A CASE OF TRANSIENT RENAL TUBULAR ACIDOSIS TYPE 1,4 HYBRID RTA: A STUDY OF THE PATHOPHYSIOLOGIC CHARACTERISTICS OF THE ACIDIFICATION DEFECT

Abstract

Summary: The diagnosis of transient renal tubular acidosis was made in a 16 months old boy. Bicarbonate titration studies revealed that the acidification defect consisted of an association of proximal and distal tubular acidosis. The effect of experimentally induced potassium depletion revealed that hyperkalemia contributed to the acidification defect. After correction of the acidification disorder a defect in urinary concentration was still present.

Speculation: The different tubular defects of transient renal tubular acidosis are due to reversible (toxic) damage of the tubular membrane. Assessment of distal tubular H⁺ secretion by measurement of (U-B)pCO₂ after oral NAHCO₃ administration is impossible in patients with decreased urinary concentration capacity. The incidence of transient renal tubular acidosis (R.T.A.) reached a peak between 1948 and 1953. This condition was first called idiopathic renal acidosis in infancy and subsequently transient R.T.A. (12). The clinical picture and biochemical disorder as well as longterm prognosis have been studied in great detail (2, 3, 4, 13). However accurate biochemical micro-methods for clinical use allowing a detailed study of the pathophysiologic characteristics of the acidification defect were lacking at that time. In recent years few cases of transient R.T.A. have been published (7, 11, 14, 15). We report a case of transient R.T.A. in which a detailed analysis of the acidification defect was made.

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