Hypouricemia causes

Tazawa M, Morooka M, Takeichi S, Minowa S, Yasaki T (1996) Exercise-induced acute renal failure observed in a boy with idiopathic renal hypouricemia caused by postsecretory reabsorption defect of uric acid (in Japanese with English abstract). Nippon Jinzo Gakkai Shi (Jpn J Nephrol) 38 407-412... 

Trimethoprim 15 mg/kg/day increased urinary uric acid excretion and reduced the plasma uric acid concentration in five healthy volunteers from 333 gmol/l (5.6 mg/dl) to 226 pmol/l (3.8 mg/dl) (1149). In 90 in-patients with hypouricemia co-trimoxazole was identified as the likely cause in four patients (1150). However, since the study was limited to patients with hypouricemia and since exposure rates for co-trimoxazole were not reported for hypouricemic or non-hypouricemic patients, no conclusions about the incidence and the relevance of trimethoprim-associated hypouricemia can be made. 

It remains to be clarified why patients with renal hypouricemia frequently develop acute renal failure. The following hypothesis has been proposed. Oxidative stress is essential for the onset of ischemic acute renal failure. In the kidney, uric acid acts as a protective mechanism against oxidative stress. However, in patients with renal hypouricemia, a decrease in uric acid may allow exposure of the kidney to oxidative stress, causing ALPE [152,153]. 

Hisatome I, Ogino K, Kotake H, Ishiko R, Saito M, Hasegawa J, Mashiba H, Nakamoto S (1989) Cause of resistent hypouricemia in outpatients. Nephron 51 13-16... 

The finding of a hyperchloremic metabohc acidosis in a patient without evidence of gastrointestinal bicarbonate losses and with no obvious pharmacological cause should prompt suspicion of an RTA. The presence of suggestive clinical (e.g., nephrocalcinosis in dRTA) or biochemical (e.g., hypophosphatemia and hypouricemia as a result of proximal tubular wasting in pRTA) features should also be considered. 

ADA deficiency causes death from massive infection before the patient reaches the age of 2 years. Some children with ADA or PNP deficiency have benefited from pe-riodie infusions of irradiated erythrocytes (which contain ADA and PNP). Irradiation of erythrocytes is necessary to inactivate any white blood cells that may be present and thereby to reduce the risk of graft-versus-host disease (Chapter 35). PNP deficiency usually causes hypouricemia and hypouricosuria and excretion of inosine, guanosine, deoxyinosine, and deoxyguanosine. 

A total of 6,629 consecutive serum urate determinations were monitored at two large hospitals in Durham, North Carolina. Hypouricemia was defined as a serum urate concentration of 2 mg/100 ml or less. Periodic checks showed that a value in this range was always more than two standard deviations below the mean of measurements made at either hospital on a given day. When significant hypouricemia was noted, the patient and his record was examined to determine the cause. If an obvious cause could not be ascertained by this method, another serum sample was obtained for measurement of uric acid, creatinine, phosphate, and salicylate, and a 24 hour urine specimen was collected in order to estimate uric acid, oxypurine, creatinine, phosphate, glucose, amino acid, and porphobilinogen excretion. 

From the total of 6,629 uric acid measurements, 0.97% including 66 men and two women, had a serum urate concentration of 2 mg/100 ml or less. In 4 of these 68 patients, the serum urate was found to be falsely low, since a value of greater than 2 mg/100 ml was obtained on the same serum sample by the uricase assay. The other 64 patients were separated into two groups, those with hypouricemia of known cause (53 patients) and those with hypouricemia of unknown cause (11 patients). 

In the group of 53 patients with hypouricemia of known cause, drugs seemed to be responsible in 44 subjects (Table 2). The drugs implicated were aspirin, allopurinol, and X-ray contrast agents. 

In summary, it is clear that hypouricemia is a relatively common finding, as would be expected on statistical grounds. Although hypouricemia previously has been reported to be a manifestation of some relatively rare diseases, these illnesses are unusual causes of the hypouricemia found in a general hospital population. 

Urinary tract An 11-year-old boy presented with hypouricemia manifesting as cyclic coma and psychosis along with tremor, ataxia, nystagmus, and hypotonia in the setting of a CBZ overdose after taking 2.6 g of CBZ (74 mg/ kg). Other causes of hypouricemia were ruled out. The serum uric acid remained low xmtil the CBZ levels retmned to normal [53 ]. The mechanism by which CBZ might lower luic acid levels is xmclear. 

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