste rile p yu ria co n sid e r ch ro n ic u re th ritis, p ro statitis,
in te rstitial n e p h ritis e sp e cially if WB C casts) , re n al T B , viral
in fe ctio n s, calcu li, p ap illary n e cro sis
J e o sin o p h ilu ria su gge sts alle rgic in te rstitial n e p h ritis, ch o le ste ro l
e m b o li syn d ro m e
Cas ts
J p ro te in m atrix fo rm e d b y ge latio n o f Tam m -H o rsfall m u co p ro te in
glyco p ro te in e xcre te d b y re n al tu b u le ) trap p in g ce llu lar d e b ris in
tu b u lar lu m e n an d m o u ld in g it in th e sh ap e o f th e tu b u le s
Table 2. Inte rpre tation of Cas ts
h yalin e n o t in d icative o f d ise ase
co n ce n trate d u rin e
fe ve r
e xe rcise
R B C glo m e ru lar b le e d in g
e .g. glo m e ru lo n e p h ritis)
= active se d im e n t
le u ko cyte p ye lo n e p h ritis
in te rstitial n e p h ritis
h e m e gran u lar AT N
p ro life rative G N
fatty casts/o val fat b o d ie s n e p h ro tic syn d ro m e
CRYSTALS
J m o st h ave n o p ath o lo gic sign ifican ce , re su ltin g fro m u rin ary
co n ce n tratio n , acid ificatio n an d co o lin g o f u rin e
J calciu m o xalate : d o u b le p yram id s ap p e arin g as a sq u are co n tain in g
a cro ss; m igh t in d icate e th yle n e glyco l to xicity
J calciu m p h o sp h ate : n arro w re ctan gle n e e d le s, clu m p e d in a rad iatin g p atte rn
J u ric acid : re d /b ro wn , rh o m b o id sh ap e d
J calciu m m agn e siu m am m o n iu m p yro p h o sp h ate trip le p h o sp h ate ) :
co ffin lid s; asso ciate d with re cu rre n t U T I b y u re a-sp littin g o rgan ism s
Proteus, Klebsiella
URINE ELECTROLYTES
J can b e u se d to e valu ate th e so u rce o f an e le ctro lyte ab n o rm ality o r
to gro ssly asse ss tu b u lar fu n ctio n
J N a
+
, K
+
, C l
, o sm o lality an d p H are co m m o n ly m e asu re d

J th e re are n o 'n o rm al' valu e s; o u tp u t is b ase d o n in take in p ro p e rly
fu n ctio n in g kid n e ys an d in d ise ase state s, th e valu e s are in te rp re te d
in ligh t o f th e p ath o lo gy
Example s of Common Urine Ele ctrolyte Abnormalitie s
Table 3. Dis tinguis hing Pre -Re nal from Intra-Re nal
Dis e as e in Acute Re nal Failure
Inde x Pre -Re nal Intra-Re nal (e .g. ATN)
U rin e O sm o lality > 500 < 350
U rin e S o d iu m m m o l/L ) < 20 > 40
F E N a
+
< 1 % > 3%
P lasm a B U N /C r S I U n its) > 80:1 < 40:1
N o te s
URINE STUDIES . . . CONT.
J h igh u rin e N a
+
in th e se ttin g o f acu te re n al failu re in d icate s in tra-re n al
d ise ase o r th e p re se n ce o f n o n -re ab so rb ab le an io n s e .g. ke to n e s)
J h igh u rin e N a
+
in th e se ttin g o f h yp o n atre m ia: d iu re tics, tu b u lar
d ise ase B artte rs syn d ro m e , se e b e lo w) , S IAD H
J a h igh F E N a
+
b u t lo w F E C 1

is se e n in m e tab o lic alkalo sis se co n d ary to vo m itin g
J o sm o lality is u se fu l to e stim ate th e kid n e y s co n ce n tratin g ab ility
J th e valu e fo r N a
+
K
+
) -C l
, also kn o wn as th e u rin e n e t ch arge is

