Presecretory reabsorption defect

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). 

On June 6, this patient developed severe loin pain after he participated in two 150-m sprints at a town athletics meeting. After 5 days, he was referred to the outpatient clinic of our department. His serum creatinine and uric acid levels and FEUA, were 2.9mg/dl, 2.1 mg/dl, and 49.7%, respectively. His creatine phosphokinase (CPK) level was normal. When his serum creatinine level decreased to 1.58 mg/dl, a contrast medium was administered. A delayed computed tomography (CT) scan after 24 and 48 h confirmed patchy wedge-shaped contrast enhancement (Fig. 58). Under a diagnosis of ALPE, his body water balance (hydration) was controlled. In this patient, recovery was achieved 4 weeks after onset, and his serum creatinine and uric acid levels were then 1.0 mg/dl and 0.6 mg/dl, respectively. Furthermore, load tests with a uric acid reabsorption inhibitor (benzbromarone) and a uric acid excretion inhibitor (pyrazinamide) suggested presecretory reabsorption defect-related renal hypouricemia. A kidney biopsy 16 days after onset confirmed the recovery from acute tubular necrosis. 

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. 

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