Renal Integration Cases

1) Effective circulating volume, 2) Na⁺ concentration (a water question), 3) K⁺ handling, 4) Acid–base status, 5) Which segment/hormone explains all of it.

Sodium CONTENT determines volume; sodium CONCENTRATION determines water balance. The kidney sacrifices concentration to defend volume.

Sweat is hypotonic (~40 mEq/L Na⁺), so proportionally more water than salt is lost → hypernatremia with volume depletion.

BUN/Cr ratio >20 (e.g., 35), urine osmolality >800–1200, urine Na⁺ <20 mEq/L; low flow boosts proximal water and passive urea reabsorption.

0.6 × weight(kg) × (Na⁺/140 − 1); e.g., 0.6 × 70 × (152/140 − 1) ≈ 3.6 L.

Brain cells generate idiogenic osmoles; correcting faster than ~10 mEq/L per 24 h pulls water into neurons → cerebral edema.

Blocks NKCC2 in the thick ascending limb → loses Na⁺/K⁺/Cl⁻, abolishes lumen-positive potential → Ca²⁺ and Mg²⁺ wasting; ↑distal Na⁺ + aldosterone → K⁺/H⁺ secretion → hypokalemic metabolic alkalosis.

Low Mg²⁺ disinhibits ROMK channels, increasing renal K⁺ secretion — K⁺ won't correct until Mg²⁺ is replaced.

pCO₂ ≈ 40 + 0.7 × ΔHCO₃⁻; e.g., HCO₃⁻ 36 → expected ~48, measured 46 = appropriate single disorder.

Vomiting (HCl loss) → hypochloremic metabolic alkalosis with hypokalemia; diarrhea (HCO₃⁻ loss) → normal anion gap hyperchloremic acidosis with hypokalemia.

U_Na + U_K − U_Cl: NEGATIVE = appropriate NH₄Cl excretion (diarrhea); POSITIVE = renal tubular acidosis (failure to excrete NH₄⁺).

Urine Cl⁻ <20 mEq/L (contraction/hypochloremic alkalosis) — treat with volume, KCl, and magnesium.