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

Recently a technique to measure intact parathyroid hormone (PTH), i.e. the biologically active hormone, has been available. The aim of the present study was to apply this method to evaluate the parathyroid function in a material of recurrent renal stone formers (n = 324). Intact PTH was found to be inversely related to both urinary calcium (r = -0.15; p less than 0.01) and serum calcium (p less than 0.02) indicating that in the majority of the patients with hypercalciuria this was accounted for by intestinal hyperabsorption and not by high serum PTH. Hyperabsorption was also the likely explanation for the finding of a positive relationship between the urinary calcium and oxalate excretions (r = 0.22; p less than 0.001) in medication-free patients without intestinal disorders, i.e. without enteric hyperoxaluria. Altogether 25 patients (7%) had elevated serum PTH concentrations. They were followed up with fasting serum and urinary electrolytes and an oral calcium loading test (1 g of calcium) in order to evaluate the importance of renal and intestinal factors responsible for the elevated serum PTH concentrations. The investigation was carried out on a free diet and on low and high calcium intakes, respectively. The incidence of intestinal malfunction, which was sometimes present without clinical symptoms, was found to be approximately the same as that of impaired renal conservation of calcium. The findings in the patients with intestinal malfunction were a reduced intestinal absorption of calcium and an enhanced tubular reabsorption of calcium (TRCa), with greater reabsorption of calcium for higher PTH values. In patients with impaired renal conservation of calcium despite the raised PTH there was no correlation between PTH and TRCa. When PTH was suppressed during the oral calcium load the TRCa was found to be inappropriately low and the renal defect obvious. The intestinal calcium absorption was secondarily increased to compensate for the renal losses.
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PMID:Parathyroid function in relation to intestinal function and renal calcium reabsorption in patients with nephrolithiasis. 163 8

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.
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PMID:Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions. 212 87

Hyperoxaluria and hypercalciuria are common features of renal calcium stone disease. The purpose of the present investigation was to examine the relationships between the intestinal absorption and the renal handling of oxalate and calcium in patients with idiopathic renal stone disease and in patients with enteric hyperoxaluria following jejunoileal bypass (JIB), in comparison with healthy controls. Hyperoxaluria was associated with a higher frequency of both stone episodes and stone operations than a lower urinary oxalate concentration. Patients with idiopathic stone disease showed increased intestinal uptake of both oxalate and calcium, which was probably of importance for their propensity to form calcium oxalate-containing stones. Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued urinary excretion of orally administered 14C-oxalate for more than 48 hours. The prolonged excretion is assumed to be due to a prolonged absorption and/or an increased oxalate pool. Malabsorption of calcium and low fasting urinary calcium excretion in the JIB patients were associated with high tubular reabsorption of calcium, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (PTH). In most recurrent renal stone formers the urinary calcium concentration was increased, with an inverse relationship to serum PTH, indicating intestinal hyperabsorption of calcium. A subgroup of hypercalciuric patients showed increased urinary calcium due to reduced tubular reabsorption of calcium. It is suggested that this is a renal defect resulting in a compensatory rise in PTH. Two different mechanisms of similar prevalence might explain enhanced secretion of PTH in normocalcaemic stone disease, namely reduced calcium absorption and a renal defect in the form of reduced tubular reabsorption of calcium. Glycosaminoglycans efficiently inhibit calcium oxalate crystal growth by binding to the surface of calcium oxalate crystals. In this study the binding was dependent on ionic strength. Higher affinity to the crystals may be the reason why highly charged glycosaminoglycans were more efficient inhibitors of calcium oxalate crystal growth. A calcium-containing organic marine hydrocolloid with the capacity to bind oxalate in vitro was shown to reduce enteric hyperoxaluria. In addition to biochemical effects considerable improvements in diarrhoeal symptoms were reported.
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PMID:Oxalate metabolism in renal stone disease with special reference to calcium metabolism and intestinal absorption. 266 21

In the present study Farnolith (a granular powder consisting of different dietary fibres) was given to normals (n = 6), patients suffering from absorptive hypercalciuria type I (n = 6) and to one patient suffering from renal hypercalciuria. Farnolith binds calcium and reduces the calcium absorption from the intestine. In normals the urine- and serum parameters of calcium metabolism (total- and ionised calcium, parathyroid hormone and vitamin-D-metabolites) remained unchanged. In patients suffering from absorptive hypercalciuria type I a significant reduction of hypercalciuria was found; oxalic acid excretion had decreased as well. Lowered parathyroid hormone values returned to normal, vitamin-D-metabolites remained unaffected. In one patient suffering from renal hypercalciuria parathyroid hormone and 1,25-dihydroxy-vitamin D values increased, calcium excretion had not decreased, though. Our investigation shows that Farnolith is suitable for the treatment of absorptive hypercalciuria. Calcium homoeostasis is returned to normal by Farnolith, at the same time it does not produce secondary hyperoxaluria (as e.g. sodium cellulose phosphate). Patients with primary renal calcium loss should not be treated by Farnolith.
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PMID:Calcium metabolism in normal and in hypercalciuric patients on Farnolith, a dietary fibre preparation. 285 67

The initial part of this presentation deals with the sensitivity of tests commonly used in the diagnosis of primary hyperparathyroidism. Total serum calcium levels often are normal in patients with small parathyroid adenomas but levels of serum ultrafilterable and/or ionized calcium usually are elevated in these patients. The recent introduction of improved radioimmunoassays for measurement of circulating parathyroid hormone has led to greatly improved sensitivity of this test for the diagnosis of primary hyperparathyroidism. However, measurement of total urinary cyclic adenosine monophosphate, even when expressed as a function of glomerular filtration rate, is an extremely insensitive test in patients who have parathyroid adenomas weighing less than 1 gm. Consequently, this test no longer is used for diagnostic purposes in our laboratory. Data relating to the prevalence and causes of hyperoxaluria in patients with idiopathic calcium oxalate stones also are presented. Hyperoxaluria (more than 450 mumol. per 24 hours) was found in 21 of 99 consecutive untreated male patients. Approximately a third of the patients with high normal or increased urinary oxalate excretion also have increased urinary glycolate excretion, which is indicative of increased endogenous oxalate production. This metabolic abnormality was unresponsive to pyridoxine administration but preliminary findings suggest that it may be corrected by restricting dietary protein.
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PMID:Clinical and laboratory approaches for evaluation of nephrolithiasis. 291 16

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 +/- 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 +/- 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 +/- 2.10 nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 +/- 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 +/- 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 +/- 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 +/- 0.12) and high urinary pH (6.69 +/- 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 +/- 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.
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PMID:Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria. 624 14

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

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

When hypercalcemia is detected in a kidney stone formation, an intact parathyroid hormone measurement should be made. Detection of hyperparathyroidism (HPT) is important to prevent further stone episodes and to avoid the complications of high serum calcium in other organ systems. Stones in patients with HPT often contain apatite salts in addition to calcium oxalate because parathyroid excess may create a renal tubular acidosis. The calculi seen in patients with sarcoidosis, another hypercalcemic state that may cause stone formation, however, are usually pure calcium oxalate. Excess generation of 1,25-dihydroxyvitamin D results in intestinal hyperabsorption of calcium and secondary hyperoxaluria.
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PMID:Kidney stones as a manifestation of hypercalcemic disorders. Hyperparathyroidism and sarcoidosis. 1077 70

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


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