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

Urinary excretion rate of oxalate was measured in 79 patients with idiopathic calcium (Ca) nephrolithiasis and the results were compared with those obtained in 28 healthy volunteers. The group of stone formers consisted of 20 patients with idiopathic hypercalciuria (IHC) of the absorptive type, 23 patients with IHC of the renal type, 11 patients with hypercalciuria secondary to dietary factors, 1 patient with hyperuricosuria (as an isolated finding) and 24 patients without hypercalciuria nor hyperuricosuria. Classification was based upon the urinary excretion rate of uric acid, as well as that of calcium measured under 3 different dietary conditions (i.e. free diet, free diet supplemented with 3 g Ca/day for 3 days, and diet free of dairy products for 5 days). On a free diet, normal values of oxaluria ranged from 125 to 435 mumol/24 h; an elevated value was observed in 11 (14%) patients, 5 of whom belonged to the subgroup without hypercalciuria nor hyperuricosuria. On a low Ca diet, mild hyperoxaluria occurred in 3 controls and in 19 patients, the tendency to develop hyperoxaluria being particularly marked in the subgroup with absorptive-IHC. Moreover, there was a positive correlation between oxaluria on a low Ca diet and the estimated degree of intestinal absorption of Ca. This study confirms the finding that on a free diet, the incidence of mild hyperoxaluria amongst idiopathic stone formers is rather low. It shows, however, that a significant percentage of patients classically referred to as "without metabolic disorder" have in fact slight hyperoxaluria, an observation with a potential therapeutic impact. Finally, it shows that on a low Ca diet, patients with absorptive-IHC are particularly prone to develop hyperoxaluria: the latter observation renders questionable the relevance of a low Ca diet for patients with absorptive IHC, unless their intake of oxalate is simultaneously reduced.
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PMID:[Incidence of hyperoxaluria in idiopathic calcium nephrolithiasis]. 717 77

Oral sodium cellulose phosphate, an inhibitor of intestinal calcium absorption, may reduce urinary magnesium, increase urinary oxalate, and have a limited hypocalciuric action or cause negative calcium balance in the absence of increased calcium absorption or in the presence of renal calcium "leak". To overcome these potential complications, we have taken the following precautions: oral magnesium supplements were given, a moderate oxalate restriction was imposed, a modest dose of sodium cellulose phosphate was used (usually 10 g per day), and only patients with documented absorptive hypercalciuria were treated. During a cumulative treatment period of 42.8 years, 18 patients with recurrent calcium nephrolithiasis showed a sustained reduction in urinary calcium, without developing consistent or substantial reduction in urinary magnesium, hyperoxaluria, hyperparathyroidism, or reduced bone density, Urinary saturation (relative saturation ratio) of calcium oxalate and brushite typically decreased. Remission of stone disease was found in 78 per cent of patients. We conclude that sodium cellulose phosphate is a useful drug for absorptive hypercalciuria when used appropriately.
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PMID:A cautious use of sodium cellulose phosphate in the management of calcium nephrolithiasis. 729 89

A 54-year old man who had been taking triamterene (150 mg daily) over a period of 8 months, passed a 3 mm stone partly coated with mustard-colored substance. Metabolic evaluation showed only mild-hyperoxaluria. Through IR spectrography after microdissection, thin-layer chromatography, UV light examination, and mass spectrometry, the stone if found to consist of 70% whewellite, 5% protein, 5% carbapatite and 20% triamterene and hydroxylated triamterene, and perhaps also the sulfate conjugate of this metabolite. In spite of the few number of observations (two cases have been reported previously), triamterene seems likely to induce stone formation, both alone and associated with urate or oxalate, and triamterene should be used cautiously in patients with a predisposition for nephrolithiasis.
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PMID:[Drug induced nephrolithiasis: observation of an oxalate and hydroxylated triamterene stone (author's transl)]. 730 Oct 28

A 32-year-old women was treated for overweight by gastrointestinal bypass surgery. Following surgery, repeated calcium oxalate nephrolithiasis was observed and secondary hyperoxaluria was diagnosed. Treatment with low oxalate and fat diet resulted in normal urinary oxalic acid excretion; no further stone formation was observed.
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PMID:[Nephrolithiasis after intestinal bypass: successful treatment with a low-fat diet]. 731 47

