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PubMed1999

Ammonium acid urate calculi: a reevaluation of risk factors.

PURPOSE: We reevaluate the demographic and metabolic risk factors for ammonium acid urate stones. MATERIALS AND METHODS: Since 1986, 23 women and 21 men ranging in age from 20 to 81 years (mean 48.7) were treated for stones partly composed of ammonium acid urate. Stone composition ranged from 2 to 60% ammonium acid urate (mean 24.1) of the total stone mass. No patient had a pure ammonium acid urate stone, although 11 (25%) had stones with ammonium acid urate as the predominant crystal. RESULTS: In the 44 patients 1 or more potential risk factors for ammonium acid urate were identified. Of the patients 11 (25%) had a history of inflammatory bowel disease with 10 (22.7%) having undergone ileostomy diversion, 6 (13.6%) admitted to a history of significant laxative use or abuse, 18 (40.9%) were morbidly obese, 16 (36.4%) had a history of recurrent urinary tract infections and 9 (20.5%) had a history of recurrent uric acid stones. CONCLUSIONS: Patients clearly at risk for stones with an ammonium acid urate component include those with a history of inflammatory bowel disease and ileostomy diversion or laxative abuse. Other factors that may potentially enhance ammonium acid urate stone formation include morbid obesity, recurrent uric acid calculi and recurrent urinary tract infection. A careful history followed by further metabolic evaluation is warranted in these patients.

Adult↗
PubMed1992

Abnormal urate transport in patients with intracranial disease.

Based on our demonstration of a high incidence of hypouricemia, tubular urate transport abnormality, and cerebral atrophy in patients with acquired immunodeficiency syndrome (AIDS), we performed prospective renal clearance studies in 29 consecutive neurosurgical patients with intracranial diseases of multiple etiologies to test our hypothesis that patients with intracranial disorders had defective tubular urate transport. Similar studies were performed in 21 age-matched controls. None of the subjects had serum creatinine greater than 123.8 mumol/L (1.4 mg/dL), sickle cell or liver diseases, or received intravenous fluid or uricosuric drugs at the time of study. Seven patients had no surgical procedures, 12 were studied after a neurosurgical procedure, and 10 had preoperative and postoperative studies. Ten had more than one postoperative study. Twelve had 24-hour urine collections. We found that 18 of 29 patients had elevated fractional excretion (FE) of urate greater than 10%. There was no difference in preoperative and postoperative FE urate by nonpaired t test for all patients and by paired t test in the 10 patients who had preoperative and postoperative studies performed. Seven patients had hypouricemia, defined as serum urate less than or equal to 0.18 mmol/L (3 mg/dL). Only one had hyponatremia (serum sodium less than 130 mmol/L). Urate excretion averaged 3.6 +/- 0.32 mmol (603 +/- 52.7 mg)/24 h, suggesting that the hypouricemia was not due to decreased urate production. None of the medications or surgical procedures could be considered to have caused the urate transport abnormality, nor was it associated with any specific intracranial location or type of disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport↗
PubMed1979

The binding of urate by plasma proteins.

Protein binding of urate may have some pertinence to the pathogenesis of gout. However, binding studies have been hampered by problems with in vitro methodology and by the problem of relating the results of in vitro studies to the physiological situation. In the present study urate binding was determined by an ultrafiltration procedure. All manipulations were performed anaerobically and at 37 degrees in order to maintain the sample under physiological conditions. Normal urate bound was 15 +/- 7.5% in males and 10 +/- 6.6% in females. Urate binding did not correlate significantly with either the albumin or total urate concentration. It is suggested that the interaction between protein and urate is influenced by a number of factors other than the concentrations of free urate and binding protein. Some possible ones are discussed. The techniques described might usefully be applied to a study of urate binding in various pathological states.

Female↗
PubMed1980

Effect of flow rate and the extracellular fluid volume on proximal urate and water absorption.

