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

The importance of dietary and urinary oxalate in the formation of calcium oxalate kidney stones is widely accepted. Although the epidemiologic evidence for the role of oxalate remains largely indirect, recent prospective observations suggest its importance. The inverse association between dietary calcium intake and the risk of stone formation may be attributable to decreased gastrointestinal absorption of dietary oxalate and, thus, lower urinary oxalate concentrations. Further, the decreased risk of stone formation in women who consume large doses of vitamin B6 may be secondary to decreased oxalate production. The increased risk of nephrolithiasis observed with increasing body size may also be secondary to increased endogenous oxalate production. However, the frequency of hyperoxaluria is not substantially different in cases and controls for either sex. Notably, men have both higher stone incidence rates and higher mean urinary oxalate concentrations than women. Additional studies are needed to determine more precisely the role of dietary oxalate. More valid and comprehensive information on the oxalate content of food are desperately needed. Because the data on dietary oxalate are inconclusive, the routine restriction of dietary oxalate needs to be reexamined.
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PMID:Epidemiologic evidence for the role of oxalate in idiopathic nephrolithiasis. 1060 13

Nephrolithiasis effects 1% to 5% of the general population in industrialized countries. The majority of stones is made of calcium oxalate. The formation of calcium oxalate nephrolithiasis depends on several factors: hypercalciuria, hyperoxaluria, adhesion of crystals on the surface of renal epithelial cells, quantitative or qualitative deficit of inhibitors of crystallization in urine, intervention of promotors of crystallization. In this review we report the new insights into calcium oxalate stone formation.
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PMID:[Idiopathic calcium oxalate urinary lithiasis: new physiopathological approaches]. 1064 84

Nephrolithiasis is one of the most frequent pathologies of the urinary tract. Its prevalence in the city of Buenos Aires is 4%. Different biochemical and physiological disturbances may create an environment conductive to renal stone formation. We present the results of an ambulatory evaluation in 2612 patients for the purpose of updating the classification of nephrolithiasis. An abnormal urinary biochemistry was observed in 2423 patients (92.8%) that could be classified in 15 categories. A single diagnosis was documented in 61.5% of the patients, and the remaining 31.2% had more than one diagnosis (concurrent abnormalities). No abnormality was found in 189 stone formers (7.2%). Idiopathic hypercalciuria was the most frequent abnormality, it was encountered in 31.2%; hyperuricosuria and gouty diathesis (presence of urine pH < 5.5, with normal or high uricemia) accounted for 9.4% and 5.4% of patients, respectively. On the other hand, hypomagnesuria affected 6.7% of the stone formers and hypocitraturia was observed in 4.5%. Primary hyperparathiriodism, hyperoxaluria and cystinuria were seen less frequently in 2.6%, 1.3 and 0.45% of patients. Low urine volume was found in 12% of the patients. Among those patients with more than one abnormality, we found that hypercalciuria together with hyperuricosuria and hypocitraturia (12%) was the prevalent association followed by hypercalciuria with hyperuricosuria (9.1%). Our results show the importance of studying nephrolithiasis patients from a biochemical point of view, since this is the only way to achieve a diagnosis of the metabolic abnormality and introduce a specific therapy to prevent recurrence.
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PMID:[Metabolic changes in 2612 patients with nephrolithiasis]. 1068 59

Inhibitors of crystallization process play an important role in renal-stone forming patients. One of well-known inhibitor is citrate. The aim of the study was to define the type of metabolic abnormality in children with nephrolithiasis and the role of urinary citrate excretion. 52 children with nephrolithiasis were examined. Hypocitraturia was observed in 42.3% of patients, most frequently in children with hypercalciuria, hyperoxaluria, and hyperoxaluria with hyperuricosuria. Low urinary citrate excretion found in patients with nephrolithiasis may play an important role in the pathogenesis of the disease. Urinary citrate excretion should be examined in patients with nephrolithiasis.
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PMID:[Hypocitraturia in children with urolithiasis]. 1089 2

