Disorders of distal acidification

The final site of titration of the urinary buffers is the collecting tubule. When this process fails urinary acid excretion is unable to match the 1 to 1.5 mEq/kg body weight of nonvolatile acid generated daily as a consequence of the high protein diet consumed by most Westerners. The clinical expression of such a defect is distal renal tubular acidosis (dRTA). Over the past decade numerous laboratory and clinical studies have clearly demonstrated that dRTA is a group of syndromes which results from a variety of defects in distal urinary acidification.If 100mEq of nonvolatile acid are generated a day, the kidney must reclaim all of the filtered bicarbonate and excrete 100mEq of acid to preserve homeostasis. Since the urine pH cannot fall below about 4.5, the acid must be excreted in buffered form as titratable acid or as ammonium. Though the nephron can reabsorb bicarbonate along its entire length, bicarbonate reclamation is mainly a proximal event. Similarly, the tubule titrates the urinary buffers at all sites. The collecting tubule, however, is the location of the greatest lowering of urinary pH and bears the major responsibility for acid excretion.In this paper I will discuss the mechanisms that might be responsible for the clinical syndromes of renal tubular acidosis and present a classification of these disorders. Many of these mechanisms can only tentatively be offered as a model since our knowledge is not far enough advanced to be certain about them. The model will doubtless require modification as more information is obtained