The in vivo microperfusion technique was used to examine the effect of variations in tubular flow rate and the extracellular fluid volume onf [2-14C]-urate and water absorption in the proximal tubule of the rat. In nondiuretic animals, fractional urate absorption was highest at the lowest perfusion rate examined and decreased as the rate of perfusion was increased. Increasing the initial concentration of urate in the perfusion solution had no effect on the fractional absorption of urate. Fractional water absorption was also inversely related to the rate of perfusion. Expansion of the extracellular fluid volume with isotonic saline resulted in rates of urate absorption similar to control values at any given microperfusion rate. Fractional water absorption showed the same flow rate dependency pattern observed in control animals, but at a significantly lower rate of absorption. These studies indicate that fractional urate absorption is dependent upon some parameter of tubular flow rate and that the relationship between urate absorption and perfusion rate is not related to the delivered load of urate per se and is not affected by the state of hydration of the extracellular fluid.

Absorption↗
PubMed1997

Release of the antioxidants ascorbate and urate from a nitrergically-innervated smooth muscle.

1. The main object of the present study was to determine whether ascorbate, an antioxidant which has been shown to protect nitric oxide (NO) from attack by scavenger molecules, might be released from nitrergically-innervated smooth muscle; ascorbate release from the rat anococcygeus was measured by use of h.p.l.c. with electrochemical detection. 2. Incubation of rat anococcygeus muscles in normal physiological salt solution (PSS; 30 min) resulted in release of ascorbate into the bathing medium (7.7 +/- 0.9 nmol g-1 tissue). This release was increased by 96% when muscles were incubated in high K+ (70 mM) PSS. The resting release of ascorbate was unaffected by tetrodotoxin (TTX; 1 microM), omega-conotoxin GVIA (10 nM) or omission of calcium ions from the PSS (with addition of 0.2 mM EGTA), but all three procedures attenuated the increased release observed under depolarizing conditions. Resting release of ascorbate was unaffected by glutamate (100 microM), aspartate (100 microM), gamma-aminobutyric acid (100 microM) or carbachol (50 microM). 3. A second h.p.l.c. peak, which always preceded the ascorbate peak, was identified as urate. Urate release from the anococcygeus, following 30 min incubation in normal PSS, was 64.6 +/- 12.7 nmol g-1 tissue but, unlike ascorbate, urate release was unchanged in high K+ PSS. In functional experiments, urate (100-400 microM) partially protected NO (15 microM)-induced relaxations of the rat anococcygeus from inhibition by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO; 50 microM), but not from inhibition by hydroquinone or duroquinone (both 100 microM). 4. Muscles chemically sympathectomized with 6-hydroxydopamine (6-OHDA, 500 microM; 2 h) still exhibited release of ascorbate (2.5 +/- 0.4 nmol g-1 tissue) and urate (22.2 +/- 2.9 nmol g-1 tissue); in both cases the release was similar to that observed in time-matched control tissues not exposed to 6-OHDA. High K+ PSS produced a TTX-sensitive increase in release of ascorbate, but not urate, from 6-OHDA-treated muscles. 5. The results demonstrate that significant amounts of ascorbate and urate are released from the rat anococcygeus muscle. Ascorbate, but not urate, release appears to be enhanced by activation of nerves which are resistant to 6-OHDA pretreatment. Since both antioxidants can protect NO from attack by scavenger molecules, their release in nitrergically-innervated tissues may be important for the provision of the correct redox environment to allow NO to fulfill its proposed neurotransmitter role.

Adrenergic Agents↗
PubMed1978

Rate-limiting factors in urate synthesis and gluconeogenesis in avian liver.

