Tubular reabsorption renal handling

Renal magnesium wasting is the main mechanism responsible for the hypomagnesemia associated with cisplatin (172), and it can be associated with enhanced tubular reabsorption of calcium and consequent hypocalciuria (173). This dissociation in the renal handling of calcium and magnesium is similar to what is found in Bartter s syndrome. The site of the renal tubular defect in these conditions is not known, but there is evidence that active renal tubular transport systems are disrupted. 

All the hyperuricosuric patients in this investigation had a urate clearance of the same order as the controls. Only one hyperuricosuric patient had a clearance urate/clearance creatinine of 14.5%, thus exceeding the 95% tolerance limit in the controls. In this patient, however, 95% of the excretion was PZA suppressible. The PZA-suppressible fraction of urate excretion and the tubular reabsorption of filtered urate in hyperuricosuric stone formers did not differ from the controls. Thus it is concluded that the renal tubular handling of urate in hyperuricosuric calcium stone patients does not differ from that of healthy subjects. 

Table 1 shows daily uric acid excretion, serum urate levels, and the different tubular phases of the renal handling of uric acid under the three uricemia states. Presecretory reabsorption of filtered uric acid was always above 99%. Tubular secretion of uric acid expressed as the percentage of filtered urate, was significantly higher in hyperuricemia with respect to the hypouricemia state. Tubular reabsorption of secreted uric acid was similar in normouri-cemia and hypouricemia, but in the sate of hyperuricemia a significant diminution of uric acid postsecretory reabsorption could be evidenced. 

A group of patients forming calcium oxalate stones are hyperuri-cosuric and it is thought that their excessive urate excretion contributes to calcium-stones formationl. The pathomechanisms invoked are dietary purine excess and endogenous uric acid overproduction, being defective tubular reabsorption of urate "unattractive because uricemia was found to be normal in patients with recurrent calcium nephrolithiasis (RCN) and hyperuricosuria. Current studies were undertaken to define the incidence, role of diet, abnormalities of the renal handling of urate, and associated metabolic disturban-c"es in patients with RCN and hyperuricosuria. 

According to the four-component model for the renal handling of urate, renal uric acid wasting might result from defects either of of presecretory or postsecretory reabsorption, or enhaced secretion of urate in the tubule. Future studies are required in order to delineate the tubular phases that may account for the uricosuric action of calcitonin. 

Animal studies and studies using brush border membrane vesicles from human kidney cortex indicate that biotin is reclaimed from the glomerular filtrate against a concentration gradient by a saturable, Na -depen-dent, structurally specific system, but biocytin does not inhibit tubular reabsorption of biotin. Subsequent egress of biotin from the tubular cells occurs via a basolateral membrane transport system that is not dependent on Na. Studies of patients with biotinidase deficiency surest that there may be a role for biotinidase in the renal handling of biotin. 

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