Pathogenesis of distal renal tubular acidosis (incomplete form) in cirrhosis: Normal urinary Pco2 after bicarbonate loading

In liver cirrhosis, an associated defect in urinary acidification is well known but its pathophysiologic nature is not well defined. Recent studies suggest that the urine P co₂ during maximal alkalinization of the urine is an adequate index of distal hydrogen ion secretion. To evaluate the nature of distal renal tubular acidosis (distal RTA) in cirrhosis, the urine minus blood P co₂ gradient [(U – B) P co₂] in alkaline urine was determined in four patients with cirrhosis and distal RTA, and compared with that in four patients without distal RTA (control subjects), as well as with that in one patient with Sjögren's syndrome and distal RTA (subject with impaired distal acidification). As expected, the (U – B) P co₂ after sodium bicarbonate loading was low (10.6 mmHg) in the subjects with impaired distal acidification and normal (32.5 mmHg, s.e.m. = 4.8) in control subjects. By contrast, all four patients with cirrhosis and distal RTA were able to achieve a normal (U – B) P co₂ gradient (33.8 mmHg, s.e.m. = 4.0) after sodium bicarbonate loading, even in the presence of the defect in urinary acidification under acid loading. These results suggest that the pathophysiology of the urinary acidification defect in liver cirrhosis is distinct from that in ordinary distal RTA; the latter signifies a defect in H⁺ secretion (secretory or voltage-dependent RTA), whereas, in cirrhosis, an increased permeability for H⁺ may cause the inability to acidify the urine.