1. Urate synthesis and other metabolic characteristics of isolated chicken hepatocytes were studied. 2. The distinction is made between immediate precursors of the purine ring (glycine, glutamine, aspartate, formyltetrahydrofolate, bicarbonate) and ultimate precursors from which the immediate precursors are formed in the liver. 3. In hepatocytes from well-fed chickens the rate of urate synthesis was not greatly increased by the addition of amino acids or NH(4)Cl, but in hepatocytes from 72h-starved chickens the rate was much increased when alanine or asparagine was added as the only substrate. Other amino acids, when added alone, did not affect the rate. The exceptional effect of alanine and asparagine is due to the ready formation of the immediate precursors. 4. Conditions are described under which glutamine, serine, glycine plus formate, ribose and glucose increased the rate of urate synthesis. 5. At 1mm-NH(4)Cl (a concentration not much higher than that of blood plasma) the rate of urate synthesis in the presence of lactate was increased, but higher concentrations inhibited urate synthesis in the presence of lactate or alanine; with alanine even 1mm-NH(4)Cl was inhibitory. 6. Glucose synthesis from lactate, alanine or dihydroxyacetone was also inhibited by 1mm-NH(4)Cl. 7. NH(4)Cl inhibition of urate and glucose synthesis was paralleled by an increased rate of glutamine synthesis. Thus in the presence of NH(4)Cl the gluconeogenic precursors are diverted from the pathway of gluconeogenesis to that of glutamate and glutamine synthesis. This implies that the synthesis of these amino acids is the primary process in the detoxication of ammonia in the avian liver. 8. Urate synthesis, like urea synthesis, can be looked on as a cyclic process with either phosphoribosyl pyrophosphate or ribose acting as the carrier on which the purine ring is assembled. 9. The energy requirements of urate synthesis depend on whether phosphoribosyl pyrophosphate is regenerated from IMP by pyrophosphorylase or by phosphorylation and pyrophosphorylation of ribose. It is 6 or 9 pyrophosphate bonds of ATP respectively.

Acetates↗
PubMed2001

Urate and arteriosclerosis in primary hyperparathyroidism.

OBJECTIVE: An increased mortality due to cardiovascular disease has been reported in patients with primary hyperparathyroidism (pHPT). An association between urate and cardiovascular disease has been suggested. Metabolic abnormalities in pHPT may include urate. We therefore evaluated the metabolic arteriosclerotic risk profile in pHPT with special focus on the role of urate. DESIGN: Retrospective analysis of data before and 1 year after surgery for pHPT. PATIENTS: 130 consecutive patients, over the age of 44 years, who underwent surgery for pHPT. MEASUREMENTS: Biochemical variables known to reflect risk of arteriosclerotic disease (AD) and renal function tests including measurement of glomerular filtration rate (GFR) were investigated before and 1 year after surgery. RESULTS: pHPT patients with AD (n = 40) were older and had higher serum levels of urate and triglyceride, and more impaired renal function in comparison with patients without AD. PTH and calcium values did not differ. Multiple logistic regression analysis indicated that urate was an independent risk factor for AD in pHPT (P < 0.01). Three variables were shown to be positively associated with urate; male gender (P < 0.01), fasting blood glucose (P < 0.05) and serum level of triglyceride (P < 0.05). CONCLUSIONS: Urate was found to be an independent risk factor for arteriosclerotic disease in primary hyperparathyroidism. Serum level of urate could (in addition to gender) be associated with a metabolic disorder comprising increased glucose and triglyceride levels.

Adult↗
PubMed1999

Urate synthesis in the blood-sucking insect rhodnius prolixus. Stimulation by hemin is mediated by protein kinase C.