u se fu l in d isce rn in g th e cau se o f m e tab o lic acid o sis; a n e gative
valu e in d icate s th e p re se n ce o f u n m e asu re d p o sitive io n s
i.e . am m o n iu m ) wh ich is se e n in m e tab o lic acid o sis 2 to n o n -re n al
cau se s e .g. d iarrh e a) in co n trast to R TA, wh e re am m o n iu m e xcre tio n is
n o t e le vate d an d th e u rin e n e t n e gative ch arge is p o sitive
J u rin e p H is u se fu l to gro ssly asse ss re n al acid ificatio n
'lo w' p H < 5.5) in th e p re se n ce o f lo w se ru m p H is an ap p ro p riate
re n al re sp o n se
a h igh p H in th is se ttin g m igh t in d icate a re n al acid ificatio n
d e fe ct R TA wh ich is a co lle ctio n o f lo w am m o n iu m
e xcre tio n d ise ase s)
ABNORMAL RENAL FUNCTION
PROTEINURIA
Table 4. Quantitative Prote inuria
Daily Prote in Excre tion Me aning
< 1 50 m g n o rm al
1 50 m g - 2 g glo m e ru lar d ise ase
tu b u lar d ise ase
o rth o static
o ve rflo w
2 g - 3 g u su ally glo m e ru lar
m ay b e tu b u lar
> 3 g alm o st always glo m e ru lar
u n le ss ligh t ch ain s m u ltip le m ye lo m a)
Prote inuria
d e te rm in e u sin g d ip stick an d /o r 24 h o u r u rin e co lle ctio n )
Phys iological Pathological
yo u n g h e alth y p e rso n s d e te rm in e with p ro te in e le ctro p h o re sis an d 24 h o u r u rin e co lle ctio n )
Orthos tatic Cons tant
p ro te in u ria ru le -o u t u n d e rlyin g
o ccu rs with d ise ase an d fo llo w-u p
stan d in g m ay d e ve lo p re n al d ise ase
5% o f ad o le sce n ts in th e fu tu re
ge n e rally re so lve s b io p sy if co n stan t fo r
sp o n tan e o u sly se ve ral m o n th s an d n o
u n d e rlyin g d ise ase
Tubulointe rs titial Glome rular Ove rflow
< 2g/24 h o u r > 2g/24 h o u r < 2g/24 h o u r
m ixe d L M W p ro te in s p rim arily alb u m in p rim arily ligh t ch ain s
an d L M W p ro te in s
o ccu rs with in cre ase d
G F R , in cre ase d p lasm a
p ro te in co n ce n tratio n
Primary Se condary
P ro life rative N o n p ro life rative P ro life rative N o n p ro life rative
Figure 3. An Approach to Prote inuria
N o te s
ABNORMAL RENAL FUNCTION . . . CONT.
J n o rm ally < 1 50 m g p ro te in /d ay is lo st in th e u rin e
40% alb u m in
40% Tam m -H o rsfall m u co p ro te in fro m ce lls o f th e asce n d in g
lim b o f th e L o o p o f H e n le i.e . d o e s n o t arise fro m th e
p lasm a an d fo rm s th e m atrix fo r casts)
1 5% im m u n o glo b u lin
5% o th e r p lasm a p ro te in s
J p lasm a p ro te in s are filte re d at th e glo m e ru lar cap illary in te rface
b ase d o n ch arge an d size
J fe n e stratio n s in th e glo m e ru lar b ase m e n t m e m b ran e e xclu d e
p ro te in s o f m o le cu lar we igh t M W) gre ate r th an an d e q u al to
alb u m in M W 60 000)
J p ro te in s o f M W le ss th an alb u m in m ay filte r th ro u gh th e
glo m e ru lar b arrie r b u t are n o rm ally re ab so rb e d an d catab o lize d b y
re n al tu b u lar ce lls
J th e re fo re , tu b u lar d ysfu n ctio n can give m o d e st e xcre tio n o f L M W
p ro te in s u p to 2 g/d ay
J glo m e ru lar d ysfu n ctio n p ro d u ce s p ro te in u ria, u su ally > 2 g/d ay
co n sistin g o f h igh e r M W p ro te in s e sp e cially alb u m in )
J alb u m in lo ss cau se s d e cre ase d o n co tic p re ssu re with re su ltin g
tissu e e d e m a an d h yp e rlip id e m ia
J h yp e rlip id e m ia re su lts fro m h e p atic lip o p ro te in syn th e sis
stim u late d b y th e d e cre ase d p lasm a o n co tic p re ssu re
J with tu b u lar d ysfu n ctio n th e re is n o asso ciate d e d e m a o r
h yp e rlip id e m ia b e cau se alb u m in is n o t lo st
J rare ly, " o ve rflo w" p ro te in u ria o ccu rs wh e re th e filte re d lo ad o f
p ro te in s u su ally L M W) o ve rwh e lm s tu b u lar cap acity fo r re ab so rp tio n
filte re d lo ad = G F R x p lasm a p ro te in co n ce n tratio n
" o ve rflo w" p ro te in u ria o ccu rs se co n d ary to :
in cre ase d G F R e .g. in p re gn an cy)
in cre ase d p lasm a p ro te in co n ce n tratio n e .g. im m u n o glo b u lin
ligh t ch ain s - m u ltip le m ye lo m a)
HEMATURIA
J gro ss h e m atu ria: p in k, re d , o r te a-co lo u re d u rin e
J m icro sco p ic h e m atu ria: ap p e ars n o rm al, m ay b e d e te cte d b y d ip stick
J iso late d h e m atu ria: n o sign ifican t p ro te in u ria, ce lls o r u rin ary casts
like ly se co n d ary to a U R O L O G IC AL p ro b le m
J h e m atu ria asso ciate d with p ro te in u ria, ce lls o r casts
like ly se co n d ary to a N E P H R O L O G IC AL p ro b le m
J cau se s are also age -re late d
glo m e ru lar cau se s p re d o m in ate in ch ild re n an d yo u n g ad u lts
fe we r th an 5% o f case s o f h e m atu ria in p atie n ts age > 40 re su lt
fro m glo m e ru lar le sio n s
N o te s
ABNORMAL RENAL FUNCTION . . . CONT.
HEMATURIA
Ps e udohe maturia He maturia True He maturia
co lo u re d u rin e b u t n e gative d ip stick but NO RBCs on
d iffe re n tial d iagn o sis micros copy
fo o d e .g. b e e ts) m yo glo b in u ria
d ye s h e m o glo b in u ria
m e d icatio n e .g. rifam p in ) d u e to h e m o lysis)
N B : m yo glo b in u ria an d
h e m o glo b in u ria will re giste r
o n d ip stick as b lo o d
Urological Ne phrological
n o casts o r p ro te in ) casts an d /o r p ro te in )
if n o u ro lo gical so u rce fo u n d th e n
m ay b e n e p h ro lo gical
d iffe re n tial d iagn o sis
u rin ary tract sto n e s
n e o p lasm s o f u rin ary tract
T B
trau m a
p ro statitis
As s ociate d with As s ociate d with As s ociate d with Cas ts
Urinary Tract Infe ction Prote inuria
d iffe re n tial d iagn o sis se e Tab le 1 fo r typ e s o f casts
glo m e ru lo n e p h ritis an d th e ir cau se s
tu b u lo in te rstitial n e p h ritis
Figure 4. An Approach to He maturia o th e r re n al p are n ch ym al d ise ase
Table 5. An Approach to He maturia
Ne phrologic Urologic
S ym p to m s co n stitu tio n al if 2 to syste m ic d ise ase ) p ain
arth ralgia gro ss b lo o d
rash p ro statism
d e afn e ss Alp o rt s syn d ro m e )
S ign s in cre ase d b lo o d p re ssu re o ccasio n ally)
U rin e p ro te in R B C s o n ly
casts
L ab s in cre ase d C r o ccasio n ally) n o rm al C r u n le ss o b stru cte d )
P o ssib le in ve stigatio n s d e p e n d in g o n se ttin g)
se ru m co m p le m e n t, AS O , AN A, AN C A, an ti-G B M an tib o d ie s, cryo glo b u lin s, h e p B an d C , H IV
ELECTROLYTE DISORDERS
HYPONATREMIA/HYPERNATREMIA
Introduction
J h yp o n atre m ia/h yp e rn atre m ia are d iso rd e rs o f wate r b alan ce
J h yp o n atre m ia su gge sts to o m u ch an d h yp e rn atre m ia is to o little
wate r in th e e xtrace llu lar flu id re lative to N a
+
J h yp o n atre m ia an d h yp e rn atre m ia can e ach b e asso ciate d with
n o rm al, d e cre ase d o r in cre ase d to tal b o d y N a
+
J E C F vo lu m e is d e te rm in e d b y N a
+
co n te n t n o t N a
+
co n ce n tratio n
N a
+
d e ficie n cy o r e xce ss le ad s to E C F vo lu m e d e p le tio n o r
e xp an sio n , re sp e ctive ly)
J wate r m o ve s o u t o f ce lls in re sp o n se to in cre ase d o sm o lality an d in to
ce lls in re sp o n se to d e cre ase d o sm o lality o f E C F as lo n g as th e
o sm o le s d o n o t fre e ly trave rse th e p lasm a m e m b ran e , as d o e s u re a
fo r e xam p le )
J clin ical sign s an d sym p to m s o f h yp o n atre m ia/h yp e rn atre m ia are
se co n d ary to ce lls e sp e cially in b rain ) sh rin kin g h yp e rn atre m ia)
o r swe llin g h yp o n atre m ia)
N o te s
ELECTROLYTE DISORDERS . . . CONT.
Table 6. Clinical As s e s s me nt of ECF Volume
(Total Body Na
+
)
Hypovole mic Hype rvole mic
Intravas cular
JVP d e cre ase d in cre ase d
b lo o d p re ssu re o rth o static d ro p n o rm al to in cre ase d
au scu ltatio n o f h e art tach ycard ia S 3
au scu ltatio n o f lu n gs n o rm al p u lm o n ary e d e m a
Inte rs titial
skin tu rgo r d e cre ase d e d e m a
Othe r
b o d y we igh t d e cre ase d in cre ase d
H ct, se ru m p ro te in in cre ase d d e cre ase d
Hyponatre mia
N a
+
H 2O N a
+
H 2O N a
+
H 2O N a
+
H 2O
n o rm al h yp o vo le m ic e u vo le m ic h yp e rvo le m ic
h yp o n atre m ia h yp o n atre m ia h yp o n atre m ia
e .g. d iu re tics, e .g. S IAD H ) e .g. C H F,
gastro e n te ritis) cirrh o sis +ascite s,
n e p h ro sis +e d e m a)
Hype rnatre mia
N a
+
H 2O N a
+
H 2O N a
+
H 2O N a
+
H 2O
n o rm al h yp o vo le m ic e u vo le m ic h yp e rvo le m ic
h yp e rn atre m ia h yp e rn atre m ia h yp e rn atre m ia
e .g. n o acce ss e .g. d iab e te s rare , e .g. N a
+
to wate r: co m a, in sip id u s) in ge stio n ,
b ab ie s) h yp e rto n ic salin e )
Figure 5. Clas s ification of Hyponatre mia/Hype rnatre mia
HYPONATREMIA
Clinical Fe ature s
J d e p e n d o n d e gre e o f h yp o n atre m ia an d m o re im p o rtan tly rap id ity o f o n se t
J n e u ro lo gic sym p to m s p re d o m in ate , se co n d ary to ce re b ral e d e m a
J e arly: n au se a, an o re xia, m alaise , le th argy, we akn e ss, so m n o le n ce
J late : h e ad ach e , d e cre ase d le ve l o f co n scio u sn e ss L O C ) , se izu re s, d e ath
J wo rk-u p in clu d e s E C F vo lu m e statu s asse ssm e n t, se ru m o sm o lality,
u rin e o sm o lality, u rin e N a
+
co n ce n tratio n , se ru m e le ctro lyte s,
glu co se , cre atin in e , an d u rin e R & M
N e p h ro lo gy 1 0 2000 M C C Q E R e vi e w N o te s
M C C Q E 2000 R e vi e w N o te s an d L e ctu re S e ri e s N e p h ro lo gy 1 1
N o te s
HYPONATREMIA
Hype r-Os molar Is o-Os molar (factitious ) Hypo-Os molar (dilutional)
e xtra o sm o le s in E C F n o rm al E C F o sm o lality b u t m o st co m m o n cau se s o f h yp o n atre m ia
d raw wate r o u t o f ce lls in cre ase d p lasm a so lid s
d ilu tin g th e N a
+
in E C F lip id s o r p ro te in s)
u su ally glu co se rare ly h yp e rlip id e m ia e .g. fam ilial,
m an n ito l) n e p h ro tic syn d ro m e , p an cre atitis)
e ve ry 1 0 m m o l/L in cre ase h yp e rp ro te in e m ia
in b lo o d glu co se re su lts e .g. m u ltip le m ye lo m a)
in 3 m m o l/L d e cre ase in N a
+
Hype rvole mic Euvole mic Hypovole mic
d iffe re n tial d iffe re n tial d iffe re n tial
C H F S IAD H re n al lo ss e .g. d iu re tics)
re n al failu re h yp o co rtiso l G I lo ss e .g. vo m itin g)
cirrh o sis an d ascite s h yp o th yro id ism h e m o rrh age
p sych o ge n ic p o lyd yp sia skin lo ss e .g. b u rn s)
tre atm e n t go al is N a
+
lo ss with tre at with wate r tre atm e n t go al is to re p le n ish lo st
re lative ly m o re wate r lo ss re strictio n an d so d iu m AN D wate r
tre at with salt an d wate r re strictio n tre at u n d e rlyin g tre at with n o rm al o r rare ly)
an d so m e tim e s d iu re tics d ise ase h yp e rto n ic salin e
fo r faste r tre atm e n t u se
n o rm al salin e +fu ro se m id e
Figure 6. An Approach to Hyponatre mia
J it is d an ge ro u s to co rre ct h yp o n atre m ia to o q u ickly
J h yp o n atre m ia with C N S sym p to m s is an e m e rge n cy
J can co n sid e r tre atm e n t in two ste p s: acu te co rre ctio n o f sym p to m atic
h yp o N a
+
an d lo n ge r te rm co rre ctio n o f asym p to m atic o r re sid u al
h yp o N a
+
J acu te co rre ctio n : u se n o rm al salin e o r h yp e rto n ic 3% o r 5%) salin e
J aim fo r raisin g th e N a
+
co n ce n tratio n b y 1 -2 m E q /L /h r o ve r 4-6 h o u rs
to valu e s b e twe e n 1 20 an d 1 25 m E q /L b u t n o m o re th an 8 m E q /L in
first d ay)
J can e stim ate th e so d iu m re q u ire m e n t as: [d e sire d N a
+
co n ce n tratio n
ch an ge x 0.6 x b o d y we igh t]
J rap id co rre ctio n o f h yp o n atre m ia can le ad to o sm o tic d e m ye lin atio n
m o st co m m o n ly o f th e ce n tral p o n s calle d C e n tral P o n tin e
M ye lin o sis - d ysarth ria, d ysp h agia, le th argy, co m a, p aralysis, ataxia,
p se u d o b u lb ar p alsy - wh ich can take we e ks to re co ve r an d u su ally
in cu rs p e rm an e n t se q u e lae )
Syndrome of Inappropriate Antidiure tic Hormone
Se cre tion (SIADH)
J ch aracte rize d b y a h yp e ro sm o lar u rin e o u t o f p ro p o rtio n to se ru m
o sm o lality, an d a n o n -lo w u rin e so d iu m e .g. > 30 m e q /L ) an d F E N a
+
J in ad d itio n to S IAD H , d ru gs wh ich cau se n au se a n arco tics,
an tin e o p lastic age n ts) N S AID s, b arb itu rate s, carb am aze p in e , T C A s,
o xyto cin m ay also cau se in cre ase d AD H as can trau m a an d su rge ry
Table 7. Dis orde rs As s ociate d with SIADH
Tumour Pulmonary CNS
o at ce ll C A p n e u m o n ia b rain tu m o u r
b ro n ch o ge n ic C A lu n g ab sce ss e n ce p h alitis
ad e n o C A o f p an cre as T B su b arach n o id h e m o rrh age
H o d gkin 's d ise ase acu te in te rm itte n t p o rp h yria
th ym o m a h e ad trau m a
N e p h ro lo gy 1 2 M C C Q E 2000 R e vi e w N o te s an d L e ctu re S e ri e s
N o te s
HYPERNATREMIA
J to o little wate r re lative to to tal b o d y N a
+
; always a h yp e ro sm o lar state
J m u ch le ss co m m o n th an h yp o n atre m ia b e cau se p ro te cte d b y th irst an d
th e in cre ase d re le ase o f AD H
Clinical Fe ature s
J d u e to b rain ce ll sh rin kage : alte re d m e n tal statu s, we akn e ss,
n e u ro m u scu lar irritab ility, fo cal n e u ro lo gic d e ficits, co m a, se izu re s, d e ath
p o lyu ria, th irst e vid e n ce o f vo lu m e d e p le tio n
J in cre ase d risk o f su b arach n o id o r in trace re b ral h e m o rrh age
J acu te in cre ase s are m o re d an ge ro u s sin ce in ch ro n ic in cre ase th e re is
co m p e n satio n b y in trace llu lar re te n tio n o f p o tassiu m , so d iu m , am in o
acid s, m yo in o sito l
HYPERNATREMIA
Hype rvole mic Non-Hype rvole mic
iatro ge n ic
h yp e rto n ic salin e o r N aH C O 3- Is p atie n t p u ttin g o u t a sm all vo lu m e 500 m L /d )
C u sh in g s syn d ro m e o f m axim ally co n ce n trate d > 800 m O sm /kg) u rin e ?
h yp e rald o ste ro n ism
tre at with salt re strictio n ,
d iu re tics, wate r N o Ye s
u rin e o sm o le in se n sib le wate r lo ss
e xcre tio n rate re sp irato ry
> 750 m O sm /d skin
G I d iarrh e a)
o sm o tic lactu lo se ,
m alab so rp tio n )
re m o te re n al lo ss
N o Ye s
ru le o u t D I: d iu re tics lo o p )
re n al re sp o n se o sm o tic d iu re sis
to d e sm o p re ssin - h yp e rglyce m ia
50% in cre ase - e n d o ge n o u s u re a with
in u rin e o sm o lality) e xce ss N G p ro te in fe e d s)
Ye s N o
C e n tral D I N e p h ro ge n ic D I
Figure 7. An Approach to Hype rnatre mia
Tre atme nt of Hype rnatre mia
J give n o rm al salin e first to b o o st E C F an d ach ie ve h e m o d yn am ic stab ility
J th e n P O o r N G tu b e wate r o r IV 1 /2 N S o r D 5W wh ile m o n ito rin g N a
+
J can e stim ate fre e wate r d e ficit b y th e fo rm u la [N a
+
] 1 40) /1 40 x to tal
b o d y wate r wh e re to tal b o d y wate r is we igh t x 0.5) fo r m e n an d
we igh t x 0.4) fo r wo m e n
J aim to re p le n ish th is d e ficit o ve r 48-72 h o u rs, lo we rin g se ru m N a
+
b y
n o m o re th an 0.5 m E q /L /h 1 2 m E q /L /d )
J rap id co rre ctio n m ay le ad to ce re b ral e d e m a; th e b rain cre ate s
ad d itio n al in trace llu lar o sm o le s in th e se ttin g o f h yp e rn atre m ia in
o rd e r to re tain wate r; if vo lu m e is th e n q u ickly re sto re d flu id is
d rawn in to th e b rain cau sin g e d e m a
J b e sid e s co rre ctin g d e ficit, n e e d to give flu id s fo r m ain te n an ce an d
o n go in g lo sse s e .g. 1 /2 n o rm al salin e ) ; th is is h e lp e d b y m o n ito rin g
u rin e /sto o l lo sse s an d co m p o sitio n
Diabe te s Ins ipidus (DI)
J m ay b e ce n tral o r n e p h ro ge n ic
J ce n tral D I e tio lo gy: n e u ro su rge ry, gran u lo m ato u s d ise ase s, trau m a, vascu lar e ve n ts, C A
J n e p h ro ge n ic D I e tio lo gy: lith iu m m o st co m m o n ) , h yp o K
+
, h yp e rC a
+
J d iagn o sis o f D iab e te s In sip id u s
th e u rin e 24 h o u r o sm o le e xcre tio n is n o t e le vate d
H 2O d e p rivatio n fo r 1 2-1 8 h o u rs: if fails to co n ce n trate u rin e ,
D I p ro b ab ly p re se n t
if th e n re sp o n d s to e xo ge n o u s AD H 1 0 m icro gram s in tran asally) ,
ce n tral D I p re se n t an d tre at with D D AVP AD H an alo gu e )
if still fails to co n ce n trate u rin e , n e p h ro ge n ic D I p re se n t; m u st
tre at with wate r D 5W o r P O ) , as kid n e ys d o n o t re sp o n d to
AD H ; th iazid e s m ay h e lp as we ll
N o te s
HYPOKALEMIA
Factors which Incre as e Re nal K
+
Los s
J in cre ase d d istal tu b u lar flo w rate an d N a
+
d e live ry
J in cre ase d ald o ste ro n e
J in cre ase d u n re ab so rb ab le an io n s in tu b u le lu m e n : P O 4
3
, H C O 3
, p e n icillin
J K
+
e xcre tio n is re fle cte d b y th e fo llo win g fo rm u la
K
+
E xcre tio n = U rin e flo w rate ) U rin e K
+
co n ce n tratio n )
Caus e s of Hypokale mia
J d e cre ase d in take u n u su al as a so le cau se b u t m ay e xace rb ate o th e r cau se s)
lim ite d d ie tary in take
clay in ge stio n
J re d istrib u tio n in to ce lls
m e tab o lic alkalo sis
h o rm o n e s: in su lin , b e ta-2 ago n ists, alp h a-b lo cke rs
u p take in to n e wly fo rm in g b lo o d ce lls: vitam in B 1 2 in je ctio n s in p e rn icio u s
an e m ia, co lo n y stim u latin g facto rs in cre asin g WB C p ro d u ctio n
J in cre ase d lo sse s
G I: d iarrh e a e sp e cially se cre to ry: carb o h yd rate in to le ran ce , lactu lo se )
skin : swe atin g
re n al
in cre ase d d istal flo w: d iu re tics, o sm o tic d iu re sis h yp e rglyce m ia, u re a)
in cre ase d K
+
se cre tio n : p rim ary h yp e rald o ste ro n ism , se co n d ary
h yp e rald o ste ro n ism re n in se cre tin g tu m o u rs, re n al arte ry ste n o sis,
h yp o vo le m ia) , co n ge n ital ad re n al h yp e rp lasia, B artte rs syn d ro m e , C u sh in g s
syn d ro m e , L id d le s syn d ro m e , vo m itin g, e xce ss N G su ctio n , D K A,
p e n icillin s, p ro xim al Typ e 2) R TA
Clinical Fe ature s
J sym p to m s rare u n til K
+
< 3.0 m E q /L
J first se e fatigu e , m u scle we akn e ss, cram p s, m yalgia, an d late r can p ro gre ss to
h yp o ve n tilatio n , p aralytic ile u s, rh ab d o m yo lysis, arrh yth m ias
J E C G ch an ge s are m o re p re d ictive o f clin ical p ictu re th an K
+
le ve ls
J E C G ch an ge s
flatte n e d o r in ve rte d T wave s
U wave s
d e p re sse d S T se gm e n t
p ro lo n gatio n o f Q -U in te rval
with se ve re h yp o K
+
se e P -R p ro lo n gatio n , wid e Q R S ,
arrh yth m ias
J in cre ase s risk o f d igitalis to xicity
J can d istin gu ish d istal re n al fro m o th e r cau se s o f h yp o K
+
b y lo o kin g at th e T T K G :
T T K G > 4 su gge sts K
+
lo ss d u e to se cre tio n at th e le ve l o f th e d istal tu b u le s
T T K G < 2 su gge sts n o n re n al o r p ro xim al re n al lo sse s o sm o tic d iu re sis, d iu re tics)
J can also asse ss se ru m re n in an d ald o ste ro n e , as we ll as acid -b ase statu s, u rin ary
e le ctro lyte s, an d se ru m M g
2+
fo r cau se s o f h yp o kale m ia
Tre atme nt
J se ru m le ve ls d o n o t co rre late we ll with d e ficit can h ave fro m 200-600
o r m o re m m o l d e ficit)
J h yp o kale m ia d u e to ce llu lar sh ifts sh o u ld b e co rre cte d with P O K
+
n o t IV
J risk o f h yp e rkale m ia se co n d ary to h yp o K
+
su p p le m e n ts is e sp e cially
h igh in e ld e rly, d iab e tics, an d p atie n ts with d e cre ase d re n al fu n ctio n
J if u rin e o u tp u t an d re n al fu n ctio n are im p aire d , co rre ct with e xtre m e cau tio n
J o ral so u rce s - fo o d , tab le ts
J IV - u su ally K C l m ay u se K H C O 3
o r K citrate in R TA o r d iarrh e a)
in itially u se salin e so lu tio n s to m ix, n o t d e xtro se , sin ce th is
m ay e xace rb ate h yp o K
+
via in su lin re le ase
m axim u m 40 m m o l/L via p e rip h e ral ve in , 60 m m o l/L via ce n tral ve in
m axim u m in fu sio n 20 m m o l/h r
HYPERKALEMIA
Caus e s
J factitio u s p se u d o h yp e rkale m ia)
co m m o n
p ro lo n ge d u se o f a to u rn iq u e t
sam p le h e m o lysis
N o te s
le u ko cyto sis, th ro m b o cyto sis
d rawin g b lo o d o u t o f ve in in to wh ich IV is ru n n in g
J in cre ase d in take rare ly so le ly re sp o n sib le )
m ay b e iatro ge n ic K
+
p ills, IV K C l) e sp e cially in p atie n ts
with o th e r co n d itio n s se e b e lo w) p re d isp o sin g to h yp e rkale m ia
J ce llu lar re le ase
in travascu lar h e m o lysis, tu m o u r lysis syn d ro m e , rh ab d o m yo lysis
in su lin d e ficie n cy
h yp e ro sm o lar state s e .g. h yp e rglyce m ia)
m e tab o lic acid o sis e sp e cially in o rgan ic)
b e ta-b lo cke rs rare ly a so le cau se )
d igitalis o ve rd o se
d e p o larizin g m u scle re laxan ts su ccin ylch o lin e )
J d e cre ase d o u tp u t
d e cre ase d d istal so lu te d e live ry
E C F vo lu m e co n tractio n
p ro te in m aln u tritio n
AR F, C R F
N S AID s in re n al in su fficie n cy
in ad e q u ate se cre tio n o f K
+
in d istal n e p h ro n
h yp o re n i n e m i c h yp o ald o ste ro n i sm re n al i n su ffi ci e n cy
d iab e tic n e p h ro p ath y, ch ro n ic tu b u lo in te rstitial d ise ase )
1 h yp o ald o ste ro n ism ad re n al in su fficie n cy, ad re n al
e n zym e d e ficie n cy)
2 h yp o ald o ste ro n ism AC E in h ib ito rs, N S AID s, h e p arin )
re sistan ce to ald o ste ro n e p se u d o h yp o ald o ste ro n ism ,
tu b u lo in te rstitial d ise ase , K
+
sp arin g d iu re tics,
trim e th o p rim , p e n tam id in e )
e n h an ce d C l
re ab so rp tio n ch lo rid e sh u n t) in G o rd o n s
syn d ro m e , cyclo sp o rin , h yp e rK
+
, d istal Typ e 4) R TA
Clinical Fe ature s
J u su ally asym p to m atic b u t m ay d e ve lo p m u scle we akn e ss, p are sth e sias,
are fle xia, asce n d in g p aralysis, an d h yp o ve n tilatio n
J im p aire d am m o n iage n e sis an d m e tab o lic acid o sis
J if se ve re E C G ch an ge s an d card io to xicity n o t co rre late we ll with K
+
co n ce n tratio n )
p e ake d an d n arro w T wave s
d e cre ase d am p litu d e an d e ve n tu al lo ss o f P wave s
p ro lo n ge d P R in te rval
wid e n in g o f Q R S an d e ve n tu al m e rgin g with T wave sin e -wave p atte rn )
AV b lo ck
ve n tricu lar fib rillatio n , asysto le
J can m e asu re T T K G : valu e s le ss th an 1 0 su gge st in ad e q u ate K
+
se cre tio n
at th e d istal tu b u le s se e ab o ve fo r p o te n tial cau se s)
Tre atme nt
J acu te th e rap y is warran te d if K
+
h igh , sym p to m s p re se n t, E C G ch an ge s
p e rfo rm E C G , re p e at b lo o d te st, r/o p se u d o h yp e rkale m ia
h o ld e xo ge n o u s K
+
an d K
+
re tain in g m e d s
C a
2+
glu co n ate 1 -2 am p s O N LY 1 0 m L o f 1 0% so lu tio n ) IV
card io p ro te ctan t) ; givin g m o re can re su lt in calciu m to xicity an d d e ath !
re gu lar in su lin In su lin R ) 1 0-20 u n its IV, with 1 /2 to 1 am p D 50W
N aH C O 3
1 -3 am p s give n as 3 am p s o f 7.5% o r 8.4%

