Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 19 patients with active nephrolithiasis, 14 patients with non-active nephrolithiasis and 17 healthy subjects were examined under standardized intake of calcium, phosphorus, purine and protein. In patients with both active and non-active renal stone disease the following abnormalities were found: elevated plasma levels of PTH and osteocalcin, increased activity of the bone isozyme of alkaline phosphatase, low plasma levels of phosphate and increased urinary excretion of calcium and oxalic acid. These abnormalities were more marked in patients with active than non-active nephrolithiasis. No correlation was found between plasma PTH levels and parameters of bone turnover as well as calciuria and oxaluria. Results presented in this paper suggest that (a) Smith's criteria of active renal stone disease are of minor pathogenetic and therapeutic value and (b) patients with active nephrolithiasis differ from non-active renal stone formers by more elevated oxaluria and markers of bone turnover and more marked abnormalities in calcium-phosphate metabolism related parameters.
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PMID:Markers of bone turnover in patients with nephrolithiasis. 941 56

Supersaturation with respect to calcium salts (oxalate and phosphate) is the driving force leading to crystalluria and nephrolithiasis. High-molecular-weight urinary inhibitors are recently described molecules capable of altering the process of kidney stone formation. By inhibition of crystal nucleation, growth and aggregation and by inhibition of crystal interaction with tubular cells, these proteins efficiently prevent stone formation and retention in the urinary tract. But in spite of considerable efforts, characterization of these proteins is still under way. Besides the pathophysiology of risk factors for calcium salts supersaturation such as idiopathic hypercalciuria or hyperoxaluria, the renal involvement of protein inhibitors is the most exciting field in the comprehensive approach of nephrolithiasis, a disease that affects up to 10% of people in Western countries.
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PMID:Urinary kidney stone inhibitors. What is the news? 956 42

Idiopathic calcium nephrolithiasis (ICN) is a frequent disease in Western countries. The physicochemical theory of lithogenesis, which explains stone formation by the precipitation, growth, and crystalline aggregation of lithogenic salts in the urine, has contributed greatly to the understanding of the pathogenesis of calcium urolithiasis. However, several aspects are still unexplained; the co-existence of familial occurrence, primary tubular dysfunctions with ICN, and anomalies in the systemic handling of oxalate and calcium led to the development of a cellular hypothesis of ICN. A number of cellular defects in the handling of ions has been reported that involves both anion and cation transport. These anomalies are probably the expression of a still unknown cellular defect in idiopathic calcium stone formers. We suggested that an anomaly in the cell membrane composition might be responsible for the complex array of cell ion flux abnormalities observed in ICN. Recently, a disorder in the n-6 polyunsaturated fatty acid series has been described; it is characterized by a lower linoleic acid content and a higher arachidonic acid concentration in both plasma and erythrocyte membrane phospholipids of renal calcium stone patients. This anomaly could cause an increased activity of ion carriers; furthermore, it may lead to increased prostaglandin synthesis and to secondary phenomena at the kidney, skeletal, and intestinal level. As a consequence, critical conditions for lithogenesis in the kidney may ensue. The data suggest a common pathogenesis for hypercalciuria and hyperoxaluria. The systemic defect in the phospholipid arachidonic acid level may be both of dietary or genetic origin; experimental data suggest that the increase in delta-6 desaturase activity, the limiting enzyme in the metabolic pathway of polyunsaturated fatty acids, might be relevant to the pathogenesis of lipid abnormalities observed in nephrolithiasis and to the pathogenesis of ICN and its related problems (at the kidney, intestinal, and bone level).
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PMID:Pathogenesis of idiopathic calcium nephrolithiasis: update 1997. 959 25

The primary care physician has a responsibility not only to recognize and treat acute stone passage but to ensure that the patient with recurrent stones has metabolic evaluation and appropriate preventive care. Renal colic is typically severe, radiates to the groin, is associated with hematuria, and may cause ileus. About 90% of stones that cause renal colic pass spontaneously. The patient with acute renal colic should be treated with fluids and analgesics and should strain the urine to recover stone for analysis. Highgrade obstruction or failure of oral analgesics to relieve pain may require hospitalization; a urinary tract infection in the setting of an obstruction is a urologic emergency requiring immediate drainage, usually with a ureteral stent. Several approaches are available when stones do not pass spontaneously, including extracorporeal shock wave lithotripsy, percutaneous lithotripsy, and ureteroscopic laser lithotripsy. Calcium stone disease has a lifetime prevalence of 10% in men and causes significant morbidity. Renal failure is unusual. Stone types include calcium oxalate, uric acid, struvite, and cystine. Stone analysis is particularly important when a noncalcareous constituent is identified. The majority of patients with nephrolithiasis will have recurrence, so prevention is a high priority. High fluid intake is a mainstay of prevention. Metabolic evaluation will indicate other appropriate preventive measures, which may include dietary salt and protein restriction, and use of thiazide diuretics, neutral phosphate, potassium citrate, allopurinol, and magnesium salts. Dietary calcium restriction may worsen oxaluria and negative calcium balance (osteoporosis).
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PMID:Nephrolithiasis: acute management and prevention. 965 69