Hemin is a catalyst of the formation of reactive oxygen species. We proposed that hematophagous insects are exposed to intense oxidative stress because of hemoglobin hydrolysis in their midgut (Petretsky, M. D., Ribeiro, J. M. C., Atella, G. C., Masuda, H., and Oliveira, P. L. (1995) J. Biol. Chem. 270, 10893-10896). We have shown that hemin stimulates urate synthesis in the blood-sucking insect Rhodnius prolixus (Graça-Souza, A. V., Petretsky, J. H., Demasi, M., Bechara, E. J. H., and Oliveira, P. L. (1997) Free Radical Biol. Med. 22, 209-214). Once released by fat body cells, urate accumulates in the hemolymph, where this radical scavenger constitutes an important defense against blood-feeding derived oxidative stress. Incubation of Rhodnius fat bodies with okadaic acid raises the level of urate synthesis, suggesting that urate production can be controlled by protein phosphorylation/dephosphorylation. Urate synthesis is stimulated by dibutyryl cAMP and inhibited by N(2((p-bromocinnamil)amino)ethyl)-5-isoquinolinesulfonamide (H-89), an inhibitor of protein kinase A, as well as activated by the protein kinase C activator phorbol 12-myristate 13-acetate. In the presence of hemin, however, inhibition of urate synthesis by H-89 does not occur, suggesting that the hemin stimulatory effect is not mediated by protein kinase A. Calphostin C completely inhibits the hemin-induced urate production, suggesting that the triggering of urate antioxidant response depends on protein kinase C activation. This conclusion is reinforced by the observation that in fat bodies exposed to hemin, both protein kinase C activity and phosphorylation of specific endogenous polypeptides are significantly increased.

Animals↗
PubMed2000

Does a relationship exist between the urate pool in the body and lipid peroxidation during exercise?

In this study, we investigated whether a relationship exists between the levels of urate in vivo and lipid peroxidation during exercise. Seven healthy male subjects performed exhaustive cycling exercise under the following three conditions. The levels of urate, thiobarbituric acid reactive substances (TBARS) and allantoin in plasma and urine were examined before exercise and during a 3h recovery period. (1) Benzbromarone administration experiment: benzbromarone (an uricosuric agent) was administered orally the day before exercise. (2) IMP administration experiment: inosine 5'-monophosphate disodium salt (a precursor of urate) was administered orally the day before exercise. (3) Control experiment: no test substance was administered. The main results obtained were as follows. Plasma urate levels and total peroxyl radical-trapping antioxidant parameter (TRAP) for deproteinized plasma in the resting period significantly decreased depending on the treatment, in the order of IMP> control > benzbromarone. A significant positive correlation was evident between plasma urate levels and TRAP values for deproteinized plasma. The increase in plasma levels of allantoin was observed only in the case of IMP treatment. A significant negative correlation between plasma levels of urate in the resting period and the amounts of urinary TBARS excreted during the recovery period was recognized. These results suggest that the urate level in vivo before exercise is a factor influencing lipid peroxidation during exhaustive exercise. Furthermore, these findings support the view that urate may serve as an important freeradical scavenger in vivo.

Adult↗
PubMed1982

Effects of prolonged, purine-free total parenteral and enteral nutrition on urate homeostasis in man.

The influence on human urate homeostasis of prolonged, totally purine-free nutritional support, using total parenteral (TPN) or elemental enteral (EN) nutrition, is not well known. In a prospective study, we measured weekly serum uric acid, renal urate excretion and clearance, together with parameters of hydration, in 58 normally hydrated patients receiving prolonged (15 to 170 days) purine-free TPN (30 patients) or EN (28 patients) for various gastrointestinal disorders. A marked, early and sustained decrease (p less than 0.001) in serum uric acid was observed in TPN (155 +/- 9 mumol/l at day 7 versus 318 +/- 13 mumol/l before nutrition, mean +/- SEM) as well as in EN patients (192 +/- 11 mumol/l at day 7 versus 320 +/- 16 mumol/l before nutrition), together with a significant (p less than 0.01) rise in renal urate clearance. The urate clearance/glomerular filtration rate ratio increased significantly, while there was no significant change in natremia or plasma osmolarity. Serum urate and urate clearance returned to normal within 8 days of refeeding with a normally purine-containing diet. Replacement of TPN by EN or vice versa, or substitution of glucose by fructose resulted in no change in hypouricemia. A 4-day oral supply of purines (125 mg/day) in EN patients was associated with a 53% rise (p less than 0.01) in serum urate. We conclude that prolonged, purine-free TPN and elemental EN are a new cause of marked hypouricemia which is mainly due to increased urate clearance, the mechanism of the latter is still poorly known, but is not related to extracellular volume expansion.