N aH C O 3
in 1 L D 5W)
2-ago n ist alb u te ro l = ve n to lin ) in n e b u lize d fo rm
catio n -e xch an ge re sin s: K aye xalate o r C alciu m R e so n iu m
d ialysis re n al failu re , life th re ate n in g h yp e rK
+
u n re sp o n sive to th e rap y)
Clinical Pe arl
J In diabe tics with incre as e d K
+
and hype rglyce mia, s imply
give ins ulin to re s tore e uglyce mia and monitor K
+
rathe r
than initiating K
+
lowe ring the rapy
N o te s
ACID-BASE DISORDERS
J an ap p ro ach se e F igu re 8)
lo o k at arte rial p H to e stab lish acid e m ia vs. alkale m ia
lo o k at H C O 3
an d p C O 2 to e stab lish m ajo r p ro ce ss re sp irato ry/m e tab o lic)

d e te rm in e e xp e cte d an d actu al co m p e n satio n s to e stab lish
se co n d ary p ro ce ss
d e te rm in e an io n gap AG ) an d co m p are AG with H C O 3
ch an ge s
in cre ase in AG sh o u ld e q u al d e cre ase in H C O 3
in p u re
AG acid o sis)
if AG acid o sis, calcu late o sm o lar gap to d e te ct n o n -io n ic o sm o le s alco h o ls)
J n o rm al H C O 3
= 25 m E q /L
J n o rm al p C O 2 = 40 m m H g
pH
low normal high
ACIDEMIA NO DISTURBANCE ALKALEMIA
OR
MIXED DISTURBANCE
lo w h igh m ixe d if p C O 2 +H C O 3
h igh lo w
H C O 3
p C O 2 b o th lo w o r b o th h igh H C O 3
p C O 2
o r p lasm a AG wid e
m e tab o lic re sp irato ry m e tab o lic re sp irato ry
acid o sis acid o sis alkalo sis alkalo sis
Figure 8. An Approach to Acid-Bas e Dis orde rs
RENAL CONTRIBUTION TO ACID-BASE BALANCE
J p ro xim al tu b u le re ab so rb s filte re d H C O 3
stim u late d b y AII, h yp o vo le m ia)

J p ro xim al tu b u le ge n e rate s am m o n iu m an d H C O 3
stim u late d b y AII, h yp o vo le m ia,

h yp o kale m ia, in trace llu lar acid o sis)
J d istal tu b u le e xcre te s H
+
p ro d u ce d b y th e b o d y stim u late d b y
in trace llu lar acid o sis, h yp o kale m ia, h yp o vo le m ia, ald o ste ro n e )
J d ysfu n ctio n o f e ith e r o f th e se tu b u lar p ro ce sse s m ay cau se
syste m ic acid e m ia h e n ce R TA)
J Typ e I R TA d istal)
u n ab le to fu lly e xcre te d aily H
+
lo ad an d accu m u late s in b o d y
J Typ e II R TA p ro xim al)
im p aire d H C O 3
re ab so rp tio n : lo st in u rin e an d b u ffe r is d e p le te d

J Typ e IV R TA
d e cre ase d ald o ste ro n e activity o r ald o ste ro n e re sp o n sive n e ss
d istal tu b u le can t e xcre te H
+
, K
+
in su fficie n t am m o n iage n e sis to ge n e rate H C O 3
an d to acce p t H
+
d istally
asso ciate d with h yp e rkale m ia u n like p ro xim al an d d istal R TA)
1 METABOLIC ACIDOSIS
J to d e te rm in e cau se , first calcu late th e AG in b lo o d sam p le
= N a
+
H C O 3
+C l
)
J in cre ase d AG m e tab o lic acid o sis
ke to acid o sis
lactic acid o sis, D -lactic acid o sis
re n al failu re with G F R < 20% o f n o rm al
d ru gs: salicylate s, e th yle n e glyco l, m e th an o l
o sm o lar gap = m e asu re d p lasm a o sm o lality m in u s
calcu late d p lasm a o sm o lality 2N a
+
+B U N +glu co se )
n o rm al o sm o lar gap < 1 0 m o sm /kg
if gap > 1 0, co n sid e r u n m e asu re d o sm o le s e .g. alco h o ls)
J n o rm al AG m e tab o lic acid o sis
lo ss o f H C O 3
in u rin e p ro xim al R TA) o r G I tract d iarrh e a)

failu re o f kid n e y to m ake n e w H C O 3
d istal R TA)
J fo r m e tab o lic acid o sis, if th e fall in H C O 3
m atch e s th e rise in AG ,
it is a p u re AG acid o sis
N o te s
ACID-BASE DISORDERS . . . CONT.
J if th e fall in H C O 3
> rise in an io n gap , co n sid e r m ixe d AG /n o n -AG

m e tab o lic acid o sis i.e . re n al failu re an d d iarrh e a)
J if AG rise is > H C O 3
fall, co n sid e r a co n cu rre n t m e tab o lic o r re sp irato ry alkalo sis

Re s piratory Compe ns ation in Me tabolic Acidos is
J h yp e rve n tilatio n su ch th at th e d e cre ase in p C O 2 = d e cre ase H C O 3
e xp e cte d : 1 -1 .3 m m H g d e cre ase d P C O 2 fo r e ve ry 1 m E q /L

d e cre ase d H C O 3
if p C O 2 d e cre ase s m o re th an e xp e cte d , th e re is also a

p rim ary re sp irato ry alkalo sis
if p C O 2 d e cre ase s le ss th an e xp e cte d , th e re is also a
p rim ary re sp irato ry acid o sis
e xam p le :
if H C O 3
= 1 5 d e cre ase b y 1 0) ,
e xp e cte d p C O 2 = 27-30 40-[1 0 to 1 3]
if in ste ad p C O 2 = 35, a re sp irato ry acid o sis is also
p re se n t o r, if m e asu re d p C O 2 = 20, a re sp irato ry
alkalo sis is also p re se n t
1 METABOLIC ALKALOSIS
J e tio lo gy
ge n e ratio n o f n e w H C O 3
G I lo ss vo m itin g, N G su ctio n )
d iu re tics
m ilk alkali syn d ro m e , e xo ge n o u s N aH C O 3
h yp o kale m ia
im p aire d H C O 3
e xcre tio n
re d u ce d G F R
vo lu m e co n tractio n alkalo sis
p rim ary o r se co n d ary h yp e rald o ste ro n ism ;
ald o ste ro n e cau se s gre ate r H
+
lo ss via D C T H
+
p u m p
le ad in g to H C O 3
ge n e ratio n ; ald o ste ro n e p ro m o te s h yp o kale m ia

wh ich is a stim u lu s fo r am m o n iage n e sis an d H C O 3
ge n e ratio n
o th e r
B artte rs syn d ro m e
h yp o m agn e se m ia
Cate gorie s and Tre atme nt
J salin e ch lo rid e ) se n sitive m e tab o lic alkalo sis m o st co m m o n )
E C F vo lu m e d e p le tio n
tre atm e n t: N aC l vo lu m e re p le tio n )
J salin e ch lo rid e ) in se n sitive m e tab o lic alkalo sis
E C F vo lu m e n o rm al o r h igh
u su ally ald o ste ro n e o r glu co co rtico id e xce ss
tre atm e n t in vo lve s co rre ctio n o f u n d e rlyin g d ise ase ,
re p le n ish in g K
+
an d M g
+
d e ficits, an d p o ssib ly sp iro n o lacto n e
Re s piratory Compe ns ation in Me tabolic Alkalos is
J h yp o ve n tilatio n an u p p e r lim it to co m p e n satio n e xists - b re ath in g
can n o t b e sto p p e d )
J p C O 2 in cre ase s 0.5-0.7 m m H g fo r e ve ry 1 m E q /L in cre ase in H C O 3
1 RESPIRATORY ACIDOSIS
(HYPOVENTILATION)
Caus e s
J se ve re C O P D , d ru gs se d ative s) , alte re d le ve l o f co n scio u sn e ss,
sle e p ap n e a, n e u ro m u scu lar d iso rd e rs
Re nal Compe ns ation in Re s piratory Acidos is
J th e kid n e y re tain s H C O 3
to co m b at th e acid e m ia
J acu te ly, in cre ase in H C O 3
= 0.1 x in cre ase in p C O 2

n o tim e fo r re n al co m p e n satio n )
J ch ro n ically, in cre ase in H C O 3
= 0.3 x in cre ase in p C O 2

kid n e ys are d o in g a b e tte r jo b o f re d u cin g acid e m ia)
N o te s
ACID-BASE DISORDERS . . . CONT.
1 RESPIRATORY ALKALOSIS
(HYPERVENTILATION)
Caus e s
J p n e u m o n ia, se p sis, p u lm o n ary e m b o lism , live r d ise ase ,
p re gn an cy, salicylate s, h e art failu re
Re nal Compe ns ation in Re s piratory Alkalos is
J th e kid n e y e xcre te s H C O 3
J acu te ly, d e cre ase in H C O 3
= 0.2 x d e cre ase in p C O 2

J ch ro n ically, d e cre ase in H C O 3
= 0.5 x d e cre ase in p C O 2

J re m e m b e r - a p atie n t with d e cre ase d H C O 3
m ay sim p ly b e
h yp e rve n tilatin g 1 re sp irato ry alkalo sis) an d n o t acid e m ic
d o n t give H C O 3
with o u t ch e ckin g syste m ic p H )

MIXED DISTURBANCES
J m ixe d acid -b ase d iso rd e rs id e n tifie d b y n e u tral p H with p C O 2 an d
H C O 3
th at are b o th lo w o r b o th h igh o r wid e p lasm a AG