Primary or secondary hyperoxaluria is associated with calcium oxalate nephrolithiasis, interstitial fibrosis and progressive renal insufficiency. Monolayer cultures of nontransformed monkey kidney epithelial cells (BSC-1 line) and calcium oxalate monohydrate (COM) crystals were used as a model system to study cell responses to crystal interactions that might occur in the nephrons of patients during periods of hyperoxaluria. To determine if COM crystals signal a change in gene expression, Northern blots were prepared from total renal cellular RNA after the cells were exposed to crystals. The immediate early genes c-myc, EGR-1, and Nur-77 were induced at one hour. At two to six hours stimulated expression of the genes encoding plasminogen activator inhibitor (PAI-1) and platelet-derived growth factor (PDGF)-A chain was detected, but constitutive expression of urokinase-type plasminogen activator (u-PA) was not altered. Expression of connective tissue growth factor (CTGF) was induced at one hour and persisted up to 24 hours. The stimulation of gene expression by COM crystals was relatively crystal- and renal cell-type specific. Thus the interaction of kidney epithelial cells with COM crystals alters expression of genes that encode three classes of proteins: transcriptional activators, a regulator of extracellular matrix (ECM), and growth factors. Activation of PAI-1 gene expression without a change in u-PA favors accumulation of ECM proteins, as does increased expression of PDGF and CTGF which can also stimulate fibroblast proliferation in a paracrine manner. These results suggest that COM crystal-mediated stimulation of specific genes in renal tubular cells may contribute to the development of interstitial fibrosis in hyperoxaluric states.
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PMID:Calcium oxalate monohydrate crystals stimulate gene expression in renal epithelial cells. 756 19

The aetiology of nephrolithiasis was investigated in 32 north Indian children (25 boys, 7 girls, mean age 7.9 +/- 3.3 years). An underlying disorder was detected in 16 (50%) patients and included idiopathic hypercalciuria (8 patients), hyperoxaluria (3 patients) and renal tubular acidosis, primary hyperparathyroidism and hyperuricosuria (1 patient each). Magnesium ammonium phosphate calculi were found in 2 patients with recurrent urinary tract infections, 1 of whom had a duplex pelvic collecting system. In 16 patients (50%) a cause for renal calculi was not identified. Our findings suggest that an underlying disorder is present in a large proportion of children with nephrolithiasis where appropriate treatment may be beneficial.
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PMID:Aetiology of nephrolithiasis in north Indian children. 757 12

Hyperoxaluria is characterized by nephrocalcinosis and nephrolithiasis on radiological examination and may also result in diffuse deposition of calcium oxalate crystals in multiple extrarenal organs (oxalosis). In two cases, the renal findings of primary hyperoxaluria were diagnosed by ultrasound and computed tomography scans. In addition to renal involvement, both patients had liver involvement, and one patient had cardiac involvement.
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PMID:Systemic oxalosis: pathognomonic renal and specific extrarenal findings on US and CT. 776 Nov 52

Enteric hyperoxaluria complicates extensive disease or resection of the small intestine in the presence of an intact colon, and is associated with calcium oxalate nephrolithiasis. In addition to hyperoxaluria these patients have a low urine volume, low urinary ionic strength and hypocitraturia. Many forms of treatment have been recommended, but none has been subjected to a prospective clinical trial. Mild idiopathic hyperoxaluria is reported in 8-50% of idiopathic calcium oxalate stoneformers. Several pathophysiological mechanisms have been proposed, including low dietary calcium and possible oxalate transport defects in the gut and/or the kidney. Mild hyperoxaluria, or a high oxalate:calcium ratio in the urine, may be particularly important risk factors for calcium oxalate stone formation; an approach to the correction of these abnormalities is proposed.
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PMID:Enteric and mild hyperoxaluria. 778 97

Calcium phosphate (CaP) and calcium oxalate (CaOx) are the two most common crystalline constituents of human urinary stones. Calcium phosphate is often recognized as the nucleator of CaOx crystals, but the relationship between the two is not yet clearly understood. Using rat models of nephrolithiasis, we studied the role of CaP in renal deposition of CaOx. Calcium oxalate nephrolithiasis was brought about by inducing hyperoxaluria, while CaP CaOx nephrolithiasis was produced by dietary manipulation. Under similar urinary CaOx or CaP supersaturations, male rats were prone to form CaOx deposits while female rats were susceptible to produce CaP deposits in their kidneys. Crystal deposition in females was generally localized to the corticomedullary junction and in males to the renal papillae. The results indicate that gender plays an important role in the type and location of crystal deposition in the kidneys. In addition, deposition of CaP does not appear to influence the deposition of CaOx.
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PMID:Deposition of calcium phosphate and calcium oxalate crystals in the kidneys. 786 45

The prevalence of nephrolithiasis (12% of the population) is directly related to environmental risk factors including nutrition. Correlations have been demonstrated between activity of renal stone disease and excessive protein intake or low fiber diets, and cause-and-effect relationships have been suggested between prevalence of the disease and low urine volume due to underhydration. Indeed eating too much meat and drinking too little can expose certain subjects, but not all, to nephrolithiasis. Why? Populations at risk include subjects with medullary sponge kidneys who represent 10% of the patients with idiopathic calcium nephrolithiasis and those with mild metabolic hyperoxaluria who cannot activate pyridoxin to 5' pyridoxal phosphate. Defective intestinal absorption of citrate and modifications in protein structures which inhibit urinary crystallization have also been observed. Clearly, many apparently normal subjects are overly susceptible to nephrolithiasis and the "explosion" would appear to be programmed if they are exposed to additional risk factors. Thus our theory of the powder keg and the tinderbox.
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PMID:[Pathogenesis of renal calculi]. 797 43


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