Adolescent↗
PubMed2000

Serum urate is associated with baseline renal dysfunction but not survival or deterioration in renal function in malignant phase hypertension.

BACKGROUND: There has been speculation whether serum uric acid levels are an independent prognostic factor in patients with hypertension. OBJECTIVE: To investigate the clinical associations and prognostic value of serum urate in patients with malignant phase hypertension (MHT), by comparing clinical features in patients with serum urate levels above and below the median levels for this population, and secondly, by performing a survival analysis in these patients. PATIENTS AND METHODS: Review of the data on 153 patients (98 males; mean age 50.3 years, SD 13.5) with MHT on the west Birmingham MHT register. Median uric acid levels in this population was 0.41 mmol/l (6.9 mg/dl), with an interquartile range of 0.34-0.50 mmol/l (5.7-8.4 mg/dl). Clinical characteristics of patients with a serum urate <0.41mmol/1 (group 1) were compared to those with levels above the median (0.41 mmol/l, group 2). RESULTS: Mean duration of follow-up was similar in both groups. The mean diastolic blood pressure at presentation and both mean systolic and diastolic blood pressures at follow-up were significantly higher in group 2 (that is, those with high serum urate levels) (unpaired t test, P= 0.039). There was also more renal dysfunction in group 2 patients with MHT, with higher mean serum urea and creatinine levels, both at presentation and at follow-up (unpaired t test, P< 0.01). The commonest causes of death were myocardial infarction (n = 7), heart failure (n = 4), stroke (n = 10) and renal failure (n = 5). There was no difference in mean survival duration between groups 1 and 2 (Kaplan-Meier, 64.6 versus 66.8 months; log-rank test, P= 0.519). Serum urate levels also did not predict the rise in serum creatinine levels (log-rank test, P= 0.84) or urea (P= 0.4033) amongst these patients. Using a multivariate Cox proportional hazards analysis, the only independent predictors of outcomes (death or the need for dialysis) were age (P = 0.007) and serum creatinine levels at presentation (P = 0.0046). CONCLUSION: Our analysis of a large series of patients with MHT shows that those with high urate levels had higher diastolic blood pressures and greater renal impairment at baseline. At follow-up, patients with median serum urate >0.41 mmol/l showed a greater deterioration in renal function and higher blood pressures, but no significant difference in survival. Serum urate levels also do not appear to be predictive of the deterioration in renal function or overall survival in patients with MHT.

Aged↗
PubMed1992

Genetic control of the renal clearance of urate: a study of twins.

Although a genetic predisposition to gout has been recognised for centuries, its mechanism has never been defined. This study was designed to determine whether this factor might be the renal clearance of urate, which is an important determinant of the concentration of urate in serum. In this study the renal clearance of urate was examined in 37 pairs of normouricaemic twins to determine whether this resemblance was genetically mediated. Monozygotic twins had more similar values of urate clearance and fractional excretion of urate than dizygotic twins. The heritability of the renal clearance of urate was estimated as about 60% (95% confidence limits 40 to 100%), whereas the heritability of the fractional excretion of urate was 87% (confidence limits 45 to 100%). This study supports the hypothesis that genetic factors exert an important control on the renal clearance of urate, which determines some of the familiarity of hyperuricaemia and gout.

Adolescent↗
PubMed1994

Transport of PAH, urate, TEA, and fluid by isolated perfused and nonperfused avian renal proximal tubules.

