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

In 222 random spot urine specimens, the calcium concentration and calcium oxalate saturation [DG(CaOx)] were significantly higher among stone formers than among non-stone formers, while the citrate and creatinine-corrected citrate concentrations were lower. In 188 24-hour urine specimens, magnesium excretion was lower among stone formers than non-stone formers, while the creatinine-corrected calcium concentration and DG(CaOx) were higher. Among stone formers, there was no gender difference in the urinary concentrations of calcium, oxalate, citrate, magnesium, and DG(CaOx), but the creatinine-corrected calcium, citrate, and magnesium concentrations were higher in women, as well as 24-hour citrate excretion. The levels of calcium and oxalate have a major influence on DG(CaOx), while citrate and magnesium levels have a minor influence. DG(CaOx) was correlated with calcium and oxalate excretion, as well as with the creatinine-corrected calcium and oxalate concentrations. Approximately 5% of 24-hour urine specimens showed critical supersaturation, 80% showed metastable supersaturation, and 15% were unsaturated. Hypercalciuria or hyperoxaluria was fairly common (30% and 40%) in critically supersaturated urine, while it was less common (22.4% and 8.6%) in metastably supersaturated urine and was not detected in unsaturated urine. Hypocitraturia and/or hypomagnesiuria was more common (63.8-80%) at any saturation. The urinary calcium, oxalate, and citrate concentrations, as well as the creatinine-corrected calcium, oxalate, citrate, and magnesium concentrations and DG(CaOx), showed a significant correlation between 57 paired early morning spot urine and 24-hour urine specimens. The creatinine-corrected calcium and citrate concentrations of the early morning urine specimens were significantly correlated with the levels of calcium and citrate excretion in the paired 24-hour urine specimens. In conclusion, no parameter other than urinary saturation gives more than a vague indication of the risk of lithogenesis, so DG(CaOx) in either early morning urine or 24-hour urine specimens appears to be the best predictor of stone risk. Finally, the creatinine-corrected calcium and citrate concentrations in early morning urine can be used as a substitute for measuring 24-hour excretion.
Front Biosci 2003 Sep 01
PMID:Urinary saturation and risk factors for calcium oxalate stone disease based on spot and 24-hour urine specimens. 1295 83

The incidence of stones in patients with enterocystoplasty is reported as 12-52.5%. Most patients will have multiple physical factors such as immobility, need for self catheterisation and poor urine drainage, so that it is not certain that an intestinal reservoir is the cause of stones on its own. There is little or no evidence that mucus is an aetiological factor. Foreign bodies in the reservoir, such as staples, increase the risk of stone formation from 13% to 43%. Stones require surgical removal. Minimally invasive techniques may be used for small stones. A low velocity disintegrator is required so that fragments are not propelled into the intestinal mucosa. Stones are infective in origin in 86% of cases, but 14% are sterile. Metabolic screen shows that 80% of patients have risk factors for at least three different types of stone. All patients have raised pH (mean 6.93) and hypocitraturia. Raised serum and urinary calcium, hyperoxaluria and hyperuricosuria are found in up to 33% of patients.
World J Urol 2004 Sep
PMID:Urolithiasis in enterocystoplasties. 1534 48

Ethylene glycol (EG) consumption is commonly employed as an experimental regimen to induce hyperoxaluria in animal models of calcium oxalate nephrolithiasis. This approach has, however, been criticized because EG overdose induces metabolic acidosis in humans. We tested the hypothesis that EG consumption (0.75% in drinking water for 4 wk) induces metabolic acidosis by comparing arterial blood gases, serum electrolytes, and urinary chemistries in five groups of Sprague-Dawley rats: normal controls (CON), those made hyperoxaluric (HYP) with EG administration, unilaterally nephrectomized controls (UNI), unilaterally nephrectomized rats fed EG (HRF), and a metabolic acidosis (MA) reference group imbibing sweetened drinking water (5% sucrose) containing 0.28 M NH4Cl. Arterial pH, plasma bicarbonate concentrations, anion gap, urinary pH, and the excretion of titratable acid, ammonium, phosphate, citrate, and calcium in HYP rats were not significantly different from CON rats, indicating that metabolic acidosis did not develop in HYP rats with two kidneys. Unilateral nephrectomy alone (UNI group) did not significantly affect arterial pH, plasma bicarbonate, anion gap, or urinary pH compared with CON rats; however, HRF rats exhibited some signs of a nascent acidosis in having an elevated anion gap, higher phosphate excretion, lower urinary pH, and an increase in titratable acid. Frank metabolic acidosis was observed in the MA rats: decreased arterial pH and plasma HCO3(-) concentration with lower urinary pH and citrate excretion with elevated excretion of ammonium, phosphate and, hence, titratable acid. We conclude that metabolic acidosis does not develop in conventional EG treatments but may ensue with renal insufficiency resulting from an oxalate load.
Am J Physiol Renal Physiol 2005 Sep
PMID:Ethylene glycol induces hyperoxaluria without metabolic acidosis in rats. 1585 60

