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

Despite intensive research the knowledge of stone pathogenesis, which is the basis of every rational stone metaphylaxis, has remained rather scanty. Epidemiology shows that stone formation in most patients is only a sporadic event, probably resulting from a coincidence of different factors. The hypercalciuria, hypocitraturia, hyperuricosuria and hyperoxaluria frequently found in calcium stone formers can be influenced therapeutically and, in affluent societies, seem to be the result of protein over-consumption. These four factors favour crystallization processes in urine. However, urine is normally protected from nucleation, growth and aggregation of calcium minerals by crystallization inhibitors. In urine, crystallization of calcium oxalate can only be induced by an extreme supersaturation, a deficient inhibitor activity and promoters of crystallization. To form a stone, crystals have to be retained in the urinary collecting system. Two mechanisms of retention are discussed: large crystal aggregates trapped in collecting ducts of renal papillae, or a pre-existing calcification of the papilla (mainly calcium phosphate) that may be responsible for growth of an initially fixed particle to a concretion large enough to become symptomatic. An excessive oxalate intake combined with a low calcium consumption can produce marked hyperoxaluria. In the animal model, hyperoxaluria induces not only calcium oxalate crystallization but also papillary damage and incrustations. Hypercalciuria at a low pH favours the aggregation of calcium oxalate, and at a high pH the crystallization of calcium phosphate, a promoter of heterogeneous nucleation of calcium oxalate. All these factors and further complex phenomena mentioned in this paper have to be taken in account to perform rational stone metaphylaxis.
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PMID:Stone prevention: why so little progress? 963 38

Many studies indicate that up-regulated production of 1,25(OH)2-vitamin D3 (calcitriol) with increased intestinal absorption of calcium is the primary event causing idiopathic hypercalciuria. Thus, a low calcium diet appears to be a straightforward strategy in calcium stone formers with hypercalciuria (HCSF). However, the efficacy of such a regimen has never been established, and lowering calcium intake from 1000 to 400 mg/day further enhances calcitriol production. On a diet chronically restricted in calcium, many stone formers increase their intake of animal flesh protein. The latter is known to increase renal mass, and calcitriol levels indeed are positively correlated with renal mass in animals as well as in HCSF. Thus, low calcium and high animal flesh protein consumption are independent stimuli for further up-regulation of calcitriol production. The rise in calcitriol suppresses parathyroid hormone synthesis thereby diminishing renal tubular calcium reabsorption, and increasing urinary calcium losses. Since calcitriol up-regulation also increases bone resorption, the combination of low calcium and high protein intake is particularly likely to induce negative calcium balance and thus osteopenia. Finally, low calcium intake carries the risk of insufficient intestinal binding of oxalate with subsequent increases in intestinal absorption and urinary excretion of oxalate. Indeed, most recent studies suggest that high amounts of calcium, when ingested simultaneously with oxalate-containing meals, are able to prevent hyperoxaluria during severe oral oxalate loading.
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PMID:Low calcium diet in hypercalciuric calcium nephrolithiasis: first do no harm. 981 31

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

Population based data on urinary excretion of various metabolites of pathological importance, Calcium, Magnesium, Sodium, Potassium, Oxalates, Citrates, Phosphates, Uric acid and urea have been collected from around three hundred children of the Quetta valley. The body weight was in the range of 11-50 kg and the age was in between 4-16 years. The urine excretion average was 987.5 +/- 452.5 ml per 24 hours. There was 11.5% incidence of hypercalciuria, 8.5% incidence of hyperuricosuria, 2.0% hyperphosphaturia, 2.5% hypomagnesuria, 3.5% hypocitraturia, 6.5% hypernatriuria, 43.5% hypokaliurea and 2.1% hyperoxaluria. Urea excretion average was 23.11 +/- 14.99 g per 24 hours. The study provided the basis for childhood reference pattern in urinary excretion of compounds related to various pathological conditions, in particular stone formation in this region.
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PMID:Population based data on urinary excretion of various metabolites in children of north western region of Pakistan. 1006 40

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

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

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

The exposure of the lumbar region to interference currents in combination with radon baths conducted in 37 patients with chronic pyelonephritis inhibited activity of the inflammation, hypercalciuria and hyperoxaluria, improved function of the kidneys. The same clinical effects were achieved in 32 patients who had received interference therapy in combination with intake of radon water.
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PMID:[The combined therapy of patients with chronic nonspecific pyelonephritis using interference currents and and radon procedures]. 1064 44

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


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