Flashcards in Renal Deck (65)
Renal Clearance (Cx)
= Ux*V/ Px
Volume of plasma cleared per unit time (ml/min)
Px, Ux= mg/ml
V= urine flow rate
Cx reabsorption , etc
Cl inulin = GFR
Cl pah = RPF
clearance of inulin
about 100 ml/min
= Kf (Pgc - Pbs)- (oncgc- oncbs) but oncbs = 0 mostly
Ccr = GFR but overestimates by about 10-15% bc of secretion in the PCT
285-295 mOsm/kg water
Water division between body and compartments
60% of body
20% ECF (75% interstitial, 25% plasma)
eRPF (effective renal plasma flow)
Clearance of PAH (para-aminohippuric acid)
100% cleared (secreted by carrier and saturable transport in the PCT)
underestimates RPF by about 10%
= RPF /(1-Hct)
GFR * Plasma concentration
What is the effect of prostaglandins on afferent arteriole?
dilate (increase GFR, increase RPF, FF constant)
NSAIDS block this path
At what plasma glucose does glucosuria begin?
Can be decreased in normal pregnancy (decrease ability of PCT to reabsorb glucose)
At what plasma glucose are transporters saturated ?
pH = 6.1 + log (HCO3-)/ 0.03 PCO2
compensation metabolic acidosis
Pco2= 1.5 (HCO3) + 8 +- 2
Anion gap formula
(Na)- (HCO3- + Cl-)
Correct for albumin
= Px * GFR -  reabsorbed
Most common site of ureter obstruction in fetus?
Uteropelvic junction (last to canalize)
What is horseshoe kidney associated with?
- uteropelvic junction obstruction, hydronephrosis, renal stones, chromosomal aneuploidy syndromes (turner, wiliams, patau, etc); infection, and rarely renal cancer
Filtered - excreted
excreted - filtered
Glomerulonephritis, malignant hypertension
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
Fatty casts/oval fat bodies
Granular casts (muddy brown)
acute tubular necrosis
ESRD/chronic renal failure
nonspecific, can be normal esp in concentrated urine samples
Mechanism of action mannitol?
Increases tubular fluid osmolaltiy --> increases fluid flow
Also decreases intracranial pressure
Clinical use of mannitol?
Increased ICP, drug overdose (increases renal flow)
Toxicity of mannitol?
When is mannitol contraindicated?
HF (pulmonary edema)
What is the mechanism of acetazolamide?
Carbonic anhydrase inhibitor
Acts in PCT
Decreases HCO3/Na reabsorption
Decreases total body HCO3 stores
What are the clinical uses of acetazolamide?
Glaucoma (CA in cilliary body in eye)
Urinary alkalinzation (excrete weak acids; cystein and uric acid stones)
Pseudotumor cerebri (CA in choroid plexus)
What is the toxicity of acetazolamide?
Hyperchloremic metabolic acidosis
NH3 toxcity (encephalopathy with hepatic impairment)
What is the mechanism of furosemide action?
Blocks the NKCC pump in the TAL
Stimulates PGE release to vasodilate afferent arteriole
What is furosemide used for?
What is the toxicity of furosemide?
Allergy to sulfa
When would you use ethacrynic acid?
Diuresis in sulfa allergic patients
Same action as furosemide
Phenoxyacetic acid derivative
What is the mechanism of HCTZ?
Blocks the NCC pump in the early DCT
Clinical use of HCTZ
HT, HF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis
Toxicity of HCTZ
Hypokalemic metabolic alkalosis
Mechanisms of action of Spirnolactone?
competitive MR inhibitors
Mechanism of action of triamterene/amiloride?
Block the ENaC channel
Clinical use of K sparring diuretics
HF (even without frank edema can be useful to decrease aldosterone and its fibrotic action on the heart)
Ca based nephrolithiasis
Toxicity of K sparring diuretics?
Spirnolactone can have actions on other endocrine receptors causing gynocomastia (testosterone) and other anti-androgenic effects
What are the mechanisms of action of ACE inhibitors?
Block ACE which converts ANGI to ANGII and metabolizes bradykinin into inactive metabolites
Clinical uses of Ace inhibitors?
Diabetic nephropathy (decreases constriction of efferent arteriole caused by NEG, decreased intraglomerular pressure slowing GBM thickening and mesangial expansion)
Prevent unfavorable heart remodeling
What are the toxicities of ACE inhibitors?
Teratogen (renal malformations)
Increase Creatinine (decrease in GFR)
When are ACE inhibitor counterindicated?
Cl esterase deficiency
Bilateral renal artery stenosis (decrease GFR)
What is the mechanism for ARBs?
Block the binding of ang II to ATI Rs (Gq)
Clinical use of ARBs?
Diabetic nephropathy with intolerance to ACE inhibitors (angioedema, cough)
Toxicities of ARBs?
Decrease renal function
Mechanism of action of aliskiren?
binds and inhibits the action of renin
What is the clinical use of aliskiren?
What is the toxicity of aliskiren?
Decreased renal function
When is aliskiren counterindicated?
Diabetics taking ACEs or ARBs
What are weak acid drugs that are excreted by alkalinization of the urine?
aspirin, phenobarbitol, methotrexate, and TCAs
What are weak bases that are improved by acidification of the urine?
What drugs cause DI?
What drugs cause Fanconi syndrome?
Hemorrhagic cystitis is caused by which drugs?
Interstitial nephritis is caused by which drugs?
Methicillin, furosemide, and NSAIDs
What can you administer with cyclophosphomide to prevent hemorrhagic cystitis?
What drugs cause SIADH?
Can't concentrate Serum sodium
Pentad for TTP?