[Type IV renal tubular acidosis: pathogenetic role of aldosterone deficiency and hyperkalemia]

Type IV renal tubular acidosis (RTA) is a syndrome of tubular dysfunction manifested clinically by persisting hyperkalemia and metabolic acidosis that occurs usually in patients with mild to moderate chronic glomerular insufficiency. The pathophysiologic characteristics include: reduced renal clearance of potassium; a reduced rate of renal bicarbonate reabsorption at normal plasma bicarbonate concentrations (the magnitude of which is insufficiently great to implicate the proximal tubule); an unimpaired ability to maintain a steep hydrogen ion concentration gradient between blood and urine during acidosis; and a reduced rate of renal net acid excretion despite highly acidic urine, due in part to reduced urinary excretion of ammonium, which in turn appears to be due in part to suppression of renal ammoniagenesis by hyperkalemia. Many patients with type IV RTA, but not all, have hyporeninemic hypoaldosteronism. The roles of mineralocorticoid deficiency and hyperkalemia in the pathogenesis of type IV RTA will be considered and the ameliorative effects of treatment with fludrocortisone, furosemide, and dietary potassium restriction reviewed.