We report herein a domino orthotopic liver transplantation (LT), from a 38-year-old woman undergoing liver-kidney transplantation (LKT) for primary hyperoxaluria type I (PH1) to a recipient with cirrhosis and hepatocellular carcinoma. Delayed onset of PH1 and renal failure and 10% residual alanine-glyoxylate aminotransferase (AGT) activity in domino liver justified its use for domino procedure. The clinical course after LKT was similar to that described in other series, including ours. Renal function started promptly and maintained despite sustained hyperoxaluria from dissolution of oxalotic deposits. Conversely, the domino recipient manifested severe hyperoxaluria and developed nephrolithiasis and renal insufficiency with rapid progression over 2 months. A new LT resulted in slow decrease of oxaluria and improvement of renal function. Therefore, PH1 behaved quite differently in these two patients, leading us to conclude that domino LT using livers from PH1 patients should be considered very carefully, only as a bridge to definitive LT in recipients with critical clinical conditions.
Am J Transplant 2005 Sep
PMID:Severe course of primary hyperoxaluria and renal failure after domino hepatic transplantation. 1609 18

A number of animal models have been developed to investigate calcium oxalate (CaOx) nephrolithiasis. Ethylene glycol (EG)-induced hyperoxaluria in rats is most common, but is criticized because EG and some of its metabolites are nephrotoxic and EG causes metabolic acidosis. Both oxalate (Ox) and CaOx crystals are also injurious to renal epithelial cells. Thus, it is difficult to distinguish the effects of EG and its metabolites from those induced by Ox and CaOx crystals. This study was performed to investigate hydroxy-L-proline (HLP), a common ingredient of many diets, as a hyperoxaluria-inducing agent. In rats, HLP has been shown to induce CaOx nephrolithiasis in only hypercalciuric conditions. Five percent HLP mixed with chow was given to male Sprague-Dawley rats for 63 days, resulting in hyperoxaluria, CaOx crystalluria, and nephrolithiasis. Crystal deposits were surrounded by ED-1-positive inflammatory cells. Cell injury and death was followed by regeneration, as suggested by an increase in proliferating cell nuclear antigen-positive cells. Both osteopontin (OPN) and CD44 were upregulated. Staining for CD44 and OPN was intense in cells lining the tubules that contained crystals. Along with a rise in urinary Ox and lactate dehydrogenase, there were significant increases in 8-isoprostane and hydrogen peroxide excretion, indicating that the oxidative stress induced cell injury. Thus, HLP-induced hyperoxaluria alone can induce CaOx nephrolithiasis in rats.
Kidney Int 2006 Sep
PMID:Modeling of hyperoxaluric calcium oxalate nephrolithiasis: experimental induction of hyperoxaluria by hydroxy-L-proline. 1685 24

Primary hyperoxaluria type 1 is caused by mutations in the alanine-glyoxylate aminotransferase (AGXT) gene. In cases in which no mutation was identified, linkage analysis can be used to confirm or exclude the diagnosis in other siblings. We present a family in which a sibling of the index case predicted to have primary hyperoxaluria type 1 by means of linkage analysis failed to show hyperoxaluria during the following 7 years, putting the diagnosis into question. Whole-gene sequence analysis identified 2 causative mutations in the index case, of which only 1, c.646A (Gly216Arg), was inherited. The other sequence change, c.33_34insC, was a de novo mutation occurring on the paternal allele. This particular mutation is a relatively common cause of primary hyperoxaluria type 1. It occurs in a run of 8 cytosines and therefore potentially is susceptible to polymerase slippage. This case illustrates 2 important points. First, biochemical confirmation of a genetic diagnosis should always be made in siblings diagnosed by using genetic tests. Second, de novo mutations should be considered as a potential, albeit rare, cause of primary hyperoxaluria type 1.
Am J Kidney Dis 2006 Sep
PMID:A de novo mutation in the AGXT gene causing primary hyperoxaluria type 1. 1693 Dec 22

