YKS

what are the major causes of an anion gap

patient with skin lesions; fibroblasts are cultured and fail to metabolize ceramide trihexoside. what is the patient at the greatest risk for?

MUDPILES Methanol (formic acid) Uremia Diabetic ketoacidosis Paraldehyde/ phenformin Iron tablets (INH) Lactic acidosis Ethylene glycol (oxalic acid)<-- anti-freeze Salicylates

RENAL

renal failure (the pt has Fabry disease (lysosomal storage disease)-- missing agalactosidase enzyme--earliest manifestations are angiokeratomas, hypohidrosis (little sweating) and acroparesthesia (burning sensation in extremities)

in what part of the nephron does the majority of free water reabsorption take place? bilateral masses composed of fat, smooth muscle and blood vessels are detected in a patient. what does she have

proximal tublules (no matter what) -no concentration or dilution occurs here because fluid is absorbed isomotically with solutes

Tuberous sclerosis (angiomyolipomas) -autosomal DOMINANT *can also have: -hamartomas in the brain -rhabdomyomas -facial angiofibromas -leaf-shaped patched of skin lacking pigment (ash leaf spots)

describe the location an inferior pole horseshoe kidney

what happens to the excretion of free H+ and titratable acids during metabolic acidosis in the presence of ADH, which part of the the nephron has 1.) the highest 2.) the lowest concentration of urine

the isthmus of the horseshoe kidney usually lies anterior to the aorta and IVC, and posterior to the inferior mesenteric artery

more H+ is excreted (some of which is bound to NH4+ and H2PO4-)

1.) the collecting ducts 2.) distal tubule **in the absence of ADH, the loop of Henle has the highest concentration

which are the only diuretics that increase calcium reabsorption from the nephron

thiazides (HyperGLUC)

calculation for RBF

RPF/(1-hematocrit)

calculation for renal plasma flow (RPF)

PAH clearance ([Urine-pah] x V) / [Plasma -pah]

RENAL1

YKS

RENAL

FF = GFR/RPF

calculation for Filtration fraction

patient being treated for acute leukemia develops oliguria. renal biobsy reveals multiple uric acid crystals obstructing the renal tubular lumen. the principle site of uric acid precipitation would be where?

(rPf, not rbf)

-tumor lysis syndrome -large number of tumor cells are destroyed during chemo, and intracellular ions including uric acid (a metabolite of tumor nucelic acid) are released and filtered by the kidneys. Uric acid precipates in acidic pHs, and the lowest pH along hte nephron is distal tubules/collecting duct **prevention: urine alkanization and hydration

what are the two major electrolyte disturbances seen with amphotericn B

-K+ and Mg2+ (hypo)

lymphocytic infiltrate in renal parehcnyma after renal transplant

what do you use to treat T cell mediated acute organ rejection (kidney, heart and liver)

T cell mediated allograft rejection (rejection can also be antibody mediated, but you wouldn't see the infiltrates (only antibodies would be present)

OKT3 (anti-CD3) *inhibits T-cells

pyruvate dehydrongenase (converting pyruvate into acetyl CoA for the TCA cycle) *note: lactate dehydrongenase converts pyruvate into lactic acid (anerobic respiration) **note: pyruvate carboxylase converts pyruvate into oxaloacetate

hypoxia-induced lactic acidosis is caused by a low activity of what enzyme

how do loop diuretics work?

they inhibit Na-K-2Cl symporters in the ascending limb of the loop of henle and effectively block Na and Cl transport, resulting in increased Na, Cl and fluid excretion **Loops also stimulate prostaglandin release, which increases renal blood flow, leading to increased GFR (and enhancing drug delivery) *thus, using NSAIDs at the same time can result in a decreased diuretic response

which class of diuretics is the most potent? what are the common side effects of loop diuretics? what happens to the GFR, RPF and FF in sever hypovolemia?

loop diuretics -used for treating edema

hypocalcemia, hypokalemia, hypomagnesemia and otoxoicity -usually occurs with rapid IV administration, or when loops are used in combo with other ototoxic agents like aminoglycosides, salicylates and cisplatin -hearing impairment is usually reversible

-large decrease in RPF -moderate decrease in GFR (efferent arteriole constricts) -FF increases (because the RPF drops much more than the GFR)
RENAL2

