Renal transport of uric acid

Previously, the disordered renal transport of uric acid in patients with renal hypouricemia had been explained by a 4-component model. In our review, 59% of the patients with ALPE and renal hypouricemia were classified as the presecretory reabsorption defect type, followed by the total defect in uric acid transport (no secretion and no reabsorption) and total reabsorption defect types (Table 8). 

A. Isolated defect in renal transport of uric acid. 

Unfortunately, at the present time there appears to be no alternative method for evaluating the renal transport of uric acid in man which is superior to the PZA suppression test. It would therefore appear reasonable to determine if a process is or is not blocked by PZA pretreatment. However, we would recommend that interpretation of the response be limited and that one not attempt to associate any response with a specific abnormality of transport. Perhaps, an effect blocked by PZA should be considered a Type A response and an effect not blocked by this agent a Type B response. Hopefully, in the future we will have the additional data necessary to determine the molecular or at least physiological basis for a Type A and Type B response. Indeed, with the recent demonstrations that the New World Monkey, a species that does not have uricase activity, handles uric acid in a similar if not identical manner to man, it may be possible to design micropuncture, isolated tubule and other in vitro experiments that will provide direct data on the sites and mechanisms concerned with uric acid transport in the kidney. 

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