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Highly selective proteinuria

Mostly low MW protein excretions; Minimal-change disease - defect in negatively charged molecules in GBM --> inability to repel albumin (also transferrin)


ACEi work how?

Decrease angioI->angioII, which blocks arteriolar vasoconstriction and aldosterone secretion. Ultimately lead to increased renin. B/c ACE breaks down bradykinin, increased bradykinin level.


Substances with no tubular absorption or secretion

Inulin and mannitol


Substances with net tubular secretion?

PAH (almost all secreted at PROXIMAL tube) and creatinine


Crescent formation pathogenesis?

Diagnostic for rapidly (wks-months) progresive glomerulonephritis. Dmg to BM lead to gaps where macrophages, T-cells, FIBRIN go into Bowman's space. Fibrin deposition leads to parietal cell proliferation = crescent. Linear deposits of immunoglobulin.


Renal papillary necrosis associated with?

Sickle cell disease/trait. Analgesic nephropathy (e.g. phenacetin), DM, Acute pyelo or UT obstruction. Gray-white/yellow necrosis at distal renal pyramids. Coag infarct. Abrupt gross hematuria, colicky flank pain b/c of ureteral obstruction 2/2 sloughed papillae.


RPGN types?

Type 1 = anti-GBM. associated with Goodpasture syndrome. Immuno w/ IgG and C3 deposits (Type II HS). Type 2=IC-mediated 2/2 post-strep, SLE, IgA or Henoch-Schonlein....Type 3 = "pauci immune" w/ ANCA. Associated with Wegener's.



Anti-GBM (alpha-3 chain of collagen type IV). RPGN (crescents) and pulmonary hemorrhages.



Synthesized and released by zone glomerulosa cells. Stimulated by angiotensin II and high serum K+. Promotes K+ secretion from principal cells and H+ secretion of intercalated cells of renal collecting tubules.


Drug that acts on proximal tubule

Acetazolamide - Carbonic anhydrase inhibitor. Drug blocks NaHCO3 reabsorption -> self-limited diuresis. Used for acute angle-closure glaucoma for dec. aqueous humor formation, metabolic alkalosis, pseudo tumor cerebra. Tox -hyperchloremic metabolic acidosis, parasethesias, NH3 fox, sulfa allergy


Drug that acts on descending Henle

Mannitol, an osmotic diuretic. Very permeable to water.


Drug that acts on thick ascending limb of Henle?

Loop diuretics (e.g. furosemide) Inhibits Na-K-2Cl symporters leading to increased Na, Cl-, and H2O excretion + Ca excretion.


Drug that acts on distal convoluted tubule

HCTZ. Impermeable to water and transports Na+ and Cl-.


Drugs that work on collecting duct?

K+ sparing diurects. Aldo receptor antagonists and amiloride (Na+ channel blocker)


RCC path

From renal tubular cells. Rounded or polygonal cells w/ abundant clear cytoplasm b/c had glycogen and lipids


Thiazide side effects

Decrease intravascular volume leads to aldo leads to excretion of K+ and H+ -> HypoK and metabolic ALKalosis. Hyponatremia. Hyperuricemia b/c of uric acid reabsorption in proximal tubules. HLD. Impaired carb tolerance. Hypercalcemia, hyperglycemia.


Role of mesonephros vs. metanephros?

Meta is SO VERY real. Mesonephros = interim kidney for 1st TM + ureteric bud --> ureter, pelvis, calyces, COLLECTING ducts by wk 10. Metanephros starts in wk 5. Metanephric mesenchyme interacts with ureteric bud to induce formation of glomerulus to distal convoluted tube. Last part of canalization is uretopelvic junction.



Degenerates by wk 4.


Etios of Potter sequence

ARPKD, posterior urethral valves, b/l renal agenesis


Horseshoe kidney

Fusion of inferior poles. Then get trapped as ascend from pelvis by INFErior mesenteric artery. Increased risk of ureteropelvic junction obstruction, hydronephrosis, renal stones, Wilms. Associated with TURNER's syndrome.


Multicystic dysplastic kidney

Etio is poor metanephric mesenchymal interaction with ureteric bud -> nonfunctional kidney of cysts and connective tissue. Often asymptomatic and unilateral due to hypertrophy of other kidney.


Interlobular artery vs. interlobar artery vs. arcuate artery?

Interlobar artery on either side of medullary pyramid. Arcuate arteries on cortical side. interlobular artery extend towards cortex.


Superficial cortical nephrons vs. juxtamedullary nephrons

Superficial cortical have glomeruli in outer corex with SHORT loops only descend to outer medulla. Juxtamedullary nephrons have glomeruli near corticomedullary border, larder glomeruli, LONG loops of Henle deep into papilla. Also have vasa recta, peritubular capillaries which follow loops


Where are juxtaglomerular cells compared to mesangial cells?

Juxtaglomerular cells located between afferent arteriole and macula dense (inward facing cells of distal renal tubule). Mesangial cells in the glomerulus.


Water under the bridge

Ureters under UTERINE artery and DUCTUS deferens.


What do I need to know about fluid compartments?

60-40-20 rule: 60% of body weight is water. (40% or 2/3 is ICF and 20% or 1/3 is ECF). 60-40-15-5 rule (5% or 1/4 of ECF is plasma volume and 15% or 3/4 of ECF is interstitial fluid).


How do you measure plasma volume and ECF volume?.

Radiolabeled albumin and inulin respectively.


Renal clearance

= volume of plasma cleared of a substance per unit time = substance clearance / plasma concentration = Urine conc. of X * urine flow rate / plasma concentration of X


What is glomerular filtration composed of?

Fenestrated capillary epithelium = size. Fused BM w/ HEPARAN sulfate = NEGATIVE charge barrier (lost in nephrotic syndrome -> albuminemia, hypoproteinemia, edema, hyperlipidemia). Epithelial layer of podocyte foot processes



Normally ~ 100 mL/min. Creatinine clearance slightly overestimates GFR b/c of slight secretion by renal TUBULES. GFR = [inulin]u x V / [inulin]p = Kf [ net hydrostatic pressure - net oncotic pressure)]