J tre atm e n t with H C O 3
) is gu id e d b y arte rial b lo o d gas p H , n o t

sim p ly H C O 3
le ve l alo n e a co m m o n m istake ! )
e xam p le : p atie n t with live r d ise ase o n sp iro n o lacto n e
acid e m ia d u e to sp iro n o lacto n e ald o ste ro n e in h ib itio n )
alkale m ia d u e to h yp e rve n tilatio n o f live r d ise ase
b alan ce : p H = 7.40, H C O 3
= 1 2 m E q /L re sp irato ry
alkalo sis an d m e tab o lic acid o sis b o th lo we r H C O 3
)
th is p atie n t h as a n e u tral p H an d d o e s n o t re q u ire H C O 3
RENAL FAILURE
Table 8. Clas s ification of Re nal Failure
Acute Chronic
his tory ab ru p t o n se t o f h isto ry o f kid n e y p ro b le m s,
m u ltisyste m illn e ss h yp e rte n sio n
p re vio u sly kn o wn p re vio u s p ro b le m s in
n o rm al fu n ctio n p re gn an cy
phys ical d e p e n d s o n p e rip h e ral n e u ro p ath y
u n d e rlyin g d ise ase re tin o p ath y
rash LVH
jo in t e ffu sio n le ss e n ce p h alo p ath y
m arke d e d e m a kid n e ys sm all e xce p t in
e n ce p h alo p ath y P C K D , D M , am ylo id
kid n e ys n o rm al size o r swo lle n
lab n o rm al to sligh t an e m ia
an e m ia
se ve re h yp e rkale m ia m o d e st h yp e rkale m ia
n o rm al to sligh t
h yp o calce m ia m arke d h yp o calce m ia
n o rm al to sligh t
h yp e rp h o sp h ate m ia m arke d h yp e rp h o sp h ate m ia
n o rm al alkalin e p h o sp h ate in cre ase d alkalin e p h o sp h ate
N o te s
ACUTE RENAL FAILURE
ARF
P re -R e n al R e n al P o st-R e n al
e vid e n ce o f vo lu m e d e p le tio n u p p e r tract: o b stru ctio n b y clo t,
d e cre ase d e ffe ctive circu latin g vo lu m e tu m o u r o r sto n e , e xte rn al
u se o f N S AID s o r AC E Is co m p re ssio n
re n o vascu lar d ise ase lo we r tract: B P H , ce rvical C A, clo t,
sto n e , strictu re , au to n o m ic
d ysfu n ctio n
U /S sh o ws h yd ro n e p h ro sis
Vascu lar Tu b u lo -In te rstitial G lo m e ru lar < 5%)
m align an t H T N
ch o le ste ro l e m b o li
H U S /T T P
AT N AIN
isch e m ic to xin
e xo ge n o u s e n d o ge n o u s
Figure 9. Acute Re nal Failure
J d e fin itio n : ab ru p t d e clin e in re n al fu n ctio n le ad in g to in cre ase d
u re a an d in cre ase d se ru m cre atin in e
J p lasm a cre atin in e rise s 50-1 75 M /24 h rs - if rise is gre ate r, m ay
b e rh ab d o m yo lysis, catab o lic p atie n t, o r to tal re n al sh u td o wn
TREATMENT
J always lo o k fo r an d co rre ct p re -re n al an d p o st-re n al cau se s first
always lo o k fo r e vid e n ce o f ch ro n ic re n al failu re
always p lace F o le y cath e te r in p atie n t wh ile in ve stigatin g th e
cau se o f AR F
always ge t an ab d o m in al U /S u n le ss cau se is ve ry o b vio u s
2 re aso n s
ru le o u t p o st-re n al cau se s o f re n al failu re
asse ss size o f th e kid n e ys if kid n e ys sm all;
in d icate s an u n d e rlyin g ch ro n ic co n d itio n )
Pre -Re nal
J co rre ct E C F vo lu m e d e p le tio n with n o rm al salin e n o t D 5W)
J im p ro ve card iac o u tp u t if p o ssib le )
Re nal
J re m o ve to xic/isch e m ic in su lts
J atte n tio n to flu id statu s
J su p p o rtive tre atm e n t o f:
in travascu lar vo lu m e o ve rlo ad
h yp e rkale m ia
h yp e rp h o sp h ate m ia
m e tab o lic acid o sis
h yp o calce m ia
h yp e rm agn e se m ia
Pos t-Re nal
J re lie ve o b stru ctio n sp e cific th e rap y is e tio lo gy d e p e n d e n t)
J p o ssib le th e rap ie s in clu d e :
in -d we llin g b lad d e r cath e te r
n e p h ro sto m y
ste n tin g
Clinical Pe arl
J Pos t-re nal failure not ne ce s s arily as s ociate d with anuria or e ve n oliguria
N o te s
ACUTE RENAL FAILURE . . . CONT.
Supportive The rapy For All Caus e s of Re nal Failure
J d ru g m o d ificatio n : avo id n e p h ro to xic d ru gs, d o sage m o d ificatio n
J p o tassiu m re strictio n
J salt re strictio n
INDICATIONS FOR DIALYSIS IN ARF
(vs . IN CRF)
J E C F vo lu m e o ve rlo ad u n re sp o n sive to d iu re tics
J h yp e rkale m ia u n re sp o n sive to tre atm e n t
J se ve re acid o sis
J u re m ic p e ricard itis
J u re m ic e n ce p h alo p ath y - alte ratio n o f m e n tal statu s, aste rixis,
se izu re s, co m a
J u re m ic p o lyn e u ro p ath y - m yo clo n u s, twitch in e ss
J e vil h u m o u rs - e ve n in ab se n ce o f ab o ve in d icatio n s, a ve ry h igh
u re a o r cre atin in e , o r e ve n a n o t-so -h igh u re a o r cre atin in e in an
o ligu ric/catab o lic e .g. p o st-o p ) p atie n t
PROGNOSIS
J h igh m o rtality with m u ltio rgan failu re
J re n al p ro gn o sis re late d to se ve rity o f u n d e rlyin g d ise ase an d
su b se q u e n t co m p licatio n s
CHRONIC RENAL FAILURE
J m an y e tio lo gie s: co n tin u u m o f p ro gre ssive n e p h ro n lo ss an d d e clin in g
re n al fu n ctio n
J asym p to m atic u n til se ve re in su fficie n cy d e ve lo p s
J re gio n al variatio n in le ad in g cau se s wo rld wid e
in N o rth Am e rica: d iab e te s > 30%) , h yp e rte n sive re n al
d ise ase 23%) ch ro n ic G N 1 0%) e .g. IgA n e p h ro p ath y) ,
p o lycystic kid n e y d ise ase 5%)
J fre q u e n tly p atie n ts p re se n t at e n d -stage with sm all, co n tracte d
kid n e ys, u n kn o wn e tio lo gy
CLASSIFICATION
J glo m e ru lar: p rim ary o r se co n d ary glo m e ru lo n e p h ritis
J tu b u lo in te rstitial d ise ase e .g. au to im m u n e in te rstitial n e p h ritis)
J vascu lar e .g. D M , H T N )
J h e re d itary e .g. au to so m al d o m in an t p o lycystic kid n e y d ise ase , Alp o rt s)
CLINICAL FEATURES OF UREMIA
J C N S : co n fu sio n , in ab ility to co n ce n trate , fatigu e , aste rixis, re stle ss
le g syn d ro m e , se n so ry an d m o to r n e u ro p ath y
J C VS : C H F, H T N with targe t o rgan d am age LVH , re tin o p ath y) ,
p e ricard itis, acce le rate d ath e ro scle ro sis
J G I: n au se a, vo m itin g, an o re xia, u p p e r G I h e m o rrh age , co n stip atio n
J S K IN : p ru ritu s, e cch ym o se s, h yp e rp igm e n tatio n , sallo w co lo u r , u re m ic fro st
J E N D O C R IN E : h yp e rlip id e m ia, d e cre ase d se x h o rm o n e le ve ls,
d e cre ase d se x d rive , m e n stru al irre gu laritie s, se co n d ary h yp e rp arath yro id ism
J H E M AT O L O G IC AL : n o rm o cytic an e m ia, b le e d in g, im p aire d ce llu lar im m u n ity
J M S K : n o ctu rn al m u scle cram p in g
COMPLICATIONS
J u re m ia/azo te m ia: se ru m cre atin in e m ay n o t o b vio u sly rise u n til
G F R is < 50% n o rm al
J wate r: in ab ility to co n ce n trate o r d ilu te u rin e ; p o lyu ria, n o ctu ria
J p o tassiu m im b alan ce : d u rin g ad van ce d re n al failu re
J an e m ia: d u e to d e cre ase d e ryth ro p o ie tin p ro d u ctio n n o rm o cytic)
J h yp e rp h o sp h ate m ia, h yp o calce m ia, d e cre ase d vitam in D p ro d u ctio n an d
se co n d ary h yp e rp arath yro id ism
J re n al o ste o d ystro p h y 2 h yp e rp arath yro id ism = o ste itis fib ro sa cystica,
an d o ste o m alacia)
J acid -b ase : n o rm al AG m e tab o lic acid o sis p ro gre ssin g to in cre ase d
AG m e tab o lic acid o sis wh e n G F R is 20% o f n o rm al
TREATMENT
J re strictio n o f N a
+
, K
+
40 m E q /d ay) , H 2O , P O 4
3
800-1 000 m g/d ay) ,
p ro te in m o d e stly 0.9 g/kg/d ay)
N o te s
CHRONIC RENAL FAILURE . . . CONT.
J ad ju st d ru g d o se s
J tre at H T N : d ru gs e sp e cially AC E -in h ib ito rs) , so d iu m re strictio n targe t B P < 1 25/75)
J tre at re n al o ste o d ystro p h y p h o sp h ate b in d e rs su ch as calciu m carb o n ate if
h yp e rp h o sp h ate m ic)
J calciu m su p p le m e n ts, activate d vitam in D an alo gu e s e .g. R o caltro l)
J co rre ctio n o f acid o sis with o ral N aH C O 3
wh e n se ru m H C O 3
is < 20 m E q /L
J e ryth ro p o ie tin in an e m ia h e m ato crit < 30%)
INDICATIONS FOR DIALYSIS IN CRF
J m ay b e sam e as AR F
J m o re co m m o n ly = d win d le s
an o re xia, n au se a, vo m itin g, se ve re fatigu e , p ru ritu s, m u scle cram p s
d ialyse wh e n cre atin in e cle aran ce < 1 0% o f n o rm al < 0.1 5 m l/se co n d )
J d iab e tics le ss to le ran t o f u re m ia, d ialyse wh e n cre atin in e cle aran ce < 1 5% o f n o rm al
J p ro gn o sis: all with p ro gre ssive re n al failu re p ro gre ss to d ialysis/tran sp lan t
DIALYSIS AND RENAL
TRANSPLANTATION
DIALYSIS
Goals
J u ltrafiltratio n = flu id re m o val
in ab se n ce o f re n al fu n ctio n , d aily flu id in take m u st b e
re m o ve d le ss b o we l an d in se n sib le lo sse s)
th e wate r re m o ve d is n o t p u re wate r, it d rags alo n g o th e r
so lu te s so lve n t d rag , co n ve ctio n )
J so lu te re m o val b y d iffu sio n an d u ltrafiltratio n )
p ro d u cts o f m e tab o lism u re a, u re m ic to xin s , e tc...) an d
o th e r so lu te s K
+
, p h o sp h ate s) n o rm ally e xcre te d b y
kid n e ys are re m o ve d
Pe ritone al Dialys is
J slo we r th an h e m o d ialysis b u t le ss stre ssfu l an d can b e d o n e at h o m e
J in -d we llin g cath e te r in se rte d th ro u gh ab d o m in al wall in to p e rito n e al cavity
J h igh d e xtro se flu id in fu se d in to cavity, d we lls fo r a variab le p e rio d , th e n
d rain e d
J u ltrafiltratio n o ccu rs acro ss p e rito n e u m via o sm o tic p re ssu re o f
d e xtro se in d ialysate wate r m o ve s fro m p lasm a to h yp e r-o sm o lar d ialysate ) ,
e .g. 2 L in to b lo o d an d 2.5 L o u t o f b lo o d m e an s 0.5 L u ltrafilte re d
J so lu te re m o val via d iffu sio n d o wn co n ce n tratio n grad ie n t
i.e . u re a fro m 30 m m o l/L in p lasm a to 0 m m o l/L in d ialysate )
an d also b y co n ve ctio n alo n g with u ltrafiltrate
J p ro b le m s: in fe ctio n at cath e te r e xit site , b acte rial p e rito n itis, lo n g
te rm m e tab o lic e ffe cts o f glu co se lo ad in g
He modialys is
J b lo o d trave ls alo n g tu b in g fro m ve sse l to artificial kid n e y wh e re it
is in co n tact with flu id o n o th e r sid e o f se m i-p e rm e ab le artificial
m e m b ran e
J u ltrafiltratio n via h yd rau lic p re ssu re im p o se d acro ss m e m b ran e o f
artificial kid n e y
J so lu te re m o val via co n ce n tratio n grad ie n t an d b y co n ve ctio n with
u ltrafilte re d vo lu m e
J p ro b le m s: vascu lar acce ss ve in s clo t, give o u t) , b le e d in g d u e to
h e p arin izatio n , h e m o d yn am ic stre ss o f e xtraco rp o re al b lo o d circu it,
d ise q u ilib riu m syn d ro m e
Clinical Pe arl
J The mos t common caus e of morbidity and mortality in an e nd-s tage re nal
dis e as e patie nt is cardiovas cular complications (CAD, CVD, PVD, CHF)
RENAL TRANSPLANTATION
J b e st way to re ve rse u re m ic sign s an d sym p to m s
J 2 typ e s: cad ave r d o n o r, livin g d o n o r re late d o r u n re late d )
J kid n e y tran sp lan te d in to iliac fo ssa, re n al arte ry an asto m o se d to in te rn al iliac arte ry
N o te s
DIALYSIS AND RENAL
TRANSPLANTATION . . . CONT.
Immunos uppre s s ion
J ch ro n ic th e rap y
co rtico ste ro id s
azath io p rin e
cyclo sp o rin e
C e llce p t M M F )
Tacro lim u s F K 506)
J tre atm e n t o f acu te re je ctio n s
an ti-T-ce ll m o n o clo n al an tib o d y O K T 3)
an ti-th ym o cyte glo b u lin R AT S )
Re je ction
J typ e s:
h yp e racu te with in 0.5 h rs, in o p e ratin g ro o m )
acu te : vascu lar, ce llu lar
ch ro n ic
Proble ms
J im m u n o su p p re ssio n : in fe ctio n s, n e o p lasm s
J re je ctio n
J cyclo sp o rin e n e p h ro p ath y
GLOMERULONEPHRITIS
GENERAL CONSIDERATIONS
Clinical Fe ature s
J d e p e n d s if 1 o r 2
J 1 G N
e d e m a, H T N , fatigu e , u re m ia, d e cre ase d u rin e
vo lu m e , h e m atu ria o r co la-co lo u re d u rin e , flan k d isco m fo rt
p re se n ts with n e p h ro tic syn d ro m e , n e p h ritic syn d ro m e ,
o r a m ixtu re o f b o th
J 2 G N
all o f ab o ve , p lu s sym p to m s an d sign s o f u n d e rlyin g d ise ase
co llage n vascu lar: rash , R ayn au d s, p h o to se n sitivity,
p o lyarth ralgia, o titis, an d sin u sitis
vascu litis: rash , ab d o m in al p ain , m o n o n e u ritis m u ltip le x
S L E : rash , jo in t e ffu sio n , p le u ritis, p e ricard itis
We ge n e rs G ran u lo m ato sis: n asal d e fo rm ity, m id d le e ar e ffu sio n
G o o d p astu re s syn d ro m e : h e m o p tysis, S O B , fle e tin g
p u lm o n ary in filtrate s
Ne phrotic Syndrome
J p ro te in u ria o f > 3.5 g/24 h r
J h yp o alb u m in e m ia
J e d e m a
J h yp e rlip id e m ia
J h yp e rco agu ab ility
Diffe re ntial Diagnos is of Ne phrotic Syndrome
J 1
m in im al ch an ge d ise ase m o st co m m o n cau se in ch ild re n )
m e m b ran o u s glo m e ru lo p ath y m o st co m m o n cau se o f
id io p ath ic n e p h ro tic syn d ro m e in ad u lts)
fo cal scle ro sis
J 2
d iab e tic n e p h ro p ath y
am ylo id o sis
d ru gs go ld , p e n icillam in e )
Laboratory
J u rin alysis
J b lo o d te sts
J 1 G N : cre atin in e , alb u m in , ch o le ste ro l
N o te s
GLOMERULONEPHRITIS . . . CONT.
J 2 G N : C B C , E S R , im m u n o e le ctro p h o re sis, co m p le m e n ts, AN A, AN C A,
cryo glo b u lin s, h e p atitis B se ro lo gy, h e p atitis C se ro lo gy, VD R L , H IV
J 24 h r u rin e cre atin in e an d p ro te in
J rad io lo gy
C XR in filtrate s, C H F, p le u ral e ffu sio n )
re n al u ltraso u n d
J re n al b io p sy in d icatio n s:
n e p h ro tic syn d ro m e , u n le ss yo u n g p atie n t assu m e
m in im al ch an ge d ise ase )
p ro gre ssive re n al im p airm e n t o f u n kn o wn e tio lo gy
Manage me nt of 1 and 2 GN
J re m o ve o ffe n d in g cau se
J salt re strictio n
J d iu re tics
J an tih yp e rte n sive s
J im m u n o su p p re ssive s in se le cte d case s
J 1 G N
m in im al le sio n : co rtico ste ro id s, cyclo p h o sp h am id e as
ste ro id sp arin g age n t
m e m b ran o u s co rtico ste ro id s, o th e r
fo cal scle ro sis im m u n o su p p re ssive s,
m e san gial p ro life rative } all co n tro ve rsial
m e m b ran o -p ro life rative
cre sce n tic: co rtico ste ro id s, +/ o th e r im m u n o su p p re ssive s,
+/ p lasm ap h e re sis fo r an tiG B M d ise ase )
J 2 G N
S L E /PAN : ste ro id s im m u n o su p p re ssive s
We ge n e rs G ran u lo m ato sis: cyclo p h o sp h am id e
Prognos is
se e b e lo w fo r sp e cific d ise ase e n titie s
PRIMARY GLOMERULONEPHRITIS
J glo m e ru lar d ise ase wh ich is n o t se co n d ary to syste m ic d ise ase ,
m e tab o lic d ise ase , d ru gs o r h e re d itary cau se s
I. Nonprolife rative GN
J n o e xtra ce lls in glo m e ru lu s
J in active se d im e n t
J m ay se e o val fat b o d ie s an d fatty casts wh ich re fle ct th e lip id u ria
an d d o n o t im p ly an active se d im e n t
Minimal Change
J m o st co m m o n cau se o f n e p h ro tic syn d ro m e in ch ild re n , b u t n o t rare in ad u lts e ith e r
J p re se n ts as n e p h ro tic syn d ro m e
J in active se d im e n t
J L M u su ally n o rm al
J E M sh o ws fu sio n o f fo o t p ro ce sse s o f glo m e ru lar e p ith e lial ce lls
J m o st re sp o n d to p re d n iso n e b u t m ay re lap se
J cyclo p h o sp h am id e m ay b e u se fu l in in d u cin g re m issio n o r re lap se
J n atu ral h isto ry is o f e ve n tu al re so lu tio n alth o u gh so m e p ro gre ss to
fo cal se gm e n tal scle ro sis
Me mbranous
J m o st co m m o n cau se o f id io p ath ic n e p h ro tic syn d ro m e in ad u lts
J d iffu se th icke n in g o f glo m e ru lar cap illary wall
J IF sh o ws gran u lar IgG an d C 3 in cap illary lo o p s
J E M sh o ws e p ith e lial d e p o sits
J n o d e fin itive th e rap y, trials with p re d n iso n e an d o th e r im m u n o su p p re ssive
age n ts give co n flictin g re su lts
J p o o r p ro gn o stic fe atu re s: m ale se x, h igh cre atin in e at p re se n tatio n ,
p e rsiste n t h igh grad e p ro te in u ria > 6 m o n th s
Focal Se gme ntal Scle ros is
J fo cal se gm e n tal are as o f glo m e ru lar scle ro sis
J IF sh o ws IgM in scle ro tic are as
J E M sh o ws fo o t p ro ce ss fu sio n an d scle ro sis
J p re se n ts as p ro te in u ria an d in active se d im e n t
J re n al fu n ctio n m ay b e n o rm al to re d u ce d
J H T N m ay o r m ay n o t b e p re se n t
J n atu ral h isto ry is o f grad u al d e clin e in re n al fu n ctio n
J th e rap y: h igh d o se lo n g-te rm ste ro id s
N o te s
II. Prolife rative GN
J e xtra ce lls in th e glo m e ru lu s
J u su ally p re se n ts as n e p h ritic syn d ro m e
J active se d im e n t = R B C , R B C casts, h e m e -gran u lar casts
J variab le p ro te in u ria
Me s angial Prolife rative (i.e . Be rge rs Dis e as e )
J IgA n e p h ro p ath y o r B e rge rs d ise ase
J IgA b e co m e s trap p e d in m e san giu m an d activate s co m p le m e n t
J IF sh o ws gran u lar m e san gial d e p o sits C h ristm as tre e -like )
J p re se n ts as asym p to m atic gro ss h e m atu ria a fe w d ays afte r U R T I o r
G I in fe ctio n o r as m icro sco p ic h e m atu ria o n ro u tin e u rin alysis
J o fte n se e n in ch ild re n an d yo u n g ad u lts
J m o st o fte n id io p ath ic, b u t also o ccu rs with o th e r d ise ase s,
in clu d in g h e p atic cirrh o sis an d glu te n e n te ro p ath y
J 1 5-20% p ro gre ss to C R F
Diffus e Prolife rative (Pos t-lnfe ctious )
J i.e . p o st-S tre p in fe ctio n
J im m u n e re sp o n se to G ro u p A b e ta-h e m o lytic) Strep
J p lan te d an tige n o r d e p o sitio n o f circu latin g Ag/Ab co m p le x
J L M sh o ws large glo m e ru lu s an d d e cre ase d B o wm an s sp ace
J E M sh o ws su b e p ith e lial h u m p s
J p re se n ts as acu te n e p h ritic syn d ro m e 1 0-1 2 d ays afte r b acte rial in fe ctio n
J n o tre atm e n t is o f p ro ve n b e n e fit