Urinary stone disease is recorded in the literature from the dawn of the history and has spared no segment of society irrespective of age, gender, occupation and socio-economic status. It is still termed as "Refractory Disease" as complete medical management to prevent occurrence or recurrence is not so far available. We conducted a preliminary survey from the Manipal Teaching Hospital and carried out urinalyses to ascertain risk factors in the local population. This preliminary survey indicates the prevalence of stone disease is in moderate zone. Hyperoxaluria is an important risk factor in more than one fourth of the stone formers; and hypernatriuria is distinctly most common potentiating risk factor.
Nepal Med Coll J 2006 Sep
PMID:Epidemiology and etiopathogenesis of urinary calculi in western Nepal (Pokhara). 1720 28

The present study was undertaken to explore the efficiency of the pentacyclic triterpene lupeol (1) and its ester derivative, lupeol linoleate (2), in experimental hyperoxaluria. Hyperoxaluria was induced in male Wistar rats with 0.75% ethylene glycol (EG) in drinking water for 28 days. Hyperoxaluric animals were supplemented orally with 1 and 2 (50 mg/kg body wt/day) throughout the experimental period of 28 days. The renal enzymes were assayed as markers of renal tissue integrity. The redox status and oxalate metabolism in animals under oxalate overloading was also assessed. Microscopic analysis was done to investigate the abnormalities associated with oxalate exposure in renal tissues. Increase in oxidative milieu in hyperoxaluria was evident by increased lipid peroxidation (LPO) and decreased enzymic and nonenzymic antioxidants. Decrease in the activities of renal enzymes exemplified the damage induced by oxalate, which correlated positively with increased LPO and increased oxalate synthesis. Renal microscopic analysis further emphasized the oxalate-induced damage. These abnormal biochemical and histological aberrations were attenuated with test compound treatment, with 2 more effective than 1. From the present study, it can be concluded that 1 and 2 may serve as candidates for alleviating oxalate toxicity.
J Nat Prod 2008 Sep
PMID:Antiurolithic effect of lupeol and lupeol linoleate in experimental hyperoxaluria. 1871 86

Idiopathic hypercalciuria is the most important predisposing risk factor for calcium oxalate (CaOx) renal stone formation. We assessed the associations between spontaneous CaOx crystallization based on the Bonn Risk Index (BRI), urinary pH, calciuria, oxaluria, and citraturia in 140 Caucasian patients with hypercalciuria, aged 4-17 years, and compared the findings with those in 210 normocalciuric controls. Of the 140 hypercalciuric patients, 58 had renal stones, and 82 had recurrent erythrocyturia, renal colic, or urinary obstructive symptoms-but without stones. Urinary ionized calcium ([Ca(2+)]) levels were measured using a selective electrode, while the onset of crystallization was determined using a photometer and titration with 40 mmol/L ammonium oxalate (Ox(2-)). The calculation of the BRI was based on the [Ca(2+)]:Ox(2-) ratio. The BRI values were 12-fold higher in hypercalciuric children than in healthy controls, but no differences were found in the BRI between subjects with urinary stones and those with urolithiasis-like symptoms. An increased BRI suggested an association with hypercalciuria, lower urinary pH, hypocitraturia, and hypooxaluria. These data indicate that hypercalciuria is an important factor associated with increased urinary CaOx crystallization, although the causal pathways need further investigation. Determination of the BRI in children with hypercalciuria may improve the risk assessment of kidney stones.
Pediatr Nephrol 2009 Sep
PMID:Spontaneous urinary calcium oxalate crystallization in hypercalciuric children. 1935 Feb 80

Primary hyperoxaluria type 1 (PH1) is a rare autosomal recessive inborn error of the glyoxylate metabolism that is based on absence, deficiency or mislocalization of the liver-specific peroxisomal enzyme alanine:glyoxylate aminotransferase. Hyperoxaluria leads to recurrent formation of calculi and/or nephrocalcinosis and often early end-stage renal disease (ESRD) accompanied by systemic calcium oxalate crystal deposition. In this report, we describe an adult female patient with only one stone passage before development of ESRD. With unknown diagnosis of PH, the patient received an isolated kidney graft and developed an early onset of graft failure. Although initially presumed as an acute rejection, the biopsy revealed calcium oxalate crystals, which then raised a suspicion of primary hyperoxaluria. The diagnosis was later confirmed by hyperoxaluria, elevated plasma oxalate levels and mutation of the AGXT gene, showing the patient to be compound heterozygous for the c.33_34InsC and c.508G > A mutations. Plasma oxalate levels did not decrease after high-dose pyridoxine treatment. Based on this case report, we would recommend in all patients even with a minor history of nephrolithiasis but progression to chronic renal failure to exclude primary hyperoxaluria before isolated kidney transplantation is considered.
Int Urol Nephrol 2010 Sep
PMID:Late diagnosis of primary hyperoxaluria after failed kidney transplantation. 2002 Feb 6


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