YKS

RENAL

what is the preferred method for diagnosin diabetic nephropahty

a child with selective protienuria (albumin only) due to loss of negatively charged components of the basement membrane

measuring albumin in the urine -diabetic nephropathy is the leading cause of ESRD in the US

minimal change nephrotic syndrome

what is the primary site of K+ excretion (concentrating the urine with potassium)

the collecting duct

what happens to the the concentrations of PAH, creatinine, inulin and urea as fluid runs along the proximal tubule (tubular fluid/plasma ultrafiltrate graph)

their concentration increases

what happens to the concentration of bicarb, glucose and amino acids as fluid moves along the proximal tubule (tubular fluid/ultrafiltrate graph)

decreases

what effect does vasopressin (ADH) have on excretionof urea

what is the most common cause of intrinsic renal failure in hospitalized patients
what parts are the first to suffer when blood flow (oxygen delivery) to the kidneys is low

urea reabsorption into the inner medullary INTERSTITIUM increases, thus fractional excretion of urea decreases

ATN
the proximal tubules and the ascending limb -there location in the medulla already makes them have low blood supply -they use ATP to transport ions, so they must have O2

relative risk table

what electrolyte problems will you see in a patient with renal damage from amphotericin B

exposure in the rows outcomes in the columns

hypokalemia, hypomagnesemia due to distal tubular membrane permeability
RENAL3

YKS

Kimmelsteil Wilson nodules

diabetic nephropathy -diabetic nephropathy starts with glomerular hyperfiltration and leads to an increase in mesangial matrix and thickening of the basement membrane -affects the glomeruli and arterioles

RENAL

which classes of drugs prevent the progression of diabetic nephropathy which antipsychotic drug can cause a drug-induced diabetes insipidus

ACE inhibitors and ARBs

lithium

what is calcineurin?

-protein phosphotase in T cells -allows for the production of IL-2, which stimulates the growth and differentiation of T cells

which two drugs used in kidney translpants inhibit calcineurin

what is the most important prognostic factor in post-strept glomerulonephritis

Cyclosporine and Tacrolimus

age -kids have a better prognosis than adults

it's secondary to CMV-induced retinitis, which is treated with ganciclovir, cidofovir and foscarnet
antiviral med used to treat CMV retinitis -analog of pyrophosphate that can chelate Ca++ and promote nephrotoxic renal magnesium wasting. Can result in hypocalcemia and hypomagnesemia

what is the likely etiology of visual impairment in an HIV infected patient

Foscarnet

What effect does acyclovir have on the acyclovir causes crystilline nephropathy if adequate hydration is not also provided kidneys? what often causes formation of calcium oxalate crystals
ethylene glycol (antifreeze) -antifreeze also causes an anion gap metiabolic acidosis, increased osmolar gap
RENAL4

YKS

where is glucose filtered and where is it reabsorbed?

if most of the glucose filtered is reabsorbed in hte proximal tubules, why does glycosuria occur?

glucose is normally filtered at the glomerulous and completely reabsorbed by the proximal tubule
reabsorption of glucose occurs via Na/glucose cotransporters--> because this process is carrier mediated, it can become oversaturated *notes: the renal tubules DO NOT secrete glucose

RENAL

which substances are not reabsorbed or secreted in the tubules

which substances have a net tubular reabsorption (the amount actually excreted is far less than the amount initially filtered)

Inulin and Mannitol

glucose, sodium, urea

PAH (creatinine is filtered and not reabsorbed, but only a little is secreted) **note: PAH is secreted via carrier mediated transport; similar to glucose, but glucose is being reabsorbed by NA/glucose co-transporters in the proximal tubules, whereas PAH is being SECRETED by carriers in the tubules **the secretion of PAH can become saturated (b/c it uses carriers), but the filtration cannot be saturated

which substances are filtered, secreted and not reabsorbed

spironolactone

K+ sparring aldosterone antagonist diuretic used in treating class II and IV heart failure patients *it's structurally similar to steroids, so it can cause gynecomastia, decreased libido and impotenece **Eplerenone is a newer drug with less endocrine effects.

a patient with a metabolic acidosis with a normal pCO2 a tear in the gastric mucosa near the gastroesophageal junction
why is spironolactone a part of the standard therapy for class III and IV heart failure patients

this patient has a superimposed respiratory acidosis (respiratory failure) *metabolic acidosis causes a drop in the HCO3-, adn your body will try and even things about by blowing off CO2 in an attempt to get rid of some acid. If the pCO2 remains normal, it means your body isn't able to blow off CO2

