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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

This retrospective survey examines the etiology of nephrocalcinosis (NC) in 40 patients (26 boys), over an 8-year period. The median age at onset of symptoms and presentation was 36 months and 72 months, respectively. Clinical features included marked failure to thrive (82.5%), polyuria (60%) and bony deformities (52.5%). The etiology of NC included distal renal tubular acidosis (RTA) in 50% patients and idiopathic hypercalciuria and hyperoxaluria in 7.5% each. Other causes were Bartter syndrome, primary hypomagnesemia with hypercalciuria, severe hypothyroidism and vitamin D excess. No cause for NC was found in 12.5% patients. Specific therapy, where possible, ameliorated the biochemical aberrations, although the extent of NC remained unchanged. At a median (range) follow up of 35 (14-240) months, glomerular filtration rate (GFR) had declined from 82.0 (42-114) ml/min per 1.73 m2 body surface area to 70.8 (21.3-126.5) ml/min per 1.73 m2 body surface area (P = 0.001). Our findings confirm that, even with limited diagnostic facilities, protocol-based evaluation permits determination of the etiology of NC in most patients.
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PMID:Etiology of nephrocalcinosis in northern Indian children. 1728 94

Intestinal diseases may cause the formation of urinary stones through changes in the metabolism of oxalate, calcium, and uric acid. The oxalate that is excreted into urine comes from the catabolism of ascorbic acid and some amino acids or from intestinal absorption of food oxalate. Calcium is absorbed by the gut after the stimulation of active vitamin D and is excreted by the kidney under the control of the bone/parathyroid hormone axis. Uric acid is generated by the oxidation of exogenous and endogenous purine bases, is excreted by the kidney through glomerular filtration/tubular secretion, and is soluble in alkaline urine. Several data indicate that patients with inflammatory bowel diseases are at high risk of urinary stones containing calcium-oxalate salt or uric acid. Calcium-oxalate stones are caused by colonic oxalate hyperabsorption (secondary to intestinal dysfunction) or by parenteral nutrition. Uric acid stones are typical of patients with severe diarrhea and/or intestinal neostomy, that is, in patients with hyperconcentrated acidic urine. Relationships between malabsorptive intestinal diseases and urinary stones are less well defined. Preventive countermeasures are not the same for all disorders. Hyperoxaluria should be controlled by diets with a low content of lipids and oxalate but supplemented with calcium and probiotics. The presence of hyperconcentrated acidic urine should be controlled by correct hydration and administration of citrate.
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PMID:[Nephrolithiasis in patients with intestinal diseases]. 1826 17

The prevalence of idiopathic nephrolithiasis is increasing in rich countries. Dietary manipulation could contribute to the prevention of both its first appearance and the recurrence of the disease. The target of dietary treatment is to decrease the "urinary lithogenic risk factors" such as low urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria, hyperphosphaturia, hypocitraturia, hypomagnesuria and excessively alkaline or acid urinary pH. Due to the lack of randomized controlled trials focused on this problem, there is not ample evidence to confidently recommend dietary changes. Despite this, numerous recent and past experiences support modification of diet as having a primary role in the prevention of nephrolithiasis. In particular, it is recommended to limit animal protein and salt intake, to consume milk and derivatives in amounts corresponding to calcium intake of about 1200 mg/day and to assume fiber (40 g/day), vegetables and fruit daily avoiding foods with high oxalate content. Furthermore, vitamin C intake not exceeding 1500 mg/day plays a protective role as well as avoiding vitamin B6 deficiency and abstaining, if possible, from vitamin D supplements. Lastly, it is recommended to drink enough water to bring the urinary volume up to at least 2 L/day and, as much as possible, to use fresh or frozen products rather than prepacked or precooked foods which are often too rich in sodium chloride.
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PMID:Dietary treatment of nephrolithiasis. 2246 Sep 96


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