J 95% o f kid s re co ve r
J in ad u lts th e p ro gn o sis is n o t as go o d
Cre s ce ntic (Epithe lial Prolife rative )
J 3 typ e s
typ e I: lin e ar d e p o sitio n o f an tiglo m e ru lar B M an tib o d ie s
i.e . an tiglo m e ru lar B M an tib o d y th at cro ss-re acts with
p u lm o n ary B M G o o d p astu re s d ise ase )
sm o kin g p lays a p e rm issive ro le in h e m o p tysis
IF sh o ws a lin e ar d e p o sitio n alo n g th e glo m e ru lar B M
E M : G B M d isru p tio n b u t n o e le ctro n d e n se d e p o sits
typ e II: gran u lar im m u n e co m p le x d e p o sits
typ e III: P au ci-im m u n e m ay b e asso ciate d with
AN C A-p o sitivity)
J p ro gn o sis: if d iagn o se d e arly an d tre ate d aggre ssive ly ste ro id s,
cyclo p h o sp h am id e , +/ p lasm ap h e re sis) m ay stab ilize
J if ad van ce d , p ro gn o sis p o o r
Me mbrano-Prolife rative
(Cros s -Ove r GN: Prolife rative and Nonprolife rative )
J p re se n ts as a n e p h ritic-n e p h ro tic m ixtu re
J p ro te in u ria an d active se d im e n t
J glo m e ru lar m e san giu m is e xp an d e d an d h yp e rce llu lar
J cap illary walls are th icke n e d
J tre atm e n t is co n tro ve rsial: in te rfe ro n fo r h e p atitis B -asso ciate d
SECONDARY GLOMERULONEPHRITIS
A. Sys te mic Dis e as e s
Diabe te s Me llitus se e D iab e te s an d th e K id n e y S e ctio n )
J p ro gre ssive glo m e ru lo scle ro sis
J p re se n ts as p ro te in u ria in itially m icro alb u m in u ria p ro gre ssin g to
clin ically d e te ctab le p ro te in u ria)
Sys te mic Lupus Erythe matos us
J id io p ath ic au to im m u n e d ise ase th at in vo lve s m u ltip le o rgan s
J kid n e y is in vo lve d in 60-70%
J an tin u cle ar an tib o d ie s an d im m u n e co m p le x d e p o sitio n
J WH O classificatio n
C lass 1 : n o rm al L M , m ay h ave d e p o sits b y IF o r E M
C lass 2: m e san gial d e p o sits
C lass 3: fo cal p ro life rative G N
C lass 4: d iffu se p ro life rative G N
C lass 5: m e m b ran o u s G N
C lass 6: ad van ce d scle ro sin g G N
N o te s
J p ro gn o sis d e p e n d s o n class e .g. class 4 h as th e wo rst o u tco m e )
J re sp o n sive to im m u n o su p p re ssive th e rap y
Othe r Sys te mic Dis e as e s to Cons ide r
J H e n o ch -S ch o n le in P u rp u ra
n o n -th ro m b o cyto p e n ic p u rp u ra, arth ralgia, ab d o m in al p ain
an d G N p ro te in u ria, h e m atu ria)
J sh u n t n e p h ritis S B E )
J syp h ilis
co n ge n ital an d 2
J vascu litic: PAN , We ge n e rs G ran u lo m ato sis
J th ro m b o tic m icro an gio p ath y, T T P, H U S , D IC
J scle ro d e rm a
J H IV-asso ciate d n e p h ro p ath y
B. Me tabolic Dis e as e s
Amyloidos is
J in itially se e n o d u lar d e p o sits o f am ylo id in m e san giu m
J e ve n tu ally, se e p ro gre ssive d e p o sitio n s o f am ylo id e ve rywh e re
J d e p o sits are b ire frin ge n t with C o n go R e d ap p le gre e n co lo u r
J p re se n ts as n e p h ro tic syn d ro m e with p ro gre ssive re n al in su fficie n cy
Dys prote ine mias
J cryo glo b u lin e m ia
circu latin g co ld p re cip itab le Ig
p u rp u ra, n e cro tizin g skin le sio n s, arth ralgias, fe ve r,
h e p ato sp le n o m e galy
C. He re ditary Ne phropathie s
Alports Syndrome
J h e re d itary n e p h ritis so m e tim e s asso ciate s with se n so rin e u ral d e afn e ss
J th re e m o d e s o f in h e ritan ce h ave b e e n d e scrib e d : X-lin ke d d o m in an t,
au to so m al d o m in an t, an d le ss o fte n au to so m al re ce ssive
D. Drug Induce s
J e .g. N S AID s, go ld , p e n icillam in e
E. Ne oplas ms
J lym p h o m a, le u ke m ia
J ad e n o carcin o m a o f lu n g, co lo n , sto m ach o r b re ast
J m e m b ran o u s o r m in im al le sio n
F. Infe ctions
J h e p atitis B , h e p atitis C , H IV
J syp h ilis
J m alaria
J sch isto so m iasis
N o te s
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N o te s
TUBULOINTERSTITIAL NEPHRITIS
De finition
J in flam m ato ry ce ll in filtrate affe ctin g p rim arily th e re n al in te rstitiu m
an d tu b u le ce lls, with n o p rim ary glo m e ru lar d am age
J fu n ctio n al tu b u le d e fe cts are d isp ro p o rtio n ate ly gre ate r th an th e
d e cre ase in G F R
Manife s tations
J acq u ire d n e p h ro ge n ic d iab e te s in sip id u s 2 to tu b u lar d am age ,
d e cre ase d AD H re sp o n sive n e ss
J n o n -AG m e tab o lic acid o sis p ro xim al R TA fro m im p aire d H C O 3
re ab so rp tio n ) an d h yp o p h o sp h ate m ia
J h yp e rkale m ia an d N a
+
-wastin g fro m d e cre ase d re n in p ro d u ctio n an d h yp o ald o ste ro n ism )
J p artial o r co m p le te F an co n i s syn d ro m e
J 1 ,25-d ih yd ro xy-vitam in D d e ficie n cy with h yp o calce m ia an d 2 h yp e rp arath yro id ism
J an e m ia lo w E p o )
J sign s an d sym p to m s o f re n al failu re m ay o ccu r se e ab o ve )
J rad io grap h ic, u ltraso n o grap h ic, an d rad io n u clid e stu d ie s o n ly sh o w e vid e n ce o f
acu te o r ch ro n ic re n al d ise ase , alth o u gh e tio lo gy m ay b e se e n
e .g. p o lycystic kid n e y d ise ase , u rin ary tract o b stru ctio n )
J classifie d as acu te vs. ch ro n ic can also b e classifie d as 1 vs. 2
ACUTE TIN
Etiology
J acu te alle rgic d ru g re actio n s
b e ta-lactam an tib io tics, su lfo n am id e s, rifam p in , q u in o lo n e s, N S AID s
su lfo n am id e d iu re tics fu ro se m id e ) , p h e n yto in , cim e tid in e , allo p u rin o l
J re n al in fe ctio n s: b acte rial p ye lo n e p h ritis, re n al T B , fu n gal n e p h ritis
J asso ciate d with syste m ic in fe ctio n
B ru ce llo sis, C M V, in fe ctio u s m o n o n u cle o sis,
L e gio n n aire s d ise ase , le p to sp iro sis, stre p to co ccal
in fe ctio n s, R o cky M o u n tain sp o tte d fe ve r, syp h ilis, to xo p lasm o sis,
M. pneumoniae
J im m u n e -m e d iate d
S L E , n e cro tizin g vascu litis e sp e cially with We ge n e rs) ,
acu te graft re je ctio n , asso ciate d with so m e acu te
glo m e ru lo n e p h ritid e s
J id io p ath ic
Clinical Fe ature s
J sign s an d sym p to m s asso ciate d with e le ctro lyte an d acid -b ase
ab n o rm alitie s d e scrib e d ab o ve
J o th e r m an ife statio n s d e p e n d o n u n d e rlyin g e tio lo gy e .g. in S L E ,
syste m ic in fe ctio n )
J m ay se e ab ru p t G F R d e clin e an d o ligu ria
J fe ve r, rash , e o sin o p h ilia in th e se ttin g o f d ru g-in d u ce d T IN
J flan k p ain , C VA te n d e rn e ss in re n al in fe ctio n
J o n go in g acu te T IN can p ro gre ss to ch ro n ic re n al failu re an d u re m ia
Laboratory Inve s tigations
J u rin e
WB C , WB C casts, p ro te in < 3.5 g/d ay) , h e m atu ria, glyco su ria,
am in o acid u ria
e o sin o p h ils if alle rgic in te rstitial n e p h ritis
e le ctro lyte ab n o rm alitie s: p h o sp h atu ria, b icarb o n atu ria, u rico su ria,
in cre ase d F E N a
+
, d ilu te u rin e
J b lo o d
e o sin o p h ilia if d ru g re actio n
n o n -AG m e tab o lic acid o sis
h yp o p h o sp h ate m ia, h yp e rkale m ia
in cre ase d B U N an d cre atin in e if re n al failu re d e ve lo p in g
Tre atme nt
tre at u n d e rlyin g cau se e .g. sto p o ffe n d in g m e d s,
an tib io tics if b acte rial p ye lo n e p h ritis)
co rtico ste ro id s m ay b e in d icate d in alle rgic o r im m u n e d ise ase )
su p p o rtive m e asu re s: tre at m e tab o lic ab n o rm alitie s, tre at
acu te re n al failu re if d e ve lo p s
CHRONIC TIN
J ch aracte rize d b y in te rstitial fib ro sis with atro p h y an d lo ss o f tu b u le s
N o te s
TUBULOINTERSTITIAL NEPHRITIS . . . CONT.
Etiology
J p e rsiste n ce o r p ro gre ssio n o f acu te T IN
J n e p h ro to xin s
an alge sics N S AID s, p h e n ace tin , ace tam in o p h e n )
e n d o ge n o u s h yp e rcalce m ia, h yp o kale m ia, o xalate
n e p h ro p ath y, u ric acid n e p h ro p ath y)
m e tals co p p e r, le ad , lith iu m , m e rcu ry, cisp latin )
rad iatio n
J in fe ctio u s
re n al T B
ch ro n ic b acte rial p ye lo n e p h ritis in th e se ttin g o f o b stru ctio n )
J ch ro n ic u rin ary tract o b stru ctio n m o st co m m o n )
J ve sico u re te ric re flu x
J cystic d ise ase
p o lycystic kid n e y d ise ase
m e d u llary cystic d ise ase
J im m u n e
S L E
S j gre n s
sarco id o sis
id io p ath ic
ch ro n ic re je ctio n
J n e o p lastic/p arap ro te in e m ic
m u ltip le m ye lo m a
ligh t ch ain n e p h ro p ath y
lym p h o m a/le u ke m ia
am ylo id o sis
Wald e n stro m s m acro go b u lin e m ia
cryo glo b u lin e m ia
J m isce llan e o u s
D M
sickle -ce ll h e m o glo b in o p ath ie s
Clinical Fe ature s
J m ay b e th o se o f tu b u lar d ysfu n ctio n se e ab o ve )
J m ay b e th o se o f p ro gre ssive re n al failu re an d u re m ia
J d e p e n d e n t o n u n d e rlyin g d ise ase as we ll
J WB C , WB C casts, p ro te in , glyco su ria, am in o acid u ria
J n o e o sin o p h ilia o r e o sin o p h ilu ria
J e le ctro lyte ab n o rm alitie s: p h o sp h atu ria, b icarb o n atu ria, u rico su ria,
in cre ase d F E N a
+
, d ilu te u rin e
J in cre ase d B U N , cre atin in e
J h yp e rkale m ia, h yp e rcalce m ia, m e tab o lic acid o sis
Tre atme nt
J sto p o ffe n d in g age n t if ap p licab le )
J su p p o rtive m e asu re s: co rre ct m e tab o lic d iso rd e rs, tre at C R F
N o te s
ACUTE TUBULAR NECROSIS
J o n e o f two m o st co m m o n cau se s o f AR F ; p re -re n al d ise ase b e in g th e o th e r
J u su ally re su lts fro m isch e m ia o r to xin s
Clinical Pre s e ntation
J typ ically p re se n ts ab ru p tly afte r a h yp o te n sive e p iso d e ,
rh ab d o m yo lysis, o r th e ad m in istratio n o f rad io co n trast m e d ia
J in co n trast, wh e n am in o glyco sid e n e p h ro to xicity o ccu rs, th e o n se t is
m o re in sid io u s, with th e p lasm a C r risin g slo wly with in 7 o r m o re d ays o f th e rap y
J u rin ary se d im e n t: h igh F E N a
+
, p igm e n te d gran u lar an d e p ith e lial casts in th e u rin e
ISCHEMIA
J sh o ck
J trau m a +/ rh ab d o m yo lysis
J se p sis o r se ve re h yp o vo le m ia
J p o st-o p e rative p atie n ts are at in cre ase d risk b e cau se o f p re -o p e rative
flu id d e p le tio n , an e sth e sia an d in tra-o p e rative flu id lo sse s
J N S AID s in vo lu m e d e p le tio n
TOXINS
Exoge nous
J an tib io tics
am in o glyco sid e s re m e m b e r th at 80 m g q 8h is n o t a
u n ive rsal d o se ! )
ce p h alo sp o rin s
am p h o te ricin B
J an tiviral cid o fo vir
J ch e m o th e rap e u tic d ru gs cisp latin , m e th o tre xate )
J co n trast m e d ia
J h e avy m e tals
J m isce llan e o u s
flu o rin ate d an e sth e tic age n ts
e th yle n e glyco l
o rgan ic so lve n ts
ace tam in o p h e n o ve rd o se
p araq u at
Endoge nous
e n d o to xin s b acte rial)
m yo glo b in
h e m o glo b in
B e n ce -Jo n e s p ro te in , if co m b in e d with rad io co n trast d ye o r
vo lu m e d e p le tio n
Prognos is of ATN
J o th e r th an co rre ctin g th e u n d e rlyin g p ro b le m , th e rap y fo r AT N is large ly
su p p o rtive
J kid n e ys u su ally ge t b e tte r if in su lt is re m o ve d
J p ro gn o stic facto rs in clu d e
age
se ve rity o f u n d e rlyin g d ise ase
co m p licatio n s
p re vio u s e p iso d e o f AR F
N o te s
NSAID NEPHROPATHY
J N S AID s act b y b lo ckin g th e cyclo o xyge n ase e n zym e n e e d e d in
p ro staglan d in syn th e sis
J p ro staglan d in s P G ) h ave vario u s actio n s o n th e kid n e y
vaso d ilatio n o f re n al arte rie s an d arte rio le s to m ain tain
re n al b lo o d flo w
n atriu re sis
stim u latio n o f re n in re le ase
an tago n ism o f th e e ffe cts o f AD H
J N S AID -m e d iate d re n al d ise ase can take th e fo llo win g fo rm s:
vaso m o to r AR F
p e rh ap s th e m o st co m m o n cau se o f d ru g-in d u ce d AR F
m o re co m m o n in th e e ld e rly an d in p atie n ts with
an te ce d e n t re n al d ise ase , o r b lo o d vo lu m e co n tractio n
d iu re tics, C H F, cirrh o sis, n e p h ro tic syn d ro m e )
AR F is p re cip itate d b y re n al h yp o p e rfu sio n se co n d ary to
P G syn th e sis in h ib itio n le ad in g to re n al arte rial an d
arte rio lar vaso co n strictio n
clin ically: o ligu ric with in a fe w d ays o f b e gin n in g
N S AID with lo w F E N a
+
tre atm e n t: d isco n tin u e N S AID , d ialysis rare ly n e e d e d
AIN
m ajo rity d u e to fe n o p ro fe n 60%) , ib u p ro fe n , n ap ro xe n ; can
b e an y N S AID
d istin gu ish fro m o th e r d ru g-in d u ce d AIN b y rarity o f
e o sin o p h ilia an d e o sin o p h ilu ria, th e p re se n ce o f skin
rash e s, an d th e p re se n ce o f n e p h ro tic ran ge p ro te in u ria
can ge t re gu lar AIN b u t in ad d itio n th e re is a u n iq u e
N S AID AIN wh e re b o th tu b u lar an d glo m e ru lar d am age
o ccu r an d sign ifican t p ro te in u ria re su lts)
u n like N S AID -in d u ce d AR F, re q u ire s N S AID s take n
fro m d ays to m o n th s
re so lve s with d isco n tin u atio n o f N S AID b u t m ay take a lo n g tim e
n e ce ssitatin g in te rval d ialysis
sh o rt te rm h igh d o se ste ro id s 1 m g/kg/d ay o f p re d n iso n e ) m ay
h aste n re co ve ry
J p ap illary n e cro sis
J glo m e ru lo n e p h ritis asso ciate d with d iffu se vascu litis
J so d iu m re te n tio n
J h yp e rkale m ia, m e tab o lic acid o sis 2 to h yp o re n in e m ic
h yp o ald o ste ro n ism )
J e xce ss wate r re te n tio n an d h yp o n ate re m ia e xace rb atio n d u e to
e lim in atio n o f AD H an tago n istic e ffe ct o f P G s)
VASCULAR DISEASES
OF THE KIDNEY
Large Ve s s e l Dis e as e
J re n al arte ry ste n o sis
J re n al arte ry th ro m b o sis
J re n al arte ry e m b o li
J ch o le ste ro l e m b o lic d ise ase
J re n al ve in th ro m b o sis
Small Ve s s e l Dis e as e
J h yp e rte n sive n e p h ro scle ro sis
J m align an t n e p h ro scle ro sis
J cyclo sp o rin e n e p h ro p ath y
J th ro m b o tic m icro an gio p ath y
H U S , T T P, D IC , p o st-p artu m re n al failu re
N o te s
DIABETES AND THE KIDNEY
J n u m b e r o n e cau se o f e n d -stage re n al failu re in N o rth Am e rica
J 35-50% o f Typ e 1 will d e ve lo p n e p h ro p ath y, u n kn o wn p e rce n tage
o f Typ e 2
J classic p ro te in u ria > 1 50 m g/d ay) d e ve lo p s afte r 1 5-20 ye ars
o f Typ e 1 b e gin s as m icro alb u m in u ria)
J o n ce p ro te in u ria is e stab lish e d , re n al fu n ctio n d e clin e s with 50% o f
p atie n ts re ach in g E S R D 7 to 1 0 ye ars afte r th e o n se t o f p ro te in u ria
J asso ciate d with H T N an d d iab e tic re tin al m icro an e u rysm s
J n o t all d iab e tics with ab n o rm al re n al fu n ctio n h ave d iab e tic n e p h ro p ath y,
sh o u ld h ave
p ro te in u ria
H T N
in active u rin ary se d im e n t
ap p ro p riate tim e co u rse
re tin o p ath y if Typ e 1
J fo u r b asic d iab e tic re n al co m p licatio n s:
1 ) p ro gre ssive glo m e ru lo scle ro sis
2) ath e ro scle ro sis
3) au to n o m ic n e u ro p ath y
4) p ap illary n e cro sis
J D M is o n e o f th e cau se s o f E S R D th at d o e s n o t re su lt in
sm all kid n e ys
Progre s s ive Glome rulos cle ros is
J stage I
IN C R E AS E D G F R 1 20-1 50%)
d u e to co m p e n sato ry h yp e rfiltratio n o f re m ain in g n e p h ro n s)
+/ sligh t in cre ase d m e san gial m atrix
J stage 2
D E T E C TAB L E M IC R O AL B U M IN U R IA > 30 m g/24h r
in cre ase d G F R
in cre ase d m e san gial m atrix
J stage 3
in cre ase d m icro alb u m in u ria
C L IN IC AL LY D E T E C TAB L E P R O T E IN U R IA 300 m g/24h r
n o rm al G F R
ve ry e xp an d e d m e san gial m atrix
J stage 4
in cre ase d p ro te in u ria > 500 m g/24h r
D E C R E AS E D G F R
< 20% glo m e ru lar filtratio n su rface are a p re se n t
scle ro se d glo m e ru li
Acce le rate d Athe ros cle ros is
J co m m o n fin d in g
J d e cre ase d G F R
J m ay in cre ase AII p ro d u ctio n : re su lts in in cre ase d B P
J in cre ase d risk o f AT N se co n d ary to co n trast m e d ia
Autonomic Ne uropathy
J affe cts b lad d e r
J re su lts in u rin ary re te n tio n
J re sid u al u rin e p ro m o te s in fe ctio n
J o b stru ctive re flu x n e p h ro p ath y se e b e lo w)
Papillary Ne cros is
J Typ e 1 D M su sce p tib le to isch e m ic n e cro sis o f m e d u llary p ap illa
J slo u gh e d p ap illa m ay o b stru ct u re te r: p re se n ts as re n al
co lic o r with o b stru ctive fe atu re s +/ h yd ro n e p h ro sis
Scre e ning
J all p atie n ts o ve r 1 5 ye ars o f age with a 5 ye ar h isto ry o f Typ e I d iab e te s
sh o u ld h ave an n u al scre e n s fo r m icro alb u m in u ria
J p atie n ts with Typ e 2 d iab e te s sh o u ld b e scre e n e d at th e tim e o f
d iagn o sis an d ye arly th e re afte r
J m u st se n d sp e cifically fo r m icro alb u m in u ria if n o d e te ctab le p ro te in o n d ip stick)
Tre atme nt
J m u st e valu ate th e p atie n t fo r o th e r cau se s o f p ro te in u ria b e sid e s
d iab e tic n e p h ro p ath y e .g. h yp e rglyce m ia, U T I, e sse n tial H T N , C H F )
N o te s
DIABETES AND THE KIDNEY . . . CONT.
J also m u st e n su re th at th e p atie n t is n o t e xp o se d to u n n e ce ssary in su lts
to th e ir kid n e ys e .g. N S AID s, am in o glyco sid e an tib io tics, avo id in g d ye
stu d ie s if p o ssib le , e tc...)
J aggre ssive B P co n tro l: slo ws rate o f d e clin e in re n al fu n ctio n an d
im p ro ve s p atie n t su rvival
J strict glyce m ic co n tro l: in D C C T sh o wn to re d u ce m icro alb u m in u ria in
Typ e 1 D M p rim ary an d se co n d ary p re ve n tio n )
J p ro te in re strictio n : d e cre ase s in traglo m e ru lar H T N , stu d ie s o n go in g,
wo rry o f m aln u tritio n
