Renal tubular acidosis.

Abstract

Disorders affecting the overall ability of the renal tubules either to secrete hydrogen ions (H+) or to retain bicarbonate ions (HC03) are known collectively by the term renal tubular acidosis (RTA). The condition was first described clinically in 1935,1 confirmed as a renal tubular disorder in 19462 and designated 'renal tubular acidosis' in 1951.3 It is now recognized that RTA comprises a diverse group of disorders affecting either proximal or distal tubular function. In the complete form, they are characteristically associated with the biochemical finding of hyperchloraemic acidosis; the glomerular filtration rate (GFR) is normal or only slightly reduced and there is no significant retention of anions such as phosphate or sulphate (as found in the acidosis of glomerular impairment). The average adult 'western' diet generates 1-1·5 mmol H+ per kg body weight, mainly from protein consumption, resulting in the need to excrete up to 100 mmol/day of H+ for a 70 kg man. In unbuffered form, this acid would theoretically produce a pH of 1 in 1 L of urine, but the minimum urine pH achievable physiologically is approximately 4·2. A GFR of 180 L/day results in a cumulative filtered load of 4500 mmol HC03, and the renal generation and retention of HC03 forms an important part of acid/base balance. The aim of this review is to explain current concepts of tubular function relating to acid/ base balance, match defects in function to a clinical classification of RTA, discuss diagnostic