Renal excretion of hydrogen in primary gout

Renal function abnormalities in patients with asymptomatic hyperuricemia

“…Those authors have postulated that the metabolic defect causing primary gout may be impaired renal tubular conversion of glutamine to form ammonia, a process thus leading to an enhanced hepatic conversion of glutamine to urate. T h e relatively normal ammonia excretion following the oral acid load i n the present gouty patients with normal glomerular filtration rate is evidence against this hypothesis, as are the findings previously published by Plante et al (19) and Swales et nl (20). Plante et nE (19) reported that 3 gouty patients on a low purine intake responded normally to an ammonium chloride load.…”

“…T h e relatively normal ammonia excretion following the oral acid load i n the present gouty patients with normal glomerular filtration rate is evidence against this hypothesis, as are the findings previously published by Plante et al (19) and Swales et nl (20). Plante et nE (19) reported that 3 gouty patients on a low purine intake responded normally to an ammonium chloride load. Swales et a1 (20) were unable to demonstrate a n inverse relationship between urinary ammonia and urinary or serum urate when urinary ammonia excretion was deliberately varied over a wide range by means of administration of ammonium chloride or sodium bicarbonate.…”

Pathophysiologic basis for normouricosuric uric acid nephrolithiasis

“…We also tested the ability of these subjects acid-induced crystallization of calcium salts [9][10][11].to excrete ammonium in response to an acute acid load. We compared these parameters in patients with pure uric acid stones Low baseline urinary pH levels in uric acid stones formto patients with mixed uric acid/calcium oxalate stones, pure ers have been consistently described in uric acid stone calcium stones, and normal volunteers.formers [12][13][14][15][16][17][18][19], although contradicting results have also Results: Pure uric acid stone formers have a much higher been reported [17,20,21]. The best explanation for the incidence of either diabetes or glucose intolerance.…”

“…formers [12][13][14][15][16][17][18][19], although contradicting results have also Results: Pure uric acid stone formers have a much higher been reported [17,20,21]. The best explanation for the incidence of either diabetes or glucose intolerance.…”

Uric acid nephrolithiasis: An update

“…Acid loading of ammonium chloride normally provokes a large increase in ammonia production and excretion in normal volunteers and in calcium oxalate stone formers, but this response to acid load is not seen in uric acid stone formers. 40 Patients with gout also do not get a normal urinary alkaline tide after meals. The alkaline tide is related to the secretion of hydrogen ions in the stomach, which results in increased bicarbonate reabsorption.…”