Transport of organic anions [p-aminohippurate (PAH) and urate] and organic cations [tetraethylammonium (TEA)] and reabsorption of fluid were studied for the first time in individual renal proximal tubules isolated from avian kidneys. In isolated nonperfused tubules, PAH and urate uptake occurred against electrochemical gradients, whereas TEA uptake appeared to result from the electrical gradient. Radiolabeled PAH uptake and radiolabeled urate uptake were inhibited to an equal extent by high concentrations of unlabeled PAH and probenecid, suggesting that they might share the same transport system. However, the rate of uptake of radiolabeled PAH was significantly stimulated by preloading with alpha-ketoglutarate (alpha-KG), suggesting PAH/alpha-KG countertransport as in mammals and reptiles, whereas uptake of radiolabeled urate was not clearly stimulated. In isolated perfused tubules, net fluid reabsorption averaged approximately 2 nl.min-1.mm-1 and was inhibited by ouabain with or without bicarbonate in the perfusate and bathing medium. In these perfused tubules, the unidirectional bath-to-lumen fluxes of PAH and urate exceeded the unidirectional lumen-to-bath fluxes, indicating net secretion of both compounds. During the bath-to-lumen fluxes the uptake across the basolateral membrane was against an electrochemical gradient for both compounds. However, for PAH the steady-state intracellular concentration was about half that observed in nonperfused tubules, as generally expected during net secretion, whereas for urate the steady-state intracellular concentration was about twice that observed in nonperfused tubules, suggesting stimulation of uptake during net secretion. During the PAH lumen-to-bath flux, the steady-state intracellular concentration was significantly above that in the perfusate, suggesting that this flux involved transport into the cells from the lumen against an electrochemical gradient. However, during the urate lumen-to-bath flux, there was no urate in the cells, suggesting that this flux, as in reptiles, occurred by a paracellular route.

Animals↗
PubMed1979

Effects of intraluminal D-glucose and probenecid on urate absorption in the rat proximal tubule.

The in vivo microperfusion technique was employed to examine urate absorption in the proximal convoluted tubule of the rat kidney using [2-14C]urate as the marker for fractional urate absorption. With NaCl as the perfusion solution, water absorption averaged 2.53 +/- 0.16 nl.min-1.mm tubule-1, and the fractional absorption of [2-14C]urate averages 11.6 +/- 1.0%/mm tubule. The addition of D-glucose (50 mg/100 ml) enhanced water absorption to 3.62 +/- 0.19 nl.min-1.mm tubule-1, but inhibited fractional urate absorption to 6.6 +/- 1.2%/mm tubule. Phloridzin (4.4 mg/100 ml), 2-deoxy-D-glucose (45.6 mg/100 ml), and 3-O-methyl-D-glucose (53.9 mg/100 ml) also inhibited the absorption of [2-14C]urate to the same degree as did D-glucose despite differing effects on water absorption. The addition of probenecid (2.8 mg/100 ml) to the NaCl perfusion solution had no effect on water absorption but inhibited [2-14C]urate absorption to 6.4 +/- 0.6%/mm tubule. The addition of both probenecid and phloridzin further reduced [2-14C-A1urate absorption to 3.8 +/- 0.7%/mm tubule. Probenecid alone had no effect on glucose transport. These studies suggest that the presence of either certain hexose sugars, phloridzin, or probenecid in the lumen of the proximal convoluted tubule inhibits the tubular absorption of urate.

Absorption↗
PubMed1981

Uptake of [3H]PAH and [14C]urate into isolated proximal tubular segments of the pig kidney.

