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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercalciuria and hyperoxaluria are important risk factors in the pathogenesis of kidney stones. Urinary glycolate has also been reported to be elevated in patients with renal stones. 1,25-Dihydroxyvitamin D(3), the active metabolite of vitamin D, has been reported to induce hyperoxaluria after either oral or intravenous administration. 1-alpha-D(3), a synthetic derivative of vitamin D, together with ethylene glycol, has been reported to induce renal stones in experimental rats. We have examined the effect of 1-alpha-vitamin D(3) on urinary oxalate and glycolate excretion. Our results indicate that 1-alpha-D(3), together with ethylene glycol, caused a significant increase in urinary glycolate, without a parallel rise in urinary oxalate excretion, in ethylene glycol-fed rats. This increase in urinary glycolate was due to the synergistic effect of both drugs.
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PMID:Effect of vitamin D3 on the conversion of ethylene glycol to glycolate and oxalate in ethylene glycol-fed rats. 1263 32

Calcium oxalate monohydrate (COM) crystals are the commonest component of kidney stones. Oxalate and COM crystals in renal cells are thought to contribute to pathology via prooxidant events. Using an in vivo rat model of crystalluria induced by hyperoxaluria plus hypercalciuria [ethylene glycol (EG) plus 1,25-dihydroxycholecalciferol (DHC)], we measured glutathione and energy homeostasis of kidney mitochondria. Hyperoxaluria or hypercalciuria without crystalluria was also investigated. After 1-3 wk of treatment, kidney cryosections were analyzed by light microscopy. In kidney subcellular fractions, glutathione and antioxidant enzymes were measured. In mitochondria, oxygen consumption and superoxide formation as well as cytochrome c content were measured. EG plus DHC treatment increased formation of renal birefringent crystal. Histology revealed increased renal tubular pathology characterized by obstruction, distension, and interstitial inflammation. Crystalluria at all time points led to oxidative stress manifest as decreased cytosolic and mitochondrial glutathione and increased activity of the antioxidant enzymes glutathione reductase and -peroxidase (mitochondria) and glucose-6-phosphate dehydrogenase (cytosol). These changes were followed by a significant decrease in mitochondrial cytochrome c content at 2-3 wk, suggesting the involvement of apoptosis in the renal pathology. Mitochondrial oxygen consumption was severely impaired in the crystalluria group without increased mitochondrial superoxide formation. Some of these changes were also evident in hyperoxaluria at week 1 but were absent at later times and in all calciuric groups. Our data indicate that impaired electron flow did not cause superoxide formation; however, mitochondrial dysfunction contributes to pathological events when tubular crystal-cell interactions are uncontrolled, as in kidney stones disease.
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PMID:Renal oxidative vulnerability due to changes in mitochondrial-glutathione and energy homeostasis in a rat model of calcium oxalate urolithiasis. 1667 Apr 37