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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tubular proteinuria is generally accepted as the critical effect following long-term, low-level exposure to cadmium as seen in an industrial environment. This effect may not be of immediate importance to the health of the individual, but the significance, in terms of long-term morbidity and mortality, of the renal tubular defect of which it is an indicator is not fully understood, and certain sequelae may have remained unrecognized due to inadequate follow-up.Follow-up studies have been performed in nine of 12 workers who were initially investigated in 1962. In six of the men exposures ranged from 28 to 45 years to cadmium sulfide dust and for shorter periods in the earlier years to cadmium oxide fume and dust. These six men had tubular proteinuria when first seen, and this has persisted in the five survivors. All six men had hypercalciuria, and two of them became recurrent stone formers. One man whose urinary calcium excretion later fell to a low level more recently developed vitamin D resistant osteomalacia. In addition, each of the six men had exhibited some, but not all, of a variety of biochemical abnormalities related to other proximal renal tubular defects, and the worker who developed osteomalacia had additional evidence of a distal tubular defect. The five survivors also have evidence of slowly progressive deterioration in glomerular function.Follow-up of this small group has shown that renal tubular dysfunction in cadmium workers may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may develop after a number of years.
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PMID:Renal tubular dysfunction and abnormalities of calcium metabolism in cadmium workers. 48 32

The safety and effectiveness of sodium cellulose phosphate (SCP) in the treatment of calcium urolithiasis of absorptive hypercalciuria was explored. Eighteen patients with absorptive hypercalciuria with intestinal hyperabsorption of calcium, normal or suppressed parathyroid function, and active stone disease received 10 to 15 Gm SCP daily (2.5 to 5 Gm with meals) and 2 to 3 Gm magnesium gluconate daily (1 to 1.5 Gm twice daily orally separately from SCP) for eight to 54 months, while maintained on a moderate calcium and oxalate restriction. During treatment, serum calcium, immunoreactive parathyroid hormone, and urinary cyclic AMP remained within the normal range. Serum alkaline phosphatase and bone density (measured by photon absorptiometry) did not change significantly or remained within normal limits. Serum concentrations of magnesium, copper, zinc, and iron and blood hematocrit were not significantly altered by therapy. However, urinary calcium returned toward normal, and incidence of renal stone formation markedly decreased. The results suggest that SCP is a safe and an effective drug for absorptive hypercalciuria.
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PMID:Clinical pharmacology of sodium cellulose phosphate. 48 64

Administration of gallium nitrate to rats resulted in the formation of renal precipitates which occluded tubular lumina. When analyzed with a combination of scanning electron microscopy and x-ray energy spectrometry, these precipitates were found to contain gallium complexed with calcium and phosphate. Injection of gallium nitrate also resulted in hypercalciuria, although serum calcium levels remained unaltered. Administration of an osmotic diuretic, isosorbide, prior to gallium treatment resulted in the formation of fewer renal precipitates and histopathologic changes than in the nondiuresed animals. Diuresis did not alter gallium serum pharmacokinetics, the 24 hour cumulative renal excretion of gallium or the extent of the drug-induced hypercalciuria. However, isosorbide pretreatment significantly reduced the urinary concentrations of both gallium and calcium. The data presented indicate that diuresis reduces the severity of gallium-induced renal lithiasis and subsequent renal accumulation of gallium by diluting the urinary concentration of gallium and calcium thereby lowering the incidence of interaction of these two elements within the kidney tubule.
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PMID:Gallium nitrate (NSC-15200) induced toxicity in the rat: a pharmacologic, histopathologic and microanalytical investigation. 49 44

The handling of an acute oral calcium load in 22 men with recurrent calcium stone disease was studied before and after diuretic therapy. As a group, the patients had marginal hypercalciuria (150 mg calcium per gram of creatinine in a 24-hr urine collection). Metolazone, a diuretic with an action in the cortical thick ascending limb of Henle's loop, was given in oral daily doses of 5.0 mg for periods of 9 to 34 mo. An oral calcium load induced a rapid rise in urine calcium exeretion, which was blunted markedly by metolazone. Further analysis of the subjects revealed that one group (11 subjects) had higher baseline 24-hr calcium excretion levels and higher parathyroid hormone (PTH) than the others. The effect of metolazone in reducing the calciuric response was significant only in this group. Thus, while long-term treatment with metolazone inhibited the rise in urinary calcium excretion elicited by an oral calcium load, the effect was significant only in patients who had high baseline urinary calcium and PTH values. The reduction in calcium excretion in response to an acute calcium challenge may explain in part the beneficial effects of cortical diluting segment diuretics in recurrent stone formers.
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PMID:Changes in calcium excretion after prolonged metolazone therapy in recurrent stone formers. 49 17

