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

Calcium, in the form of regular food supplementation, can improve bone metabolism, but it can also increase the risk for renal calcium stones, and may aggravate pre-existing calcium urolithiasis. To study the first of these two aspects, ten healthy volunteers were given a conventional test meal (breakfast; calcium content 28 mg) with or without two dosages of calcium (as calcium-sodium citrate, CSC 1, 680 mg; CSC 2 1,360 mg), taken after an overnight 12 h fast. To study the latter aspect, patients with idiopathic recurrent calcium urolithiasis (ICU) received a balanced test meal of fixed composition, containing 1,000 mg calcium either as CSC (Meal + CSC3; n = 6) or as calcium gluconate (Mcal; n = 8). In normals, CSC induced a dose-dependent increasing intestinal absorption of calcium, and a decrease in oxalate absorption; in serum, CSC increased calcitonin and suppressed parathyroid hormone, but left unchanged the markers of bone turnover, serum osteocalcin and bone alkaline phosphatase. In urine, CSC decreased bone resorption markers (collagen crosslinks) and phosphaturia increased citrate, created signs of metabolic alkalosis, and inhibited several parameters of CaOx crystallization. In ICU, the CSC3 load failed to promote the crystallization of CaOx and calcium phosphate. It was concluded that CSC supplementation of a meal: (1) is well tolerated by healthy subjects and ICU patients, renders calcium highly available to bone, and prevents post-prandial oxaluria from rising; and, (2) is followed by the inhibition of crystallization of renal stone forming calcium-containing substances. Long-term studies aimed at evaluating the usefulness of CSC in preserving healthy bone, and in the metaphylaxis of renal stones would appear justified.
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PMID:Acute effects of calcium sodium citrate supplementation of a test meal on mineral homeostasis, oxalate, and calcium oxalate crystallization in the urine of healthy humans--preliminary results in patients with idiopathic calcium urolithiasis. 1042 48

The careful analysis of cystine calculi may be important to detect the presence of other urinary alterations (such as hyperuricosuria, hypercalciuria, hyperoxaluria or bacterial infections) that coexist with cystinuria in many patients. For this reason, in the present study, 14 human and 17 canine cystine uroliths have been studied by infrared spectroscopy (IR), scanning electron microscopy (SEM), and energy dispersive X-ray analysis (EDX). According to the infrared analysis, most of the human and canine stones were composed of nearly pure cystine. However, in these calculi of apparently pure cystine, the study by SEM and EDX showed in many cases the presence of small amounts of calcium apatite. The infrared study of several samples heated at 750 degrees C confirmed the presence of phosphate, when it was difficult to detect this component in the spectra of the original samples owing to band overlapping. Other components detected in varying proportions in cystine calculi were magnesium ammonium phosphate hexahydrate (struvite), calcium hydrogen phosphate dihydrate (brushite), calcium oxalate (mono and/or dihydrate) and, in one case, a drug (oxolinic acid).
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PMID:Spectroscopic and ultrastructural comparative study of cystine calculi in humans and dogs. 1047 54

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

Several studies indicate that crystallization, the essential first step for stone formation, starts in the nephron. First a calcium phosphate mineral precipitates in the loop of Henle and this may induce formation of calcium oxalate in the late nephron segments. This study investigated the factors that determine the risk of the first calcium phosphate crystallization step in the loop of Henle. Data from a theoretical model that describes the fluid composition in the different nephron segments are combined with data from nucleation experiments. From this, an assessment was made regarding how changes in plasma and urine composition, tubular functions, and renal anatomy effect the chance of initial crystallization of calcium phosphate in the loop of Henle. The results show that parameters like hypercalciuria and hyperoxaluria do not completely reflect the risk for the initial nucleation step. A combination with data on plasma composition and on tubular function is needed to assess this risk. Renal growth from birth to adulthood and the concomitant increase in renal concentrating capacity are shown to increase the risk for crystallization in the loop of Henle. This coincides with the increasing incidence of calcium oxalate urolithiasis. Treating crystallization and stone formation as a nephron event opens new ways for investigating and understanding the process of urinary stone formation.
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PMID:Risk factors for crystallization in the nephron: the role of renal development. 1054 Dec 65

We report the case of a 10-year-old girl who received a cadaveric kidney transplant for oxalosis after a period of 12 months on hemodialysis. The donor was a 6-year-old child. Cold ischemia was four hours. Diuresis occurred immediately in the operating room. Mean daily diuresis was maintained at 8 liters: first by i.v. perfusion, then by nocturnal continuous nasogastric hydration. In addition to the usual immunosuppressive drugs, she received pyridoxine, sodium citrate, phosphate, hydrochlorothiazide and magnesium. Daily hemodialysis was performed from Day 1 to Day 9 and four additional sessions every other day. The postoperative course was satisfactory. Oxaluria was elevated initially at 1074 mg/24 h (normal < 50 mg/24 h). One year later, mean daily diuresis is still 8 liters, renal function is normal and oxaluria is at 296 mg/24 h. Repeated graft sonography showed no nephrocalcinosis, but mild oxalate deposits are noted on renal biopsy. Isolated renal transplantation was successful in our patient. It allowed us to stop hemodialysis and to avoid extra-renal accumulation of oxalate. Despite this success, we are convinced that long term prognosis is uncertain and liver transplantation should be realized to correct definitely the biochemical defect.
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PMID:Dilemma of oxalosis in end stage renal failure: isolated kidney allograft or hemodialysis. 1088 38