J AC E in h ib ito rs
kid n e y p ro te ctio n in d e p e n d e n t o f B P co n tro l, m ay p re se rve
G F R co n tro ve rsial)
re d u ce d p ro te in u ria, slo we d re n al d e te rio ratio n
im p ro ve d glu co se u se an d in su lin se n sitivity
J a gre ate r th e n 50% d e cre ase in C rC l n e ce ssitate s a re fe rral to a n e p h ro lo gist
HYPERTENSION
J h yp e rte n sio n o ccu rs in 1 0-20% o f p o p u latio n
J 95% o f h yp e rte n sio n is e sse n tial p rim ary)
J 5% d u e to se co n d ary cau se s in clu d in g re n al re n al p are n ch ym al o r
re n o vascu lar an d n o n -re n al
Initial Inve s tigations
J h isto ry, p h ysical targe t o rgan d am age : card iac, n e u ro lo gic, re n al, o cu lar
J se ru m C r, K
+
, u ric acid , ch o le ste ro l, triglyce rid e s
J fastin g b lo o d su gar, H gb A1 C
J u rin alysis
J E C G
Clue s to 2 Caus e s
J o n se t < 20 o r > 50 ye ars
J b ru its re n al arte ry ste n o sis)
J ab n o rm al re n al fu n ctio n , ab n o rm al u rin alysis G N o r T IN )
J h yp o kale m ia in ab se n ce o f d iu re tics in cre ase d m in e ralo co rtico id s)
J u n u su al h isto ry flan k trau m a, p h e o ch ro m o cyto m a-like sym p to m s)
J p o o r re sp o n se to th e rap y h igh B P d e sp ite 2 o r 3 an tih yp e rte n sive s)
J grad e III o r IV h yp e rte n sive re tin o p ath y
RENOVASCULAR HYPERTENSION
J 1 -2% o f all h yp e rte n sive s, 30-40% o f m align an t h yp e rte n sive s
J su sp e ct if
n e gative fam ily h isto ry
e p igastric o r flan k b ru it
sp o n tan e o u s h yp o kale m ia
su d d e n o n se t o r e xace rb atio n
yo u n g fe m ale
h isto ry o f ath e ro scle ro sis
d ifficu lt to co n tro l with an tih yp e rte n sive th e rap y
Clinical Pe arl
J Flas h pulmonary e de ma can be as s ociate d with bilate ral
re nal arte ry s te nos is
Etiology
J d e cre ase d re n al p e rfu sio n o f o n e o r b o th kid n e ys le ad s to in cre ase d
re n in re le ase , an d su b se q u e n t AII p ro d u ctio n cau sin g ge n e ralize d
arte rio co n strictio n , raisin g syste m ic B P as we ll as h yp e rald o ste ro n e m ia
le ad in g to N a
+
an d wate r re te n tio n
J th e e le vate d B P can in tu rn le ad to fu rth e r d am age o f kid n e ys an d
wo rse n in g H T N
J 2 typ e s
ath e ro scle ro tic p laq u e s p ro xim al 1 /3 re n al arte ry) , u su ally
m ale s > 55 ye ars
fib ro m u scu lar h yp e rp lasia d istal 2/3 re n al arte ry o r se gm e n tal
b ran ch e s) , u su ally fe m ale s b e twe e n 35-50 ye ars
N o te s
HYPERTENSION . . . CONT.
J p atie n ts with sin gle kid n e y an d re n al arte ry ste n o sis, o r 2 kid n e ys an d
b ilate ral re n al arte ry ste n o sis are at risk o f AR F with AC E in h ib ito r th e rap y o r N S AID s
wh e n th e re is d e cre ase d R B F, G F R is d e p e n d e n t o n
an gio te n sin II-in d u ce d e ffe re n t arte rio lar co n strictio n an d
raisin g o f filtratio n fractio n
Inve s tigations
J re n al U /S an d d o p p le rs
J d igital su b tractio n an gio grap h y ve n o u s p u n ctu re , co m p licatio n s re late d to d ye )
J re n al scan with AC E in h ib ito r acce n tu ate s d iffe re n ce in G F R )
J arte rial an gio grap h y
Tre atme nt
J B P lo we rin g m e d icatio n s AC E -in h ib ito r d ru g o f ch o ice if u n ilate ral
re n al arte ry d ise ase b u t co n train d icate d if b ilate ral re n al arte ry d ise ase )
J su rgical, an gio p lasty +/ ste n t
J ve ry co n tro ve rsial!
J p e rh ap s th e o n ly th in g e ve ryo n e agre e s o n is an gio p lasty fo r
sim p le fib ro m u scu lar d ysp lasia le sio n in yo u n g p atie n ts
HYPERTENSION CAUSED BY RENAL
PARENCHYMAL DISEASE
J an y ch ro n ic re n al d ise ase can le ad to H T N G N , T IN , d iab e tic n e p h ro p ath y)
J m o st co m m o n cau se o f se co n d ary H T N
J m e ch an ism o f H T N n o t fu lly u n d e rsto o d b u t m ay in clu d e :
e xce ss re n in -an gio te n sin -ald o ste ro n e syste m activatio n d u e to
in flam m atio n an d fib ro sis in m u ltip le sm all in tra-re n al ve sse ls
se e R e n o vascu lar H T N S e ctio n )
p ro d u ctio n o f u n kn o wn vaso p re sso rs o r lack o f p ro d u ctio n o f
u n kn o wn vaso d ilato rs, o r lack o f cle aran ce o f e n d o ge n o u s
vaso p re sso r
in e ffe ctive d isp o sal o f so d iu m with flu id o ve rlo ad
Inve s tigations
J as we ll as ab o ve in ve stigatio n s, ad d itio n al te sts m ay in clu d e :
24 h o u r u rin ary e stim atio n s o f C r cle aran ce an d p ro te in e xcre tio n
im agin g IVP, U /S , C T, rad io n u clid e scan )
im m u n o lo gic te stin g
b acte rio lo gy an d re n al b io p sy
Tre atme nt
J m o st ch ro n ic re n al d ise ase can n o t b e re ve rse d b u t tre atm e n t o f th e
H T N can slo w th e p ro gre ssio n o f re n al in su fficie n cy
J co n tro l E C F vo lu m e : N a
+
re strictio n 980 m m o l/d ay in take ) , d iu re tic,
d ialysis with e n d -stage d ise ase
PYELONEPHRITIS
ACUTE PYELONEPHRITIS
J in fe ctio n o f th e re n al p are n ch ym a with lo cal an d syste m ic
m an ife statio n s o f in fe ctio n
J m ay b e classifie d as u n co m p licate d o r co m p licate d
u n co m p licate d : in th e ab se n ce o f co n d itio n s p re d isp o sin g to
an ato m ic o r fu n ctio n al im p airm e n t o f u rin e flo w
co m p licate d : o ccu rrin g in th e se ttin g o f re n al o r u re te ric sto n e s, strictu re s,
p ro static o b stru ctio n h yp e rtro p h y o r m align an cy) , ve sico u re te ric re flu x,
n e u ro ge n ic b lad d e r, cath e te rs, d iab e te s m e llitu s, sickle -ce ll h e m o glo b in o p ath ie s,
p o lycystic kid n e y d ise ase , im m u n o su p p re ssio n , an d p o st-re n al tran sp lan t
Etiology
J u su ally asce n d in g m icro o rgan ism s, m o st o fte n b acte ria
J in fe m ale s with u n co m p licate d p ye lo n e p h ritis u su ally E . coli
J cau sative m icro o rgan ism s are u su ally E. coli, Klebsiella, Proteus,
Serratia, Pseudomonas, Enterococcus, an d S. aureus
J if S . aureusis fo u n d , su sp e ct b acte re m ic sp re ad fro m a d istan t fo cu s
e .g. se p tic e m b o li in in fe ctive e n d o card itis) an d su sp e ct p o ssib le
m u ltip le in tra-re n al m icro ab sce sse s o r p e rin e p h ric ab sce ss
N o te s
PYELONEPHRITIS . . . CONT.
Clinical Pre s e ntation
J rap id o n se t h o u rs to a d ay)
J le th argic an d u n we ll, fe ve r, tach ycard ia, sh akin g, ch ills, n au se a an d
vo m itin g, m yalgias
J m arke d C VA o r flan k te n d e rn e ss; p o ssib le ab d o m in al
p ain o n d e e p p alp atio n
J sym p to m s o f lo we r U T I m ay b e ab se n t u rge n cy, fre q u e n cy, d ysu ria)
J m ay h ave sym p to m s o f G ram n e gative se p sis
Clinical Pe arl
J Patie nts (e s pe cially the e lde rly) with acute pye lone phritis +/ s e ps is
may pre s e nt initially with only back pain, abdominal pain, s ymptoms
of dis turbe d GI function, or me ntal s tatus change s
J u rin e d ip stick: +ve fo r le u ko cyte s an d n itrite s, p o ssib le h e m atu ria
J m icro sco p y: > 5 WB C /H P F in u n sp u n u rin e o r > 1 0 WB C /H P F in sp u n
u rin e , b acte ria
J G ram stain : G ram n e gative ro d s, G ram p o sitive co cci
J cu ltu re : > 1 0
5
co lo n y fo rm in g u n its C F U ) /m L in cle an catch
m id stre am u rin e o r > 1 0
2
/m L in su p rap u b ic asp irate o r cath e te rize d
sp e cim e n
J C B C an d d iffe re n tial: le u ko cyto sis, h igh % n e u tro p h ils, le ft-sh ift in cre ase
in b an d ce lls - im m atu re n e u tro p h ils)
J b lo o d cu ltu re s: m ay b e p o sitive in 20% o f case s, e sp e cially in S . aureus
in fe ctio n
J co n sid e r in ve stigatio n o f co m p licate d p ye lo n e p h ritis: if fe ve r, p ain ,
le u ko cyto sis n o t re so lvin g with tre atm e n t with in 72 h r, if m ale p atie n t,
o r if th e re is h isto ry o f u rin ary tract ab n o rm alitie s ab d o /p e lvis U /S , C T
fo r re n al ab sce ss, sp iral C T fo r sto n e s, cysto sco p y)
Tre atme nt
J u n co m p licate d p ye lo n e p h ritis with m ild sym p to m s
1 4 d ay co u rse o f T M P /S M X o r flu o ro q u in o lo n e o r th ird
ge n e ratio n ce p h alo sp o rin
start with IV fo r se ve ral d ays an d th e n switch to P O can th e n
b e as o u tp atie n t)
J p atie n t m o re th an m ild ly sym p to m atic o r co m p licate d p ye lo n e p h ritis in
th e se ttin g o f sto n e o b stru ctio n is a u ro lo gic e m e rge n cy p lacin g p atie n t
at risk o f kid n e y lo ss)
start b ro ad sp e ctru m IV an tib io tics u n til cu ltu re s re tu rn im ip e n e m o r
e m ro p e n e m o r p ip e racillin /tazo b actam o r am p icillin +ge n tam ycin )
an d tre at 2-3 we e ks
fo llo w-u p cu ltu re s 24 we e ks afte r sto p p in g tre atm e n t
J if n o im p ro ve m e n t in 48-72 h r, n e e d to co n tin u e o n IV an tib io tics,
asse ss fo r co m p licate d p ye lo n e p h ritis o r p o ssib le re n al o r p e rin e p h ric
ab sce ss
Prognos is
J tre ate d acu te p ye lo n e p h ritis rare ly p ro gre sse s to ch ro n ic re n al d ise ase
J re cu rre n t in fe ctio n s o fte n co n stitu te re lap se rath e r th e n re -in fe ctio n
CHRONIC PYELONEPHRITIS
J a fo rm o f ch ro n ic tu b u lo in te rstitial n e p h ritis o f b acte rial o rigin
J co rtical scarrin g, tu b u lo in te rstitial d am age , an d calyce al
d e fo rm itie s se e n
J m ay b e active p e rsiste n t in fe ctio n ) o r in active p e rsiste n t fo cal ste rile
scars p o st-in fe ctio n )
J h isto lo gically in d istin gu ish ab le fro m m an y o th e r fo rm s o f T IN se ve re
ve sico u re te ric re flu x, h yp e rte n sive d ise ase , an alge sic n e p h ro p ath y)
J active ch ro n ic p ye lo n e p h ritis m ay re sp o n d to an tib io tics
J n e e d to ru le o u t T B
CYSTIC DISEASES OF THE KIDNEY
ADULT POLYCYSTIC KIDNEY DISEASE (APCKD)
J 1 :1 000 p e o p le , acco u n ts fo r ab o u t 1 0% o f case s o f re n al failu re
J m o re co m m o n th an sickle -ce ll an e m ia, cystic fib ro sis, h e m o p h ilia an d m u scu lar d ystro p h y
J au to so m al d o m in an t, lin ke d to alp h a-glo b in ge n e lo cu s o n ch ro m o so m e 1 6p
J p ath o lo gical d e fe ct th o u gh t to b e d u e to
ab n o rm ally we ak b ase m e n t m e m b ran e le ad in g to
se gm e n tal d iste n tio n o f tu b u le o r ve sse l an d cyst fo rm atio n
p ro life ratio n o f tu b u lar e p ith e liu m
J ab n o rm al b ase m e n t m e m b ran e also p re d isp o se cyst fo rm atio n in
o th e r o rgan s
live r - 33%
ce re b ral arte ry an e u rysm - 1 0%
o th e r asso ciatio n s: d ive rticu lo sis an d m itral valve p ro lap se
le ss co m m o n : p an cre as, sp le e n , th yro id , o vary,
e n d o th e liu m , se m in al ve sicle s, an d ao rta
Clinical Cours e
J p o lycystic ch an ge s are b ilate ral an d p re se n t an ytim e fro m e arly
ch ild h o o d to as late as 80 ye ars o f age
J th e kid n e ys are n o rm al at b irth , sym p to m s are rare b e fo re 20
J ve ry co m m o n in o ld e r ad u lts, e ld e rly
J kid n e ys m ay e n large to 1 0 tim e s n o rm al vo lu m e
J sym p to m s an d sign s
o fte n asym p to m atic; d isco ve re d in cid e n tly o n im agin g
ab d o m in al p ain /lu m b ar p ain
h e m atu ria
H T N u p to 75% o f ad u lts)
p ro gre ssive re n al failu re
rare ly e xtra-re n al p re se n tatio n e .g. ru p tu re B e rry an e u rysm )
Complications
J u rin ary tract in fe ctio n
in fe cte d cysts m o st co m m o n in wo m e n d u e to asce n d in g in fe ctio n
tre atm e n t: T M P /S M X
J fo cal co m p re ssio n o f in tra-re n al arte rie s b y cysts > in cre ase d
re n in p ro d u ctio n > H T N
J if u n tre ate d will AC C E L E R AT E p ro gre ssio n to E S R D
J n e p h ro lith iasis in 5-1 5% o f AP C K D m ay fo rm d u e to p o o r d rain age
fro m d isto rte d calyce al syste m )
u su ally u rate sto n e s se e U ro lo gy N o te s)
Diagnos is
J p o sitive fam ily h isto ry
J u ltraso u n d : cysts are u su ally d e te ctab le b y age 20
J o th e r m o d alitie s: C T scan with co n trast fo r e q u ivo cal case s)
J d iffe re n tial d iagn o sis: m u ltip le sim p le cysts n o t p ro gre ssive like AP C K D )
J m u st p ro vid e ge n e tic co u n se llin g: 50% ch an ce o f tran sm issio n b y affe cte d p are n t
Manage me nt
J go al: to p re se rve re n al fu n ctio n
J m u st tre at U T I e arly
J scre e n fo r H T N , tre at aggre ssive ly with an tih yp e rte n sive s e .g. AC E in h ib ito rs)
J ad e q u ate h yd ratio n to p re ve n t sto n e fo rm atio n
J in stru m e n tatio n o f th e G U tract sh o u ld b e avo id e d
J sh o u ld avo id co n tact sp o rts d u e to gre ate r risk o f in ju ry if kid n e ys are large
J as E S R D d e ve lo p s, tre at with p e rito n e al d ialysis, h e m o d ialysis
o r re n al tran sp lan t
MEDULLARY CYSTIC DISEASE
J rare au to so m al re ce ssive d iso rd e r
J o fte n re su lts in e n d -stage re n al failu re d u rin g ad o le sce n ce /ch ild h o o d
J cysts d ifficu lt to im age
MEDULLARY SPONGE KIDNEY
J n o n fam ilial d ise ase
J p re se n ts in th e fo u rth to sixth d e cad e s
J m u ltip le cystic d ilatatio n s in th e co lle ctin g d u cts o f th e m e d u lla
J b e n ign with re sp e ct to th e d e ve lo p m e n t o f re n al in su fficie n cy
J in cre ase d in cid e n ce o f re n al calcu li, in fe ctio n s, an d H T N
J n e p h ro calcin o sis m ay b e se e n o n X-ray, m e d u llary sp o n ge
d e fe ct se e n o n IVP
N o te s
OTHER SYSTEMIC DISEASES
AND THE KIDNEY
HYPERTENSION CAUSING RENAL DISEASE
J H T N can cau se re n al d ise ase - in th is case , o n se t o f H T N an te d ate s
im p aire d re n al fu n ctio n
J re su lts in n e p h ro scle ro sis
J b o th b e n ign slo wly p ro gre ssive ) an d m align an t n e cro tizin g
arte ritis with acce le rate d H T N ) n e p h ro scle ro sis can o ccu r;
th is is d u e to in tra-re n al vascu lar scle ro sis
J m o re co m m o n in b lacks
J tre atm e n t: e arly co n tro l o f B P
MULTIPLE MYELOMA
J a m align an t p ro life ratio n o f p lasm a ce lls in th e b o n e m arro w with
th e p ro d u ctio n o f im m u n o glo b u lin s
J p atie n ts m ay p re se n t with se ve re b o n e d ise ase an d re n al failu re
J m ye lo m a kid n e y: tu b u lar d e p o sits o f ligh t ch ain s with su rro u n d in g in flam m atio n
J ligh t ch ain s are filte re d at th e glo m e ru lu s an d ap p e ar as
B e n ce -Jo n e s p ro te in s in th e u rin e
J ligh t ch ain s m ay also p re cip itate in th e tu b u le s an d fo rm d e n se
e o sin o p h ilic casts can ge t F an co n i syn d ro m e - a Typ e II R TA cast
n e p h ro p ath y with glo b al d ysfu n ctio n o f p ro xim al tu b u le s)
J h yp e rcalce m ia m ay cau se re n al failu re
J se co n d ary am ylo id o sis m ay o ccu r, p re se n ts with n e p h ro tic syn d ro m e
J p lasm a ce lls m ay in filtrate kid n e y
J B e n ce -Jo n e s p ro te in s are n o t d e te cte d o n a u rin e d ip stick
SCLERODERMA
J in te rlo b u lar arte rie s; in tim al th icke n in g an d p ro life ratio n
J fib rin o id n e cro sis o f affe re n t arte rio le s +/ glo m e ru li
J re n al d ise ase m ay p re se n t as " re n al crisis" = m align an t
H T N , m align an t n e p h ro scle ro sis
VASCULITIDES
J p ath o lo gy ch aracte rize d b y fo cal n e cro tizin g glo m e ru lo n e p h ritis
in flam m ato ry in ju ry) +/ cre sce n ts
e g. PAN , We ge n e rs G ran u lo m ato sis
J u n u su al to se e actu al vascu litis ve sse l wall in flam m atio n ) in kid n e y b io p sy
J sim ilarly, u n u su al to se e gran u lo m as in kid n e y b io p sy in We ge n e r's
G ran u lo m ato sis
RHEUMATOID ARTHRITIS
J 1 in vo lve m e n t rare
J 2 am ylo id o sis
J go ld , p e n icillam in e , N S AID n e p h ro p ath y
J if S j gre n 's, in te rstitial n e p h ritis
CANCER
J m ild p ro te in u ria is co m m o n in p atie n ts with so lid tu m o u rs,
b u t o ve rt G N is rare
J m in im al le sio n o r m e m b ran o u s G N with lym p h o m a
J m e m b ran o u s G N with so lid tu m o u rs > n e p h ro tic syn d ro m e
J h yp e rcalce m ia
J h yp e ru rice m ia with tu m o u r lysis
J ch e m o th e rap y e sp e cially cisp latin ) can le ad to AT N
J o b stru ctio n with p e lvic tu m o u rs o r m e ts
J am ylo id o sis
J rad io th e rap y rad iatio n n e p h ritis)
INFECTIONS
J h e p atitis B : m e m b ran o u s G N , p o lyarte ritis n o d o sa
J h e p atitis C : m e m b ran o p ro life rative G N +/ cryo glo b u lin s
J T B : ste rile p yu ria, gran u lo m ato u s in flam m atio n an d
case o u s n e cro sis, ab n o rm al IVP, 2 am ylo id o sis, h yp e rcalce m ia
J in fe ctio u s e n d o card itis: p ro life rative G N , cryo glo b u lin e m ic G N
J d ip h th e ria, L e gio n n aire 's, to xo p lasm o sis: in te rstitial n e p h ritis
J syp h ilis: m e m b ran o u s G N
J m alaria: variab le glo m e ru lar in vo lve m e n t
N o te s
OTHER SYSTEMIC DISEASES
AND THE KIDNEY . . . CONT.
HIV-ASSOCIATED RENAL DISEASE
J sp e cific glo m e ru lar syn d ro m e s; H IV-asso ciate d n e p h ro p ath y
fo cal an d se gm e n tal glo m e ru lo scle ro sis-like syn d ro m e
IgA n e p h ro p ath y
th ro m b o tic m icro an gio p ath y T T P )
o th e r fo rm s o f glo m e ru lo p ath y
J h igh p re d ile ctio n fo r yo u n g b lack m ale s
J AR F se co n d ary to se p sis, E C F V d e p le tio n e tc...
J flu id -e le ctro lyte an d acid -b ase d istu rb an ce s
DIURETICS
Loop Diure tics
J e xam p le s
fu ro se m id e L asix) , b u m e tan id e B u m e x) , e th acryn ate
E d e crin ) , to rse m id e D e m ad e x)
J m e ch an ism
in h ib itio n o f N a
+
/K
+
/2C l
ch an n e l in th e th ick asce n d in g lim b , ve n o d ilatio n