This review describes the supposed mechanisms leading to idiopathic hypercalciuria (IHU) in childhood, further the diagnostic criteria and the proposed treatment modalities are discussed. IHU is not only one of the main causes of renal stone disease in children but it's also at the origin of the postglomerular haematuria and the frequency-dysuria syndrome. Its role in the development of osteoporosis in adults is also documented. The diagnosis of raised calcium excretion is based on age specific values during early infancy. In older children and adults a urinary calcium/creatinine ratio exceeding 0.6 mmol/mmol is regarded as elevated. Dietary calcium restriction can no longer be recommended for the treatment of IHU because it results in secondary hyperoxaluria and on the long-term causes decreased bone mineral density. Patients should be kept on dietary sodium restriction and high fluid intake. In cases IHU associated with recurrent episodes of macroscopic haematuria or recurrent stone disease a therapeutic trial with hydrochlorothiazide in the dose of 0.5-1 mg/kg/day with potassium-citrate supplementation and possibly magnesium citrate should be started. In some special forms of hypercalciuria such as the X-linked recessive nephrolithiasis syndrome or Bartter syndrome the localization and in some cases even the molecular mechanism of the events leading to increased calcium excretion are elucidated. In IHU enhanced Ca(++)-ATPase, and Na-Li countertransport activity and decreased Na+/K+ ATPase activity were described in the erythrocyte membrane model. It is expected that with the molecular genetic development the clinical classification of the hypercalciuric syndromes will become a rational genome-based one.
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PMID:[Idiopathic hypercalciuria in childhood]. 987

Inter-alpha-inhibitor and other bikunin-containing proteins are synthesized in relatively large quantities by the liver. These proteins function as Kunitz-type serine protease inhibitors and appear capable of inhibiting calcium oxalate (CaOx) crystallization in vitro. Preliminary studies have shown that renal tubular epithelial cells synthesize bikunin in response to CaOx challenge. To examine this response in vivo, a sensitive reverse transcription-quantitative competitive template-PCR was developed to detect and quantify poly(A)+ -tailed bikunin mRNA expression in kidney tissue from normal rats and rats developing CaOx nephrolithiasis after challenge with ethylene glycol. Bikunin mRNA expression in rat liver tissue was assessed as a positive control. The expression of bikunin mRNA in liver did not differ significantly between normal control rats and experimental rats with induced hyperoxaluria and renal CaOx crystallization. In contrast, there were significant temporal increases in the levels of bikunin mRNA expression in rat kidneys during CaOx nephrolithiasis after challenge with ethylene glycol. Urinary excretion of bikunin-containing proteins seemed to increase concomitantly. These findings indicate an association between the induction of hyperoxaluria/CaOx nephrolithiasis and the expression of the bikunin gene in rat kidneys.
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PMID:Temporal changes in mRNA expression for bikunin in the kidneys of rats during calcium oxalate nephrolithiasis. 1023 84

Nephrolithiasis is a common and important condition. Several lines of evidence suggest that increased urinary calcium increases the risk of kidney stones. Since dietary calcium raises urinary calcium, it has been common practice to reduce calcium intake in stone-formers who hyperabsorb calcium from the intestine, although no trial has yet been designed to directly demonstrate the effectiveness of calcium restriction. In contrast, some have suggested that calcium restriction may be harmful due to resultant hyperoxaluria and risk of bone loss. In fact, two powerful prospective observational studies have suggested that increased dietary calcium reduces the risk of the first kidney stone. However, calcium was not the only variable, since those with the highest quintile of calcium intake also ingested more fluid, potassium, magnesium and phosphate. Moreover, the otherwise thorough analysis was not adjusted for alkali intake, which may prevent stones, or oxalate intake, which may increase stone risk. Due to limitations in available data, future prospective studies should be designed to probe the effect of specific interventions with calcium, both dietary and supplemental, on urinary parameters and stone formation, particularly in hypercalciuric stone-formers, who may respond conversely. For now, dietary calcium should be gradually increased in stone-formers as guided by the urinary calcium, and hypocalciuric agents should be added as necessary.
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PMID:The role of calcium in the prevention of kidney stones. 1051 17

