Renal Flashcards
Renal Clearance
Cx = renal clearance of substance X Cx = Ux * V / Px where Ux is the urine concentration of substance X, V is urine flow rate, and Px is the plasma concentration of substance X
Cx = GFR, no net reabsorption or secretion of substance X
Cx < GFR, net reabsorption of substance X
Glomerular filtration
Estimated w/ insulin clearance as insulin is near absorbed or secreted and freely filtered
GFR = Uinsulin * V / Pinsulin
GFR normal approximately 100 mL/min
Creatinine clearance is an approximate measure of GFR
Slightly overestimates GFR because creatinine is moderately secreted by renal tubules
Effective renal plasma flow
Can be estimated by using para-amniohippuric acid (PAH) clearance because it is both filtered and actively secreted in proximal tubule (not all PAH entering kidney is filtered, but all is excreted)
ERPF = Upah * V / Ppah = Cpah RBF = ERPF / (1-Hct)
Filtration fraction (FF)
FF = GFR/RPF
Normal FF = 20%
Glomerular dynamics
Afferent arteriole constriction: decreased RPF, GFR, no change in FF
Efferent arteriole constriction: decreased RPF, increased GFR (increased plasma hydrostatic pressure), increased FF
Increased plasma protein concentration: no change in RPF, decreased GFR (increased plasma oncotic pressure), decreased FF
Constriction of ureter: no change in RPF, decreased GFR, decreased FF
Glucose clearance
Glucose at normal plasma level ~ 100 is completed reabsorbed at the proximal tubule but Na/glucose cotransport
Glucose plasma level of ~ 200 glycosuria begins
Glucose plasma level of ~ 375 all transporters are saturated
Early proximal convoluted tubule
Reabsorbs all of the glucose and amnio acids and most ions (HCO3, Na, Cl, K, PO4) and water
Secretes NH3 to buffer H+ in tubule lumen
PTH inhibits PO4 absorption
ATII stimulates Na and HCO3 absorption
65-80% of Na reabsorbed
Thin descending loop of Henle
Passively reabsorbs H20 via medullary hypertonicity (impermeable to Na)
Concentrating segment making urine more hypertonic
Thick ascending loop of Henle
Actively reabsorbs Na, K, and Cl
Indirectly induces the paracellular reabsorption of Mg and Ca
Impermeable to water, making urine less concentrated
10-20% Na reabsorbed
Loop diuretics prevent absorption of Na at this region (NaK/2Cl cotransporter into cell lumen)
Early distal convoluted tubule (DCT)
Actively reabsorbs Na and Cl, making urine more hypotonic
PTH increased Ca/Na exchange and increasing Ca reabsorption
5-10% Na reabsorbed
Thiazide diuretics prevents absorption of Na at this region (NaCl cotransporter) and decreases Ca excretion
Collecting tubule
Reabsorbs Na in exchange for secreting K and H (regulated by aldosterone which inserts Na channel on luminal side) —-> principle cells
ADH acts to insert aquaporin H2o channels on luminal side to increase water reabsorption –> principle cells
Amiloride blocks Na channels –> principle cells
3-5% Na reabsorbed
Fanconi syndrome
Reabsorption defect in PCT
Associated w/ increased excretion of nearly all amnio acids, glucose, bicarb, and phosphate
Can result in metabolic acidosis (proximal renal tubular acidosis)
Causes include hereditary (Wilson), ischemia, and nephrotoxins
Bartter syndrome
Reabsorption defect in thick ascending loop of Henle
Affects NaK/2Cl co transporter
Results in hypokalemia and metabolic alkalosis
Gitelman syndrome
Reabsorption defect of NaCl in distal convoluted tubule
Less severe than Bartter but can still lead to hypokalemia and metabolic alkalosis
Liddle syndrome
Increased Na reabsorption in distal and collection tubules due to increased activity of epithelial Na channels
Results in hypertension, hypokalemia, metabolic alkalosis