We report our experience with the composition and management of caliceal diverticular stones for the past 13 years at our institution. Fourty patients with caliceal diverticular stones were treated percutaneously at Long Island Jewish Medical Center. The size of the diverticula ranged from 1 to 4.8 cm, with a mean size of 2.27 cm. The stone size ranged from 0.2 to 4.5 cm in diameter with an average of 1.7 cm. Twenty patients underwent a metabolic evaluation. Follow-up ranged from 8 months to 140 months with a mean of 72.5 months. We achieved a stone free rate of 95%. All 40 patients were free of pain and infection. The chemical composition of stones was identified in 38 patients. Twelve patients were found to have mainly calcium phosphate stones, 16 mainly calcium oxalate stones, 7 mainly uric acid stones and 3 were found with milk of calcium in their diverticulum. Thirty-five patients had complete resolution of their diverticula with normal urograms. The remaining 5 patients had at least 50% diminution of the diverticulum size. No one of the latter patients was found to have stone recurrence. Metabolic evaluation of the 40 patients showed in the 75% of the cases any metabolic abnormality, an absorptive hypercalciuria type II in two patients (10%), hyperuricosuric hypercalciuria in two cases (10%) and hyperoxaluria in one (5%). Percutaneous management of caliceal diverticular stones is a safe and effective modality compared to the existing alternative procedures reported in the literature.
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PMID:[Percutaneous treatment of calculosis in caliceal diverticulosis: 13-year experience]. 1095 91

The potential risk of recurrence and degradation of renal function justifies the etiological investigation of all lithiasis-associated pathologies. Therefore calculus analysis of the crystalline phases and morphological characteristics is an important factor in the etiological diagnosis of the disease. Microscopic examination and infrared spectroscopy of calculi from 727 children showed that calcium oxalate was the main component in 36.7% of cases, followed by calcium phosphate (31%), struvite (9.9%) and purine groups (7.7%). The most frequently observed crystalline from was carbapatite (26%), then whewellite (21%) and weddellite (15.7%). As regards the etiopathogenic aspect in adults, the relations between hypercalciuria and weddellite, and between hyperoxaluria and whewellite are also found in the child: in subjects with hypercalciuria, 82% of the calculi contained over 20% weddellite; and in subjects with hyperoxaluria, whewellite was the major constituent in 79% of cases (or 95% in the absence of associated hypercalciuria). In 27 calculi mainly composed of whewellite, the morphological analysis indicated primary hyperoxaluria; this diagnosis was confirmed in 25 cases by specific biological investigation. Urinary tract infection is frequently associated with lithiasis, but its lithogenic role cannot be confirmed without calculus analysis. Several criteria can be used as markers to determine the lithogenic etiology of the infection, i.e., the presence of struvite, the carbonate rate of carbapatite, and the whitlockite and/or protein content of the calculus.
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PMID:[Component analysis of urinary calculi in the etiologic diagnosis of urolithiasis in the child]. 1098 88

Urolithiasis is a frequent disorder that is characterized by its recurrence following treatment and which can affect between 3-20% of the population, with an incidence that differs from country to country. The aim of the present study was to determine the composition of the calculi, and the remain characteristics of this pathology in Morocco. A series of 80 calculi was therefore analyzed by Fourier transform infrared spectroscopy. The findings showed that calcium monohydrate oxalate was the main lithiasic component, indicating that hyperoxaluria plays a major role in the formation of the calculi. The component identified were as follows: calcium oxalate (58.75%), calcium phosphate and magnesium phosphate (17.5%), uric acid (15%), and urate (8.75%). In 91.25% of cases, the calculi were of mixed composition. Regular patient follow-up is advocated and subjects should be informed of the risk factor involved, as urolithiasic recurrence was observed in 10% of the cases in this series.
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PMID:[Infrared spectrometry and urolithiasis. Report of 80 cases]. 1114 79

To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and fat-rich experimental diet (CH-F, n = 12) for 111 +/- 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins > 100 kD and a deficit of proteins > 30-50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies.
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PMID:Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction. 1122 20

Stone disease is as old as recorded history but despite advances in diagnosis and treatment, it continues to cause significant morbidity. This review summarises the current pharmacologic management of urinary calculi based upon the stone type. All patients with stone disease are advised to increase fluid intake, limit dietary protein and limit sodium. Calcium oxalate stones can be managed on a selective or non-selective basis depending on the cause of the hypercalciuria or hyperoxaluria. Agents currently in use include sodium cellulose phosphate, thiazides, orthophosphates, oral calcium supplements, pyridoxine, cholestyramine, citrate, magnesium and allopurinol. Classically, struvite stones occur in the presence of urea splitting organisms and are composed of magnesium, ammonium phosphate and carbonate apatite. The goal of treatment is to make patients stone free as bacteria retained in stone fragments lead to stone growth. Urease inhibitors, aluminium hydroxide gel, hemiacidrin, and Suby G and M solutions are infrequently used in treatment. Cystine stones are the result of an autosomal recessive disorder. D-Penicillamine, captopril and alpha-mercaptopropionylglycine (MPG) are all oral agents that have proven to be efficacious. As more randomised trials are conducted and the understanding of endogenous stone inhibitors progresses, the medical management of stone disease will continue to improve.
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PMID:Pharmacology for renal calculi. 1124 28


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