Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hippuric acid (HA) originating from the conjugation of benzoic acid with glycine is a physiological component of human urine. Findings suggest that HA inhibits calcium oxalate (CaOx) growth and considerably enhances the CaOx solubility in artificial urine. Thus, it is assumed that HA is a major modifier of CaOx formation. However, only a slight CaOx growth inhibition of 1-8% was also reported. These values were also derived from artificial urine. The key mechanism, which led HA to be of interest in urolithiasis research is the fact that in presence of Ca2+ ions HA can form a hippurate complex. By forming such a complex, Ca2+ concentration in urine decreases, and as a consequence, CaOx formation is inhibited. This study was performed in order to clarify the role of HA in native and artificial urine. Biochemical analyses to calculate the relative CaOx supersaturations and crystallisation experiments using an in-line laser probe were examined. BONN Risk Indices indicating the risk of CaOx crystallisation were calculated from the results of the crystallisation experiments. The results obtained from artificial as well as from native urines showed that HA has no significant effects on CaOx formation. We suggest that HA plays only a minor role as a crystallisation modifier in human urine.
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PMID:Hippuric acid as a modifier of calcium oxalate crystallisation. 1135 18

Primary renal hypouricemia (PRH) refers to a rare condition of increased renal urate clearance, caused by an isolated inborn error of membrane transport of urate in the renal proximal tubule. Several cases of exercise-induced acute renal failure and urolithiasis have been reported. This is the first study that assessed tubular function in PRH using NMR-based metabonomic urine analysis. The study groups consisted of 36 unrelated asymptomatic subjects with PRH, defined as serum uric acid levels (sUA) <2.5 mg/dL and fractional excretion of uric acid (FEUA) >10%, after exclusion of diseases and drugs that may affect urate homeostasis, and 39 sex and age-matched healthy individuals with normal sUA levels (>4.0 mmol/L) and FEUA<10%. Individuals with primary hypouricemia presented similar biochemical profiles to the controls without significant differences with regard to FE of electrolytes and renal threshold for phosphate excretion. Individuals with primary hypouricemia were differentiated from healthy individuals in the orthogonal signal correction/partial least-squares-discriminant analysis models of the NMR data with a statistically significant separation. The components that contributed to this separation were the lower levels of hippurate, creatinine, and trimethylaminoxide, and the higher levels of phenylalanine, alanine, glycine, glutamate, acetate, and of an unidentified metabolite (3.3 ppm) observed in hypouricemic subjects compared with controls. Primary hypouricemia, though considered an isolated renal tubular defect, is often associated with a more generalized proximal tubular disorder that mimics a partial Fanconi syndrome.
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PMID:Evaluation of the proximal tubular function in individuals with primary renal hypouricemia: an NMR-based metabonomic study. 1959 59