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

In 6 male subjects the diurnal variation of urinary oxalic acid excretion was studied after ingestion of chocolate, a food stuff rich in oxalic acid. The ingestion of chocolate caused a striking but transient increase in urinary oxalic acid excretion due to its absorption in the upper gastrointestinal tract. The peak excretion rates occurred 2-4 h after the intake of the chocolate. The peak values were 235% of the fasting excretion rate in the trial with 50 g chocolate and 289% in the trial with 100 g chocolate and reached the amounts found in cases with primary hyperoxaluria. The administration of ranitidine had no influence on oxalic acid absorption. The transient hyperoxaluria observed seems to be an important factor for the formation of calcium oxalate calculi in patients on risk for stone disorders.
Nephron 1989
PMID:Transient hyperoxaluria after ingestion of chocolate as a high risk factor for calcium oxalate calculi. 291 54

Urinary excretion of oxalate, calcium and urate has been investigated in 88 patients affected by idiopathic calcium oxalate stone disease and in 20 normal subjects. Of these ions, only oxalate was found significantly higher in stone formers. Defining hyperoxaluria as urinary oxalate excretion greater than 2 SD above normal, 50% of stone-forming people were found to be hyperoxaluric. When stone formers were classified in normo- and hyperoxaluric, the prevalence of hypercalciuria, hyperuricuria, family history of stone disease and recurrencies in stone formation was the same in both groups. It is concluded that hyperoxaluria is a frequent finding in finding in idiopathic calcium oxalate renal stone disease.
Nephron 1983
PMID:Prevalence of hyperoxaluria in idiopathic calcium oxalate kidney stone disease. 688 20

Hypercalciuria is common in patients who form calcium oxalate urinary stones and is considered by many to be the cause of the disorder. This review shows that there is little relationship between either the rate of stone-formation or calcium oxalate crystalluria and the urinary excretion of calcium. There is, however, a strong relationship between these parameters and the urinary excretion of oxalate which is slightly, but significantly, elevated in stone-formers compared with normals. It is concluded that this mind degree of hyperoxaluria may be much more important than hypercalciuria in the genesis of calcium oxalate stones.
Nephron 1980
PMID:The cause of idiopathic calcium stone disease: hypercalciuria or hyperoxaluria? 741 65

Nephrocalcinosis was described in preterm infants by several authors who tried to determine its association with hypercalciuria and furosemide therapy. We evaluated these potential mechanisms along with other lithogenic factors not previously studied in 10 premature babies. Hypercalciuria was an inconsistent finding like in other reports; elevated uric acid excretion and hyperoxaluria were observed in 5 and 6 cases, respectively. The aminocid excretion was normal in all infants. Our data suggest that in addition to hypercalciuria, other lithogenic factors may play a role in the pathophysiology of nephrocalcinosis of premature infants.
Nephron 1995
PMID:Nephrocalcinosis and prematurity: importance of urate and oxalate excretion. 775 55

Serum levels of oxalate are elevated in uremic patients on dialysis. The effect of living related donor kidney transplants on serum and urine oxalate levels was studied in 8 patients. Serum and urine oxalate levels were measured prior to transplant, on the day of transplant and daily for 5 days postoperatively, and the results compared to those in 11 normal subjects. All transplanted kidneys functioned immediately. Serum oxalate fell from 55 +/- 9 mumol/l (484 +/- 79 micrograms/dl) before transplant to 21 +/- 3 mumol/l (185 +/- 26 micrograms/dl) the day after transplant, and to 9 +/- 2 mumol/l (79 +/- 18 micrograms/dl) 72 h after transplant. Serum oxalate in normal subjects was 9 +/- 2 mumol/l (79 +/- 18 micrograms/dl). During the initial 24 h after transplant urine oxalate averaged 1,244 +/- 150 mumol/l (109.5 +/- 13.2 mg), but fell to levels not statistically different from normal by 72 h after transplant. Rapid clearance of oxalate after transplant leads to transient hyperoxaluria until normal levels of serum oxalate are reached.
Nephron 1994
PMID:Effect of renal transplantation on serum oxalate and urinary oxalate excretion. 796 73

The treatment of X-linked hypophosphatemia (XLH) consists of phosphate and vitamin D3 derivatives. Transient hypercalciuria and hypercalcemia are well-known signs of vitamin D intoxication. Despite urinary calcium excretion control, the danger of nephrocalcinosis in treated patients has been emphasized. It has recently been suggested that hyperoxaluria might be a causative factor of nephrocalcinosis other than calcium in phosphate-treated XLH patients. We measured urinary oxalate and phosphate excretion in 12 patients with the syndrome of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) receiving only oral phosphates and in 5 XLH patients receiving both oral phosphates and vitamin D. No correlation was found between the dosage of phosphate supplements or urinary phosphate excretion and urinary oxalate excretion, in either group of patients. Nephrocalcinosis, presenting as hyperechogenicity of the medullary pyramids, was found in 2 of the 5 XLH patients and only in 2 HHRH patients who had been treated with excessive doses of vitamin D2 and calcium, prior to the true diagnosis being established. We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods.
Nephron 1993
PMID:Hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets. 839 9

