Hypouricemia

Hypouricemia and increased excretion of hypoxanthine and xanthine are associated with xanthine oxidase deficiency due to a genetic defect or to severe liver damage. Patients with a severe enzyme deficiency may exhibit xanthinuria and xanthine lithiasis. 

Some drugs, such as the two-substituted thiodiazole and acetazolamide (Diamox), increase serum uric acid by stimulating uric acid synthesis (K9). Others, such as chlorothiazide (Diuril), increase uric acid retention by decreasing uric acid excretion (K9). Hydrochlorothiazide inhibits tubular secretion and has been shown to increase pretreatment mean uric acid values from 6.5 mg/100 ml to 10.3 mg/100 ml by the third treatment day. In a patient with gout, the level increased from 8 mg/100 ml to 12 mg/100 ml (H6). In a single case a paradoxical hypouricemia occurred (H6). 

Hypothermic activity. Ethanol extract of the plant, administered intraperitoneally to guinea pigs, was inactive . Hypouricemic activity. An aqueous leaf extract, administered repeatedly to male and female rats at doses of 37.5, 75, 150, 300, 600, and 1200 mg/kg daily for 60 days, produced an increase of weight, hypotension, hypoglycemia, and hypouricemia 5 Immunosuppressant activity. Seed oil, administered in ration of mice, was active . Inotropic effect positive. Glycerin/etha-nol extract of the leaf, administered to rabbits at a dose of 5 mg/mL, was active on heart k Ethanol (95%), glycerin, and ethanol/glycerin extracts of the seed oil, administered to rabbits at a dose of 5 mg/mL, were active on heart ° . 

Weight increase. Aqueous leaf extract, administered repeatedly to male and female rats at doses of 37.5, 75, 150, 300, 600, and 1200 mg/kg/24 hours for 60 days, produced an increase of weight, hypotension, hypoglycemia, and hypouricemia """. 

OE232 Eehri, B., J. M. Aiache, A. Memmi, et al. Hypotension, hypoglycemia and hypouricemia recorded after repeated administration of aqueous leaf extract of Olea europaea L. J Pharm Belg 1994 49(2) 101-108. 

Hypouricemia. Deficiency of uric acid in the blood, along with xanthinuria, resulting from deficiency of xanthineoxidase, the enzyme required for conversion of hypoxan-thine to xanthine and of xanthine to uric acid. 

Hypouricemia commonly occurs after several days of parenteral nutrition, although occasional reports of gout have been reported. In one case polyarticular gout developed on two occasions after a sudden fall in serum uric acid after the start of purine-free parenteral nutrition (917). 

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. 

Hypouricemia in individuals admitted to an inpatient hospital-based facility. Am J Kidney Dis 2003 41 1225-32. 

In this text, we emphasize that ALPE should always be considered in patients who complain of severe loin pain and nausea after sprinting in an athletics meeting, and while ALPE frequently develops in patients with renal hypouricemia, it also develops in those without it. 

Serum myoglobin (ng/ml) CPK (U/l) Myoglobinuria Kidney biopsy Hypouricemia... 

This patient was the first case in which ALPE developed in the presence of renal hypouricemia [3]. On September 26,1984, he participated in a 400-m race in a school athletics meeting. On September 27, nausea and vomiting occurred about 12 h later at 0100 hours, and then bilateral loin pain and abdominal pain developed. Because... 

This patient developed ALPE in the presence of renal hypouricemia [3]. He caught a cold, and took aspirin at 400 mg, ethenzamide at 150 mg, and acetaminophen at 300 mg on October 8 and 9, 1987. On October 10, he participated in two 100-m races... 

Fig. 29. The clinical course of ALPE complicated by renal hypouricemia...

This patient (Case 1 in Fig. 57) and his son developed ALPE in the presence of renal hypouricemia [36]. After two 150-m sprints and rope skipping (40 skips) in a town athletics meeting, he developed ALPE. Gene analysis was performed to check for renal hypouricemia. The patient s son also developed ALPE (Case 2 in Fig. 57). The details are given in Chap. 10, Sect. 1. 

This patient and his father (Patient 18) developed ALPE in the presence of renal hypouricemia [36] (Case 2 in Fig. 57). The son developed ALPE after participating in two 400-m races, a mock cavalry battle, and a tug of war in an athletics meeting. At a local clinic, a nonsteroidal anti-inflammatory drug (NSAID) was administered orally under a diagnosis of muscular pain, and the condition was exacerbated. Gene... 

Renal hypouricemia was observed in 76 (57%) of the 133 patients in whom the serum levels of uric acid were recorded. Patients with a serum uric acid level of 2.0mg/dl or less at baseline were regarded as having hypouricemia. 

Risk factors for exercise-induced acute renal failure (ALPE) include anaerobic exercise, renal hypouricemia, administration of antipyretic analgesics for cold, and dehydration. We review renal hypouricemia here and in Chap.10. 

In 1990, we reported that 3 (23%) of 13 patients with ALPE had renal hypouricemia [3]. Previously, Erley et al. [28] had reported that patients with renal hypouricemia frequently developed acute renal failure. However, we were the first to report that these patients developed exercise-induced acute renal failure (ALPE) [3]. In our 3 patients with renal hypouricemia, the mean serum creatinine and uric acid levels in acute renal failure were 5.1 2.6mg/dl and 4.7 1.7mg/dl, respectively (Fig. 56). In the remaining 10 patients without renal hypouricemia, the mean serum creatinine and uric acid levels were 3.1 1.6mg/dl and 11.4 4.2mg/dl, respectively. In the recovery phase, these levels in the hypouricemia patients were 1.1 0.3 mg/dl and 0.8 0.2 mg/dl, respectively. The mean FEUA was 58.4 18.7%. In the 10 patients without hypouricemia, the mean serum creatinine, uric acid, and FEUA values were 1.1 0.1 mg/dl, 6.1 1.2 mg/dl, and 7.8 3.0%, respectively. 

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). 

Comparison of Patients With and Without Renal Hypouricemia... 

Of the 155 cases of patients with ALPE collected from the literature, we examined the presence or absence of renal hypouricemia in 133 for whom the serum levels of uric acid were reported (Table 9). The mean ages in the renal hypouricemia and non-renal hypouricemia groups were 20.2 7.4 years and 23.3 8.4 years, respectively. In the... 

Fig. 56. Serum creatinine, uric acid, and FEUA values at the onset (peak) and recovery of ALPE in patients with and without renal hypouricemia...

Table 8. Types of disordered renal uric acid transport in 76 patients with renal hypouricemia and ALPE...

Table 9. Comparison of ALPE patients with and without renal hypouricemia...

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