Interstitial calcium oxalate (CaOx) crystals can be found in primary oxalosis and in secondary hyperoxaluria. In a rat model for nephrolithiasis, we investigated whether such crystals can be removed by the surrounding interstitial cells. CaOx crystals were induced by a crystal-inducing diet based on ethylene glycol (EG) and ammonium chloride (CID). Both lithogenic compounds were added to the drinking water. After 9 days, the animals received normal drinking water for 2 days. Using this CID, only the interstitial crystals are retained. Subsequently, half of the population remained on normal drinking water (normo-oxaluria), whereas the other half received a low dose of EG alone (chronic hyperoxaluria). The rats were killed at regular times thereafter. The results showed that the kidney-associated oxalate significantly declined during normo-oxaluria, but remained high during chronic hyperoxaluria. Interstitial cells positive for the leukocyte common antigen (CD45; which identifies all types of leukocytes), the ED1 antigen (which is specific for monocytes and macrophages), and the major histocompatibility class II antigen (MCHII), respectively, had increased in number, with minor differences between both rat populations. The cells around the interstitial crystals were mostly positive for ED1. Multinucleate giant cells were regularly observed. These cells were positive for CD45 and ED1 and sometimes also for MCHII. The crystals in these cells were moderately positive for acid phosphatase and carbonic anhydrase II. It is concluded that interstitial CaOx crystals can be removed under normo-oxaluric conditions and that, in all likelihood, macrophages and multinucleate giant cells are involved in that process.
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PMID:Role of macrophages in nephrolithiasis in rats: an analysis of the renal interstitium. 1097 95

Despite intensive studies in the last decades many aspects of nephrolithiasis still remain to be elucidated. Supersaturation with respect to lithogenic substances explains stones composed of cystine, uric acid, struvite, and calcium stones secondary to systemic diseases. In this subset there is a clear separation between patients and controls, and stone activity is well related to alterations in the physicochemistry of the urine environment. The understanding of the mechanisms of idiopathic calcium nephrolithiasis, on the other hand, is controversial, because we are still unable to establish clear-cut cause-effect relations between metabolic and physicochemical abnormalities and stone formation. Recent studies have been centered on the kidney, not only as the end organ of biochemical derangements due to systemic or environmental factors, but also as a complex laboratory where some events conduct to and others defend from lithogenesis. Many of these phenomena occur in the proximal tubule. Molecular biology has explained some types of hypercalciuria, which are due to genetic mutations altering tubular function, and similar results are expected for hypocitraturia and hyperoxaluria. The latter is conducive to stone formation through several mechanisms including supersaturation, oxidative stress on tubular cells, and interference with some natural inhibitors. The long list of inhibitors includes ionic and macromolecular moieties, some being produced within the nephron in response to lithogenic insults, and some affecting not only crystallization but also crystal cell adherence. Crystal trapping is believed to anticipate a renal stone. However, much has still to be clarified on their actual role in calcium nephrolithiasis, by what mechanisms they act, if patients and controls differ in the excretion and structure of some inhibitors, and whether differences are genetically determined.
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PMID:Renal stones: from metabolic to physicochemical abnormalities. How useful are inhibitors? 1113 33

Whether specific metabolic abnormalities are related to nephrolithiasis in patients with medullary sponge kidney (MSK) remains a debated issue. The purpose of this study is to determine metabolic disorders in patients with MSK and nephrolithiasis compared with idiopathic calcium-stone-forming patients. One hundred eighty-four patients with recurrent calcium-stone formations were investigated with regard to metabolic abnormalities. Of these, 22 patients (11.9%; 13 men, 9 women) showed MSK by radiological examination. MSK was defined as a kidney that presented at least three linear or round papillary opacities in the affected papilla on urography. Multiple stones (more than five) existed in both kidneys in all patients with MSK. The remaining 162 patients (109 men, 53 women) were idiopathic calcium-stone formers. Frequencies of low urine volume (urine < 1,500 mL/24 h) and hyperoxaluria (oxalate > 40 mg/24 h) were similar between the groups. Hypercalciuria (men, calcium > 300 mg/24 h; women, calcium of 250 mg/24 h) was found less frequently in the MSK group. The frequency of hypocitraturia (citrate < 300 mg/24 h) was significantly greater in the MSK group than the idiopathic group (77.3% versus 33.9%, respectively). Mean 24-hour urinary excretions of calcium, citrate, uric acid, and magnesium were significantly less in the MSK group. No differences were found in serum calcium, phosphate, and parathyroid hormone levels between the groups. Low urinary excretions of citrate and magnesium are the most typical metabolic disorders that distinguish MSK stone patients from idiopathic calcium-stone-forming patients. In addition to such anatomic abnormalities as ectatic collecting ducts, low levels of urinary inhibitors of stones seem to contribute to the pathogenesis of nephrolithiasis in patients with MSK.
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PMID:Contributory metabolic factors in the development of nephrolithiasis in patients with medullary sponge kidney. 1138 81