J clin ical u se
re d u ce E C F vo lu m e e .g. h e art failu re , n e p h ro tic syn d ro m e ,
cirrh o tic ascite s) , in cre ase fre e wate r cle aran ce
e .g. S IAD H -in d u ce d h yp o n atre m ia) , an tih yp e rte n sive
J ad ve rse e ffe cts
alle rgy in su lfa-se n sitive in d ivid u als, e le ctro lyte ab n o rm alitie s
h yp o kale m ia, h yp o n atre m ia, h yp o calce m ia,
h yp e rcalciu ria/u rico su ria with sto n e fo rm atio n ) , vo lu m e
d e p le tio n with m e tab o lic alkalo sis)
Thiazide Diure tics
J e xam p le s
h yd ro ch lo ro th iazid e H C T Z ) , ch lo ro th iazid e D iu ril)
in d ap am id e L o zo l, L o zid e ) an d m e to lazo n e Z aro xo lyn )
are re late d co m p o u n d s
J m e ch an ism
in cre ase s th e e xcre tio n o f N a
+
/C l
/H 2O b y in h ib itin g th e N a
+
/C l
tran sp o rte r in th e d istal tu b u le an d co rtical lo o p o f H e n le

J clin ical u se
first lin e th e rap y fo r e sse n tial H T N o fte n in co m b in atio n with
o th e r an tih yp e rte n sive s o r lo o p d iu re tics) , id io p ath ic
h yp e rcalciu ria an d re cu rre n t re n al sto n e s, d iab e te s in sip id u s
h yp o kale m ia, in cre ase d se ru m u rate le ve ls, h yp e rcalce m ia,
ad ve rse ly affe cts lip id p ro file s, th iam in e d e p le tio n
Potas s ium-Sparing Diure tics
J e xam p le s
sp iro n o lacto n e Ald acto n e ) , triam te re n e D yre n iu m ) ,
am ilo rid e M id am o r
J m e ch an ism
e ach acts at a d iffe re n t ste p in th e D C T wh e re N a
+
is
re ab so rb e d an d K
+
an d H
+
are e xcre te d
th e n e t re su lt is d e cre ase d N a
+
re ab so rp tio n an d H
+
an d K
+
se cre tio n : sp iro n o lacto n e is an ald o ste ro n e an tago n ist
ald o ste ro n e p ro m o te s n o rm al fu n ctio n in g o f th e D C T N a
+
ch an n e l) am ilo rid e an d triam te re n e d ire ctly clo se ap ical N a
+
ch an n e ls
J clin ical u se
ascite s sp iro n o lacto n e ) , re d u ce s p o tassiu m e xcre tio n d u rin g
th e rap y with th iazid e o r lo o p d iu re tics, cystic fib ro sis
am ilo rid e re d u ce s visco sity o f se cre tio n s)
h yp e rkale m ia cau tio n with AC E I) , gyn e co m astia e stro ge n ic
e ffe ct o f sp iro n o lacto n e )
N o te s
DIURETICS . . . CONT.
Combination Diure tics
J e xam p le s
D yazid e , M axid e triam te re n e an d H C T Z ) , Ald acto zid e
sp iro n o lacto n e an d H C T Z ) , M o d u re tic am ilo rid e an d H C T Z ) ,
Vaso re tic e n alap ril an d H C T Z ) , Z e ste re tic lisin o p ril an d H C T Z )
J clin ical u se
p o tassiu m -sp arin g d ru gs are co m b in e d with th iazid e to re d u ce
h yp o kale m ia
AC E I are co m b in e d with th iazid e s to p ro m o te
syn e rgistic an tih yp e rte n sive e ffe ct AC E I re d u ce s
vaso co n strictio n an d in cre ase d re sistan ce wh ich re su lts
se co n d arily fro m d iu re tic-in d u ce d vo lu m e co n tractio n )
Carbonic Anhydras e Inhibitors
J e xam p le s
ace tazo lam id e , m e th azo lam id e , an d d ich lo rp h e n am id e
J m e ch an ism
in h ib its carb o n ic an h yd rase in p ro xim al tu b u le , th e re b y
in h ib itin g th e re ab so rp tio n o f N aH C O 3 b y an in d ire ct
m e ch an ism
J clin ical u se
glau co m a, to raise u rin e p H in cyste in u ria
p e rio d ic p aralysis se co n d ary to n o n -AG m e tab o lic
acid o sis an d h yp e rkale m ia) , ad ju n ctive th e rap y in e p ile p sy
Os motic Diure tics
J e xam p le s
m an n ito l, glyce ro l an d u re a
J m e ch an ism
n o n -re so rb ab le so lu te s th at e xe rt o sm o tic p re ssu re in th e
re n al tu b u le s p ro xim al an d co lle ctin g d u ct) , p ro m o tin g th e
e xcre tio n o f wate r
J clin ical u se
p ro m o te th e e xcre tio n o f b o d y wate r re fracto ry e d e m a,
h yp o n atre m ia)
lo we r in tracran ial o r in trao cu lar p re ssu re
p re ve n tio n o f AR F b y p ro m o tin g d iu re sis an d cle aran ce o f
tu b u lar d e b ris)
Drawing by VinceMazzurco

