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Course: Nephrology
Lect urer: Dr. Mora
Source: L ecture, Handout
Nephro
Week: 5-6
Topic: Chronic Kidney
Disease
Mgmt of Hpn in CKD ............................................................................................... 5
Table of Contents
Anemia ......................................................................................................................... 5
Consequences ........................................................................................................... 5
Causes ...................................................................................................................... 5
Management ............................................................................................................. 5
Abnormal hemostasis .................................................................................................... 5
Clinical Manifestations .............................................................................................. 5
Treatment ................................................................................................................. 5
Epidemiology..................................................................................1
Definition ......................................................................................1
NKF K/DOQI US Definition ..................................................................... 1
NKF K/DOQI US Classification ................................................................................ 1
Pathophysiology ..............................................................................2
Risk Factors for CKD .................................................................................... 3
Staging CKD ..................................................................................3
Estimate GFR ............................................................................................... 3
Measure Albuminuria .................................................................................... 3
EPIDEMIOLOGY
Prevalence: 120/1M
2013 opp est 97M
814200
Incidence 12,122 2012
Prev 18868
50% will die this year
1 death per hour
th
7 leading cause of death
14% newly diagnosed ESRD die w/o tx (vs 25% in 2011)
Renal failure pts go through a continuum of progressive
attrition of nephron number
o
If recognized earlier you have time intervene and
delay progression
Img: Kidney Int 2007 international society of nephrology
3
4
5
Lecture
Stage
1
DEFINITION
Description
Kidney damage w/normal or high
GFR
Kidney damage and mild decrease in
GFR
Moderate decreased in GFR
Severe decrease in GFR
Kidney failure
GFR
90
60-89
30-59
15-29
15 (or
dialysis)
mra
Med3C
Nephro
Abnormalities of kidney structure of nc, present for >3 months, with implications for health
Classified based on cause, GFR, category and albuminuria category (CauseGFRAlbuminria classification)
o
Ex Diabetic nephropathy, G3b, A3
o
Get randomalbumin
PATHOPHYSIOLOGY
Long-term reduction of
renal mass
Long term
maladapative
response (sclerosis)
the healing/scarring
process
Initial renal insult, kidney can recover but if not able goes to insuffience;
essential mxn of functional adaptation is RAAS and the ANG II, a very powerful
vasoconstrictor, causing peripheral capillary vasoconstriction, hypertension
and eventually glomerular hypertension, which once present it creates a
vicious circle and why BP control is so important and the use of ACEI comes
into play, the other thing is that Ang II is important in aldosterone release
which is produced in the zona glomerulosa and once released acts in the
mineralocorticoid receptor at the basolatoreral membrane at the _____ cell at
the cortical collecting ______. Once elaborated and epithelial Na channel in
apical membrane causing absorption of sodium Increased plasma volume
(expanded) BP and most common complication of CKD is Hpn and most
common cause of hpn in CKD is volume overload state .Culminates in
glomerlosclerosis and interstitial fibrosis two most important pathologic
hallmarks in irreversible renal injury.
The same mxn that heals and adapts is the same one that
becomes detrimental in long-term renal outcome
Lecture
mra
Med3C
MANIFESTATIONS OF CKD
Nephro
Salt/water restriction
Potassium Homeostasis
Common to see hyperK in ESRD but GFR has to be <5 already b/c
the homeostatic mxn in place will work up until that point
STAGING CKD
Estimate GFR
MDRD equation
Cockcroft-Gault equation
Hypokalemia in CKD
Measure Albuminuria
Uremic Toxins?
A Conundrum no common toxin found
Products of bacterial
metabolism as
aromatic amines,
and skatoles
Products of
nitrogenous
metabolism,
Guanidino
compounds
Uremic
toxins?
Metabolic Acidosis
Compounds
retained in
circulation, or
underproduced
Biochemistry of Uremia
Urea and Creatinine
iii.