The in vivo effect of cyclosporin A (CsA) on renal calcium oxalate (CaOx) crystal retention in experimental hyperoxaluric rats was investigated. Further, the effect of pretreatment of vitamin E on the above conditions was also studied. Male Wistar rats were divided into two major groups each containing 40 rats. One of the groups was pretreated with vitamin E. Both major groups were then subgrouped into four groups: group 1 received the vehicle (olive oil); group 2 received CsA in olive oil (50 mg/kg); group 3 received 3% ammonium oxalate (AmOx), and group 4 received CsA + AmOx. Nephrotoxicity was assessed by the activities of urinary marker enzymes and also by histopathology. Urinary oxalate excretion as well as the activities of lactate dehydrogenase, gamma-glutamyltranspeptidase, alkaline phosphatase and inorganic pyrophosphatase enzymes were elevated either in CsA-alone or AmOx-alone treated groups. On combined administration of both CsA and AmOx, further elevations of these enzymes were observed. Urinary excretion of oxalate concentration positively correlated with urinary excretion of these enzymes. Deposition of CaOx crystals was seen only in the kidneys of rats that received combined treatment. On pretreatment with vitamin E the observed increased urinary activities of the enzymes and oxalate, histopathological changes and the deposition of CaOx crystals by administration of CsA in hyperoxaluria were prevented suggesting that vitamin E could be supplemented to prevent CsA-induced membrane damage.
Nephron 1997
PMID:Vitamin E pretreatment prevents cyclosporin A-induced crystal deposition in hyperoxaluric rats. 903 Dec 74

The hyperoxaluric rat kidney nucleus exhibited a 50% increase in oxalate binding activity of control in both the residual fraction containing nuclear envelopes and the histone fraction with a concomitant increase in basal lipid peroxidation and a decrease in thiol content. However, in vitro lipid peroxidation induced by the ascorbate-ADP-Fe3+ system increased the oxalate binding activity of the residual fraction with a positive correlation but inhibited the histone oxalate binding activity with a negative correlation with depletion of thiols during peroxidation in both control and hyperoxaluric rats. A twofold increase in oxalate concentration was observed in the nucleus as well as the nuclear subfractions in hyperoxaluria. Hyperoxaluric rat kidneys showed increased H1 and oxalate binding activity, and the distribution of H1B was higher than that in the control. The present study suggests that the increased nuclear oxalate binding activity in hyperoxaluric rats was not due to lipid peroxidation but due to increased formation of histone H1.
Nephron 1997
PMID:Induction of renal nuclear oxalate binding activity in experimental hyperoxaluric rats. 904 45

Proteins are thought to play a major role in stone formation and structurally abnormal proteins have been reported to be present in the urine of stone formers. This study was aimed to determine whether hyperoxaluria modifies the kinetic properties of urinary inhibitory proteins. Hyperoxaluria was induced by feeding 1% ethylene glycol to rats. Oxalate, uric acid and calcium excretion were increased progressively during hyperoxaluria, while magnesium level was decreased. Urinary proteins were separated on a DEAE-cellulose column by eluting with stepwise increasing salt concentration in 0.05 M Tris-HCl buffer (pH 7.0). Each protein fraction was studied for its crystallization inhibitory potential by the spectrophotometric method. The protein eluted in 0.3 M NaCl containing buffer had the maximal nucleation as well as inhibitory activity. The protein had a molecular weight of 45 kD. In hyperoxaluria, the urinary excretion of this protein significantly increased. In the crystal growth assay, the control rat 45-kD protein inhibited nucleation by 75% and aggregation by 100%. In contrast, it is very interesting to note that the protein derived from 28th day hyperoxaluric urine, behaved as a promoter of nucleation (-113%, percentage inhibition) and weak inhibitor of aggregation (28%). A significantly high negative correlation (r = -0.97) between oxalate excretion and the inhibitory activity of the 45-kD protein was observed suggesting a modification of the protein by oxalate.
Nephron 2002 Feb
PMID:Effect of hyperoxaluria on the inhibitory activity of a 45-kD urinary protein. 1181 6

Proteins are thought to play a major role in stone formation. Oxalate binding protein plays a vital role in the transport of oxalate. This study was aimed at determining whether hyperoxaluria induces the expression of nuclear pore complex oxalate binding protein p62 which has the transport function. Hyperoxaluria was induced in male Wistar rats by feeding 0.75% ethylene glycol in water. The oxalate binding activity of the nuclear pore complex protein increased markedly during experimental hyperoxaluria, whereas nuclear lamina had no binding at all. There was an alteration in the elution profile of the nuclear pore complex oxalate binding protein during the hyperoxaluric condition. The protein was purified and had a molecular weight of 62 kDa (data not shown). The purified protein showed cross-reactivity with the monoclonal antibody (MAb 414) and it showed homogeneity. The expression of this protein (p62) during the hyperoxaluric condition was determined by ELISA and a 3-fold increase was observed when compared to control rats. The increased expression is further confirmed by Western blotting and immunohistochemistry. The increase in p62 protein expression may be either due to increased expression of certain genes or degradation of the cell membrane by oxalate-induced cell injury. Thus, the present study suggests that the increased expression of this protein (p62) may be due to the oxalate induction.
Nephron Exp Nephrol 2004
PMID:Expression of nuclear pore complex oxalate binding protein p62 in experimental hyperoxaluria. 1529 81


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