PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12474638

Hyperuricosuric calcium nephrolithiasis.

Carsten M Sorensen·Paramjit S Chandhoke
View original source ↗Export metadata ↓

Abstract

Since the findings of Yü and Gutman [1], the hyperuricosuric calcium stone former is a unique clinical entity. While an impressive number of clinical and epidemiologic studies implicate hyperuricosuria in calcium stone formation, the exact physicochemical mechanism by which uric acid affects calcium oxalate crystallization has not been proven. Allopurinol decreases stone recurrences and is the drug of choice for patients with isolated HCN.

Explore related subjects

AllopurinolCalcium OxalateCitratesFemaleGoutGout SuppressantsHumansKidney CalculiLithiasisMaleUric AcidJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Carsten M Sorensen, Paramjit S Chandhoke. 2002. Hyperuricosuric calcium nephrolithiasis.. https://doi.org/10.1016/s0889-8529(02)00038-5

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Induction of mitochondrial xanthine oxidase activity during apoptosis in the rat mammary gland.

Oxidative stress is an important signal for apoptosis to start. So far the mitochondrial respiratory chain has been considered as the major, if not the only, cause of such stress. Here we report that this is not the case. Xanthine oxidase, a O2(-) and H2O2 generating enzyme which is important in causing significant oxidative stress in the cytosol, is also present in the mitochondrial fraction of rat mammary gland. After weaning, during the involution of the mammary gland, massive apoptosis occurs. Mitochondrial xanthine oxidase activity increases and high mitochondrial H2O2 production takes place. Inhibition of xanthine oxidase activity by allopurinol, a specific inhibitor of xanthine oxidase activity, slows down the involution of the mammary gland due to the decrease in the number of apoptotic cells and prevents the production of H2O2 that occurs during apoptosis. Thus, mitochondrial xanthine oxidase by means of its production of O2(-) and H2O2 can maintain the apoptotic machinery during the involution of the mammary gland after weaning and could be considered necessary to maintain the apoptotic cascade during the physiological involution of tissues. Oxidative stress generated during apoptosis by mitochondria is not only due to the respiratory chain.

Allopurinol↗
PubMed2007

Effect of allopurinol supplementation on nitric oxide levels in asphyxiated newborns.

This study aimed to investigate the effect of allopurinol in the management of cerebral hypoxia-ischemia by monitoring nitric oxide levels of serum and cerebrospinal fluid. Sixty asphyxiated infants were divided randomly into two groups. Group I infants (n = 30) received allopurinol (40 mg/kg/day, 3 days) within 2 hours after birth. Group II infants (n = 30) received a placebo. Twenty healthy neonates served as control subjects. Cerebrospinal fluid and serum nitric oxide levels were measured within 0-24 hours and 72-96 hours after birth. Both serum and cerebrospinal fluid concentrations of nitric oxide were higher in severely asphyxiated infants (40.86 +/- 8.97, 17.3 +/- 3.63 micromol/L, respectively) but lower in mildly asphyxiated infants (25.85 +/- 3.57, 5.70 +/- 2.56 micromol/L, respectively) than in moderately asphyxiated infants (35.86 +/- 5.38, 11.06 +/- 3.37 micromol/L, respectively) within the first 0-24 hours after birth. Serum nitric oxide levels in control subjects were lower than those of moderately and severely asphyxiated infants. Serum nitric oxide levels of Group I infants within 72-96 hours after birth decreased significantly from their corresponding levels within 0-24 hours after birth. The asphyxiated newborns treated with allopurinol had better neurologic and neurodevelopmental outcome at 12 or more months of age.

Allopurinol↗
PubMed2007

Clarifying the role of rasburicase in tumor lysis syndrome.

Tumor lysis syndrome (TLS) is a complication of malignancies with high tumor cell proliferation, tumor burden, and chemosensitivity. It manifests with the release of intracellular components and results in hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. These biochemical abnormalities may lead to serious complications such as renal failure, cardiac dysrhythmias, and death. Rasburicase, a recombinant urate oxidase enzyme, is a new agent indicated in the treatment or prophylaxis of hyperuricemia in pediatric patients with cancer who are at high risk for TLS. We reviewed the evidence for treatment with this agent compared with standard therapy with allopurinol. Rasburicase may be considered for use in patients with hyperuricemia at presentation and in patients at high risk for TLS that would otherwise result in a delay in chemotherapy. However, randomized controlled trials are required to establish the comparative efficacy of rasburicase in the adult population. Preliminary evidence suggests that single-dose or reduced-dose rasburicase may be effective in the prophylaxis and the treatment of hyperuricemia and TLS. However, to our knowledge, there is no evidence comparing clinically relevant outcomes such as acute renal failure or dialysis.

Allopurinol↗