Renal & Urinary System
Nephron physiology
The proximal tubule reabsorbs about 65 percent of filtered sodium and water isotonically, with brush-border and carbonic anhydrase activity. The thin descending limb is water permeable; the thick ascending limb uses the sodium-potassium-2-chloride cotransporter, is water impermeable, and dilutes urine (loop diuretic site). The distal convoluted tubule uses the sodium-chloride cotransporter (thiazide site) and reabsorbs calcium. Collecting duct principal cells use ENaC under aldosterone; intercalated cells handle proton and potassium balance; ADH inserts aquaporin-2.
Clearance and acid-base
Clearance equals urine concentration times urine flow divided by plasma concentration. Inulin estimates GFR; PAH estimates renal plasma flow. Proximal renal tubular acidosis causes bicarbonaturia; distal causes stones and hypokalemia; type 4 causes hyperkalemia with hypoaldosteronism. Use the anion gap and the MUDPILES mnemonic for high-gap acidosis.
Glomerular disease and stones
Nephritic syndrome: hematuria with red cell casts, hypertension, and oliguria (post-streptococcal, IgA nephropathy, rapidly progressive glomerulonephritis). Nephrotic syndrome: proteinuria above 3.5 grams daily, edema, hypoalbuminemia, hyperlipidemia (minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy). Calcium oxalate stones are envelope shaped; struvite stones form staghorns with urease-producing bacteria; uric acid stones are radiolucent.
Traps
Using fractional excretion of sodium without diuretic status. Confusing pre-renal azotemia with acute tubular necrosis. Forgetting NSAIDs and ACE inhibitors cause prerenal injury through different mechanisms.
Worked rule
Fractional excretion of sodium under 1 percent with a BUN-to-creatinine ratio above 20 suggests prerenal azotemia; over 2 percent with muddy brown casts suggests acute tubular necrosis.