Lecture
At GFR <15
Less ammonia production (initially) less proton
excretion non-anion gap acidosis
o
Initially
o
Ammonia comes from glutamine combines with
H+ which is eliminated form body thru urine == acid
elimination by the body dysfnc means more
retention of H+/protons
Worsening renal fnc urinary net daily acid excretion
to 30-40mmol Anion gap acidosis
o
Over time
Net effect: net protein catabolism malnutrition
Management: start alkali supplementation when HCO3 falls
below 20-23 mmol/L (n AKI wait until 15 but here we have to
prevent bone problem d/t malnutrition)
o
Consider need for diuretic avoid volume overload
PTH
Classic ex: Osteitis fibrosa
cystica
Med3C
High bone turnover CM
Brown tumors
Compression syndromes
Erythropoietin resistance
blood cell forming elements
are destroyed
Muscle weakness
Constitutional sx
Excessive suppression of
PTH production (VitD,
excess calcium exposure)
Fractures
Accumulation of
unmineralized bone matrix
Traditional classic
Hypertension
Hypervolemia
Dyslipidemia
Sympathetic overactivity
Hyperhomocysteinemia
Nontraditional CKD
related
Anemia
Hyperphosphatemia
Hyperparathyroidism
Sleep apnea
(sympathetic activity
BP)
Generalized inflammation
(chronic inflamm state)
Inflammatory state
Accelerated vascular
occlusive dse & Rapid
vascular calcification(w/low
fetuin level)
Attenuated coronary
reserve
Causes
o
MI vascular calcification
o
LVH chronic hpn
o
Cardiomyopathy anemia and high output failure
o
Salt and water retention
Can be systolic or diastolic
Risk Factors
Nephro
Lecture
mra
Med3C
Targets
130/80 mmHg
Early Stage
Causes
Relative deficiency of erythropoietin
Diminished RBC survival
Bleeding diathesis
Iron deficiency
Hyperparathyroidism/BM fibrosis
Chronic inflammation
Folate or vitamin B12 deficiency
Hemoglobinopathy
Recombinant EPO
Darbepoeitn
Blood transfusion
o
Easiest way to correct in sx pt req surgery
o
Limitations: (Pre-) Sensitization, Infection, Iron
overload
Iron supplements
Studies show req to keep Hgb at pace w/EPO syn in the body
Desmopressin (DDAVP)
Cryoprecipitate
IV conjugated estrogen works well but takes time
Blood transfusion always improves
EPO therapy
Optimal dialysis pre-surgery avoid intraop coagulopathy
Neuromuscular
irritability (hiccups,
cramps, fasciculations,
muscle twitching)
Adv Untx
Asterixis
Seizures
Coma
Stage 4 CKD
Sensory nerves > motor nerves
Lower extremities > upper extremities
Distal > proximal
Restless leg syndrome
o
Ill-defined sensation
o
Debilitating
o
Relieved by frequent leg movement
Onset of sensory abn indication to start dialysis
Dialysis & KT may reverse neurologic dysfunction
Uremic fetor
o
Breakdown of urea to ammonia in saliva
o
Dysgeusia
Gastritis, peptic ulcer dse, mucosal ulceration
Constipation
o
Worsened by calcium & iron supplements
Anorexia, nausea, vomiting
o
Protein restriction
Protein-energy malnutrition
o
Protein restricted diet
o
Resistance to anabolic action of insulin & other
growth factors
o
Indication for RRT
Clinical Manifestations
Treatment
Reversal of abn bleeding and coagulopathy
Abnormal hemostasis
Late Stage
Management
Memory
Concentration
Sleep
disturbances
Peripheral neuropathy
Consequences
Clinical Manifestations
Nephro
Low testosterone
Sexual dysfunction
Oligospermia
Delayed sexual maturation
Metformin
mra
Med3C
Nephro
CLINICAL RENOPROTECTION
Reading assignment; note below taken from Harrisons
Description
Kidney damage w/ N or Inc GFR
GFR
>90
60-89
3
4
5
30-59
15-29
<15 (or
dialysis)
Action
Diagnosis & treatment, tx of comorbids, slowing progression, CVD risk
reduction
Estimating progression
Evaluating & treating complications
Preparation for RRT
Renal replacement (if uremia present)
Elevated BP proteinuria
If agent reduces BP it proteinuria and slows GFR decline;
their effectiveness is measured in proteinuria reduction
Basis for guideline of maximum 125/75 mmHg as target BP in
proteinuric CKD pts
Protein Restriction
Uremic pericarditis
Encephalopathy
Intractable muscle cramping
Anorexia
Nausia not attributable to reversible causes
Evidence of malnutrition
Fluid and electroly abn (*hyperK or ECF volume overload)
Patient Education
2 Possible Responses
Lecture
mra