A patient with long-standing type 1 diabetes develops overt nephropathy with GFR 28 mL/min. Serum K+ is 5.8 mEq/L. Urine pH is 5.2. Which renal tubular defect PRIMARILY explains the hyperkalemia?
- A Reduced GFR decreasing potassium filtration load to the tubule
- B Hypoaldosteronism from hyporeninemic state in diabetic nephropathy impairing CCD potassium secretion ✓
- C Metabolic acidosis shifting K+ extracellularly from cells
- D Impaired H+/K+-ATPase mediated acid secretion in the distal nephron retaining K+
Explanation
Diabetic nephropathy characteristically causes hyporeninemic hypoaldosteronism (type 4 RTA). Damaged juxtaglomerular cells in diabetes produce insufficient renin → low angiotensin II → low aldosterone. Without aldosterone, principal cells of the cortical collecting duct cannot adequately secrete K+ and H+, causing both hyperkalemia and non-anion gap metabolic acidosis (though urine pH can still acidify because H+ secretion is only partially impaired). Option A contributes minimally as the kidney adapts by increasing fractional K+ excretion; option C is a contributing factor; option D does not accurately describe the mechanism.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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