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NEPHROLOGY

, o sm o lality an d p H are co m m o n ly m e asu re d

, also kn o wn as th e u rin e n e t ch arge is

1 -3 am p s give n as 3 am p s o f 7.5% o r 8.4%

an d p C O 2 to e stab lish m ajo r p ro ce ss re sp irato ry/m e tab o lic)

stim u late d b y AII, h yp o vo le m ia)

stim u late d b y AII, h yp o vo le m ia,

re ab so rp tio n : lo st in u rin e an d b u ffe r is d e p le te d

in u rin e p ro xim al R TA) o r G I tract d iarrh e a)

> rise in an io n gap , co n sid e r m ixe d AG /n o n -AG

fall, co n sid e r a co n cu rre n t m e tab o lic o r re sp irato ry alkalo sis

e xp e cte d : 1 -1 .3 m m H g d e cre ase d P C O 2 fo r e ve ry 1 m E q /L

if p C O 2 d e cre ase s m o re th an e xp e cte d , th e re is also a

ge n e ratio n ; ald o ste ro n e p ro m o te s h yp o kale m ia

= 0.1 x in cre ase in p C O 2

= 0.3 x in cre ase in p C O 2

J acu te ly, d e cre ase in H C O 3

= 0.2 x d e cre ase in p C O 2

= 0.5 x d e cre ase in p C O 2

with o u t ch e ckin g syste m ic p H )

th at are b o th lo w o r b o th h igh o r wid e p lasm a AG

) is gu id e d b y arte rial b lo o d gas p H , n o t

ch an n e l in th e th ick asce n d in g lim b , ve n o d ilatio n

tran sp o rte r in th e d istal tu b u le an d co rtical lo o p o f H e n le

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