Deposition of calcium oxalate (CaOx) crystals in the renal interstitium is common in humans with primary oxalosis and secondary hyperoxaluria, as well as in kidneys of rats with CaOx nephrolithiasis. In vivo, macrophages and multinucleated giant cells mostly encapsulate these crystals. To investigate whether macrophages are able to dispose of CaOx crystals after phagocytosis, we used a nontransformed macrophage cell line derived from mouse spleen progenitors. Cytokine assays showed that in response to crystal binding and phagocytosis, these macrophages release tumor necrosis factor-alpha. This release was evident at 8 hours, maximal at 24 hours, and decreased to control values after 48 hours of incubation with crystals. A very low but significant release of interleukin-6 into the culture medium was only noticed after 32 hours. Radiochemical experiments showed that these cells bind 38.8% of the CaOx crystals added. After 4 days, all internalized crystals had been dissolved and their molecular constituents released into the extracellular environment. Confocal laser scanning microscopy followed by morphometrical analyses confirmed these results. Long-term (survival) analyses showed that in the interval under study and at the crystal doses used, cell viability was not significantly affected. These findings support the view that properly functioning macrophages are able to remove CaOx deposits from the renal interstitium and that these cells produce inflammatory cytokines before crystal dissolution.
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PMID:Cytokine production induced by binding and processing of calcium oxalate crystals in cultured macrophages. 1147 59

Dietary calcium lowers the risk of nephrolithiasis due to a decreased absorption of dietary oxalate that is bound by intestinal calcium. The aim of the present study was to evaluate oxaluria in normocalciuric and hypercalciuric lithiasic patients under different calcium intake. Fifty patients (26 females and 24 males, 41 +/- 10 years old), whose 4-day dietary records revealed a regular low calcium intake (<or=500 mg/day), received an oral calcium load (1 g/day) for 7 days. A 24-h urine was obtained before and after load and according to the calciuria under both diets, patients were considered as normocalciuric (NC, N = 15), diet-dependent hypercalciuric (DDHC, N = 9) or diet-independent hypercalciuric (DIHC, N = 26). On regular diet, mean oxaluria was 30 +/- 14 mg/24 h for all patients. The 7-day calcium load induced a significant decrease in mean oxaluria compared to the regular diet in NC and DIHC (20 +/- 12 vs 26 +/- 7 and 27 +/- 18 vs 32 +/- 15 mg/24 h, respectively, P<0.05) but not in DDHC patients (22 +/- 10 vs 23 +/- 5 mg/24 h). The lack of an oxalate decrease among DDHC patients after the calcium load might have been due to higher calcium absorption under higher calcium supply, with a consequent lower amount of calcium left in the intestine to bind with oxalate. These data suggest that a long-lasting regular calcium consumption <500 mg was not associated with high oxaluria and that a subpopulation of hypercalciuric patients who presented a higher intestinal calcium absorption (DDHC) tended to hyperabsorb oxalate as well, so that oxaluria did not change under different calcium intake.
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PMID:Effect of calcium intake on urinary oxalate excretion in calcium stone-forming patients. 1204 31

The primary hyperoxalurias (PH1 and PH2) are rare defects of oxalate overproduction. There are only 24 reported cases of PH2, which is characterized by raised urine oxalate and L-glycerate. We describe 13 previously unreported children with PH2, representing the largest single-centre cohort in the world. DNA samples were tested for a common mutation and four other documented mutations in the gene encoding the enzyme glyoxylate reductase/hydroxypyruvate reductase (GRHPR). Two of the five kindred showed homozygosity for two different mutations in the GRHPR gene. The genetic defect was not identified in the other three families. The median age at diagnosis of PH2 was 1.7 years. Five children presented with nephrolithiasis between 0.8 and 9 years. Haematuria was common, but urinary tract infection and nephrocalcinosis were not. All had normal renal function at diagnosis, and only 1 patient had a significant decline in glomerular filtration rate. We conclude that all children with nephrolithiasis secondary to hyperoxaluria should have urinary glycerate measured, as PH2 may be more prevalent than currently estimated. DNA mutational analysis may be useful in supporting the diagnosis.
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PMID:Primary hyperoxaluria type 2 in children. 1218 64


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