Segments of proximal convoluted (PCT) and proximal straight (PST) tubules of minipigs and normal-sized pigs were microdissected (without collagenase treatment) and incubated (30 min, 37 degrees C, pH 7.4) in Ringer solution (under O2) containing [3H]PAH (3.10(-5) M) or [14C]urate (9.10(-5) M) and, in inhibitor studies, probenecid, pyrazinoic acid (PZA), urate or PAH, all at 1 mM. In both strains the uptake of [3H]PAH expressed as means T/M ratio (cpm per ml tissue water/cpm per ml incubation medium) was significantly higher (P less than 0.001) in PCT than in PST. T/M was 34.7 +/- 5.6 (SE) in 34 PCT and 2.4 +/- 0.3 in 24 PST of eight minipigs. In two normal-sized pigs the T/M was 14.1 +/- 3.6 in 15 PCT and 1.4 +/- 0.1 in six PST. Similar results were obtained for [14C]urate. In eight minipigs the T/M was 4.9 +/- 0.5 in 24 PCT and 2 +/- 0.2 in 25 PST. In normal-sized pigs the T/M was 3.8 +/- 0.3 in 35 PCT (five pigs) and 1.9 +/- 0.4 in eight PST (two pigs). In inhibitor studies urate significantly depressed the uptake of [3H]PAH, and unlabeled PAH depressed the uptake of [14C]urate. PZA significantly inhibited the uptake of [14C]urate but not that of [3H]PAH, whereas probenecid had a strong inhibitory effect on the uptake of both compounds. These results suggest that [14C]urate and [3H]PAH are transported by a transport system located mainly in the proximal convoluted tubule. These findings are in contrast to the findings obtained in rabbits in which the transport system of PAH and urate is mainly located in the proximal part of the pars recta.

Aminohippuric Acids↗
PubMed1975

Intrinsic renal disease leading to abnormal urate excretion.

Since approximately two thirds of daily urate production is normally excreted by the kidney, intrinsic renal disease resulting in abnormalities of urate excretion may have a profound effect upon urate homeostasis. Alterations in the pattern of urate excretion encountered in chronic renal failure are reviewed in depth, with a description of adaptive mechanisms for urate excretion which develop in residual nephrons, as exemplified by the remaining normal kidney of transplant donors. In addition, abnormalities in urate excretion in the presence of a normal complement of nephrons are described. Diminished urate excretion per nephron appears to be responsible for hyperuricemia in some patients with gout, while a variety of tubular defects resulting in excessive renal urate excretion have been documented as the basis for some cases of hypouricemia.

Acute Kidney Injury↗
PubMed1982

Hypouricemia due to renal urate wasting. Two types of tubular transport defect.

We present 2 patients associated with hypouricemia. Serum uric acid levels were 1.6 and 1.3 mg/100 ml, and the ratios of urate clearance to creatinine clearance were 34.1 and 39.4%, respectively, while glomerular filtration rates (GFR) were normal. In the pyrazinamide (PZA) suppression test these 2 patients showed a different response of urate excretion. In the first patient urate excretion showed only a slight decrease following PZA. The load of benzbromarone did not increase urate excretion significantly. This patient is considered to have a defect of urate reabsorption in the proximal tubule, resulting in renal uricosuria. The second patient, on the contrary, showed nearly complete suppression of urate excretion after PZA. Uricosuric response to benzbromarone was far less than in the normal subjects. The suppression rate of urate excretion following PZA in benzbromarone-induced uricosuria was similar to the value of the normals. These results suggest that the latter had a defect of postsecretory reabsorption of urate in the tubule.

Adult↗
PubMed1987

Evaluation of the renal mechanisms for urate homeostasis in uremic patients by probenecid and pyrazinamide test.

The tubular transport of urate was studied in 47 uremic patients and in 20 normal subjects using probenecid and pyrazinamide tests. There was a marked increase in urate excretion per nephron as the renal function deteriorated. Presecretory reabsorption of urate per nephron, which was almost complete in normal subjects, showed a diminution with increasing severity of chronic renal failure. Until the creatinine clearance had decreased to less than 10 ml/min, the secreted urate per nephron remained almost constant, while in the end stage of renal failure it was markedly decreased. With the progression of renal disease, the postsecretory reabsorption of urate per nephron diminished. In patients with a creatinine clearance less than 10 ml/min, it was 4 times lower than in normal subjects. These findings indicate that urate secretion does not contribute to the increase of urate excretion per nephron at any level of renal failure, whereas the impairment of both reabsorptive components accounts for the augmented urate excretion per nephron in uremic patients.

Absorption↗