Mallory-Weiss tear -caused by excessive vomiting -recurrent vomiting can cause a metabolic acidosis (you're losing a lot of the acid in your stomach)

-mild diuretic effects -inhibition of the neurohormonal effects of aldosterone leading to decreased ventricular remodeling and cardiac fibrosis *in heart failure, the RAAS is activated---> leads to elevated aldosterone--> aldosterone is known to cause ventricular remodeling leading to cardiac fibrosis
-cytoplasmic antineutrophil cytoplasmic antibody -Wegener's granulomatosis (RPGN/pauci immune) includes: -nephritis -lung involvement -crescent on light microscopy (irreversible sclerosis) **there are no immune deposits on immunofluorescence, despite the fact that it's type III hypersens... just c-ANCA

c-ANCA

RENAL5

YKS

RENAL

effacement of foot processes

minimal change disease (seen on EM)

from the epithelial cells of the proximal tubule (clear cells are filled with fat and glycogen)

where in the nephron do most clear cell renal carcinomas originate from

what do the antibodies in Goodpasture syndrome react with (be specific) linear deposits of IgG and C3 along hte basement membrane on immuofluorescence

alpha3-chain of collagen type IV, found in the basement membrane

Goodpasture syndrome
-renovascular hypertension (usually associated with fibromuscular dysplasia or atherosclerosis) -diuretic use -malignant hypertension -renin-secreting tumors

what are some causes of secondary hyperaldosteronism painless hematuria 2-3 dyas after an upper repiratory tract infection
IgA nephropathy accompanied by extrarenal symptoms (abdominal pain, joints (arthralgia and arthritis) purpuric skin lesions<--buttocks and lower extremites)

IgA nephropathy (Berger disease) -IgA deposits in the mesangium of glomeruli on IF microscopy only!)

Henoch Schonlein purpura

what effect does prolonged use of NSAIDs have on the kidneys

papillary necrosis and chronic interstitial nephritis (it's reversible!)

diuretic that blocks the Na-Cl symporters in the distal convoluted tubules, thus blocking reabsorption of of Na, CL and water *since only a small amount of Na reaches the distal convoluted tubule, thiazides are not as efficacious as loops

moa of thiazides
diuretic also used to treat open-angle and secondary glaucoma and how does it work

Acetazolamide -inhibitor of carbonic anhydrase (found in the proximal tubules and the eye) -->blocks NaHCO3 and water reabsorption
RENAL6

what is the most serious concern during the recovery phase (polyuric phase) of ATN

YKS

RENAL

hypoKalemia

affect of salicylate intoxication of pH

-first causes and acute respiratory alkalosis -with high doses, a superimposed metabolic acidosis will occur (the acidosis will predominate)

cystic dilations of the MEDULLARY collecting ducts what is one of the more sever toxicities of Mannitol
what effect does ureteral constriction/obstruction have on GFR and FF what is the equation for the net excretion of a substance that is filtered and reabsorbed

medullary sponge kidney -the cysts don't involve the cortex (like in ADPKD) -kidney stones are the only problem that could arise

pulmonary edema

acutely decreases the GFR and glomerular filtration fraction

total filtration rate - total tubular reabsorption rate total filtration rate = GFR x Plasma

diffuse thickness WITHOUT hypercellularity spike and dome appearance on EM

membranous glomerulonephropathy -can occur secondary to tumors, infections and certain medicatons
-elevated anti-streptolysin O titers -elevated anti-DNAse B titers -decreased C3 -cryoglobulins
renal vein thrombosis due to decrease in antithrombin III *left testicular vein drains in to the left renal artery, then into the IVC (right testicular artery has a straight shot to the IVC); a decrease in antithrombin III can cause a renal vein thrombosis, which will back up drainage of the left testis, causing a variocele

What labs do you expect to see with post-streptglomerulonephritis?

male patient with nephrotic syndrome and a left-sided variocele (fluid in testis)

female presenting with flank pain that radiates to the groin after a hysterectomy

hydronephrosis due to damage of the ureter during the hysterectomy *the ureters lie just posterior to the uterine arteries, which are ligated during this procedure
RENAL7