It is unclear why men have a higher incidence of calcium oxalate nephrolithiasis than women. This study examined the role of sex hormones on urinary oxalate excretion and kidney stone formation in an experimental model of urolithiasis. Adult male and female Sprague Dawley rats with different sex hormone modulations were given 0.75% ethylene glycol for 2 wk to induce hyperoxaluria and kidney calcium oxalate crystal deposition. The study groups were: intact male and female rats; castrated male and female rats; intact male or female rats with opposite sex hormone implants; and castrated male and female rats with either testosterone or estradiol implants. Overall, a significant negative correlation between urinary oxalate and plasma estradiol/testosterone ratio was found. None of the estradiol-implanted rats, whether male or female, intact or castrated, developed kidney crystal deposits. The three groups of testosterone-implanted rats had a 43 to 88% rate of kidney calcium oxalate crystal deposition. These results indicate that androgens increase and estrogens decrease urinary oxalate excretion, plasma oxalate concentration, and kidney calcium oxalate crystal deposition. These findings may partly explain why nephrolithiasis is a predominantly male disease.
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PMID:Role of sex hormones in experimental calcium oxalate nephrolithiasis. 1054 Dec 67

LLC-PK1 and Madin-Darby canine kidney (MDCK) cells were used to study the role of free radicals in renal epithelial injury during exposure to oxalate ions (Ox) and calcium oxalate monohydrate (COM) crystals. The cell cultures were exposed for 120 or 240 min to 1.0 mmol Ox or 1.0 mmol Ox plus 500 microg/ml of COM crystals averaging 1.0 microm in size. Exposure of both LLC-PK1 and MDCK cells to Ox alone increased the leakage of lactate dehydrogenase, which was further enhanced when cells were exposed to Ox + COM crystals. The release of lactate dehydrogenase from the LLC-PK1 cell line, however, was significantly higher than that from MDCK cells. LLC-PK1 cells also showed a significant increase in malondialdehyde (MDA) content on Ox challenge. MDA content was even higher when LLC-PK1 cells were challenged with Ox + COM crystals. However, in MDCK cells, the elevated MDA content was similar in both treatment groups, suggesting that these cells may be more resistant to the calcium oxalate crystals. Glutathione peroxidase activity was decreased in both LLC-PK1 and MDCK cells. Challenging cells with Ox + COM resulted in decreased catalase activity in LLC-PK1, but increased catalase activity in MDCK cells. Superoxide dismutase activity and reduced glutathione content were not significantly different in either cell type when challenged with Ox or Ox + COM. Previous in vivo animal studies yielded indirect evidence for the increased lipid peroxidation during hyperoxaluria-induced nephrolithiasis. However, in an animal model, it is difficult to separate the effect of Ox from Ox in combination with COM crystals. This study suggests that the injury to renal tubular epithelial cells is accompanied by lipid peroxidation when exposed to Ox. The injury is augmented when COM crystals are included. LLC-PK1 cells are more susceptible to Ox-associated injury than MDCK cells.
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PMID:Cells of proximal and distal tubular origin respond differently to challenges of oxalate and calcium oxalate crystals. 1054 Dec 82

The first episode of nephrolithiasis provides an opportunity to advise patients about measures for preventing future stones. Low fluid intake and excessive intake of protein, salt and oxalate are important modifiable risk factors for kidney stones. Calcium restriction is not useful and may potentiate osteoporosis. Diseases such as hyperparathyroidism, sarcoidosis and renal tubular acidosis should be considered in patients with nephrolithiasis. A 24-hour urine collection with measurement of the important analytes is usually reserved for use in patients with recurrent stone formation. In these patients, the major urinary risk factors include hypercalciuria, hyperoxaluria, hypocitraturia and hyperuricosuria. Effective preventive and treatment measures include thiazide therapy to lower the urinary calcium level, citrate supplementation to increase the urinary citrate level and, sometimes, allopurinol therapy to lower uric acid excretion. Uric acid stones are most often treated with citrate supplementation. Data now support the cost-effectiveness of evaluation and treatment of patients with recurrent stones.
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PMID:Prevention of recurrent nephrolithiasis. 1059 18


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