Two siblings from a consanguineous family, suffering from nephrocalcinosis and nephrolithiasis caused by idiopathic hypercalciuria are described. The condition is associated with bilateral macular colobomata and tapeto-retinal degeneration. It is known that the latter can occur together with different nephropathies; however, until now it has never been described in combination with idiopathic hypercalciuria. Blood calcium levels were found to be normal, calcium excretion rates were, with one exception, more than 6 mg/kg/24 h corrected for 100 ml GFR. Hypomagnesemia of 1.5 and 1.2 mg/dl and hyermagnesuria of 1.9 and 2.5 mg/kg/24 h corrected for 100 ml GFR were found in both patients. Tubular phosphate reabsorption reached 87% and 84% at serum parathormone levels of 0.34 microgram/l and 0.31 microgram/l in the two patients, respectively. Under calcium and magnesium loading the clearance rates of calcium and magnesium were raised whilst there was only a small insignificant increase in the blood levels of these cations. Acid-base titrations showed normal excretion rates of acid and base in one patient and a mild proximal tubular acidosis in the other. Quantitative investigation of the renal concentrating and diluting capacity established a decrease in the formation of the medullary concentrating gradient in both patients.
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PMID:Idiopathic hypercalciuria with bilateral macular colobomata: a new variant of oculo-renal syndrome. 50 Mar 85

Increased calcium (Ca) excretion is characteristic of chronic phosphate (PO(4)) depletion (PD). To study the changes in tubular transport and the site of the hypocalciuric effect of PO(4) administration, clearance and micropuncture experiments were performed in intact rats pair fed either a control diet (0.5% PO(4)) or a PO(4)-depleted (PD) diet (0.01% PO(4)) plus Al(OH(3)) and in parathyroidectomized (PTX) PD rats, infused either with saline or with neutral sodium PO(4). Intact PD rats, compared with intact rats on a control diet, exhibited a lower plasma ultrafiltrable (UF) PO(4) (5.8+/-0.5 vs. 7.8+/-0.3 mg/dl), higher fractional excretion (FE) of Ca (4.1+/-1.2 vs. 0.6+/-0.1%), and reduced FE PO(4) (0.1+/-0.01 vs. 10.2+/-1.8%). Tubular fluid/plasma inulin was lower in the late proximal tubule of PD rats, associated with increases in fractional delivery (FD) from the proximal tubule of Na and Ca.The%FD of Ca to the early distal tubule of PD rats was increased (20+/-3 vs. 11+/-2%), but this difference was abolished by the late distal tubule (5.1+/-1.2 vs. 3.3+/-0.9%). In PTX-PD rats, PO(4) infusion increased plasma UF PO(4) (13.8+/-0.7 vs. 7.8+/-0.7 mg/dl). FE of Ca was reduced (1.08+/-0.35 vs. 4.59+/-1.57%) without correcting the increased Ca delivery to the late distal tubule. These data indicate that PD impairs Ca reabsorption in tubular segments before but not within the distal convoluted tubule, so that hypercalciuria is ultimately a result of decreased Ca transport either in the terminal nephron or in deeper nephrons where PO(4) infusion stimulates Ca transport independent of parathyroid hormone or changes in the filtered load of Ca.
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PMID:Renal tubular sites of altered calcium transport in phosphate-depleted rats. 50 Aug 33

A patient with incomplete distal renal tubular acidosis (RTA) demonstrated hypercalciuria, potassium wasting and hyperreninemia. Indomethacin administration resulted in sustained improvement of these abnormalities. The results suggest that overproduction of prostaglandins contributes to hypercalciuria, potassium wasting and hyperreninemia in some patients with RTA and that indomethacin may be useful in treating patients with this disorder.
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PMID:Improvement of hypercalciuria, potassium wasting and hyperreninemia in incomplete distal renal tubular acidosis by indomethacin. 50 64

A study of normal subjects and patients with hypercalciuria and recurrent renal stones has identified three main types of hypercalciuria: complex, absorptive and renal. Complex hypercalciuria is a combination of absorption, renal leak and resorption factors. Absorption and renal leak were examined by means of a 45Ca test. Resorption is defined as an increase of the urinary calcium:creatinine ratio while the subjects are being maintained on an intake of 400 mg of calcium per 24 h.
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PMID:Different types of hypercalciuria in patients with renal lithiasis and evidence of the calcium renal waste. 50 71

Primary hyperparathyroidism is a major cause of calcium urolithiasis and is easily recognised when it is classically manifested. However, subtle presentations of primary hyperparathyroidism may cause confusion with other causes of calcium stone disease or cause diagnostic difficulty. Several pitfalls of parathyroid evaluation and treatment are illustrated by four cases of calcium urolithiasis. Cases 1 and 2 represent ineffective or useless parathyroid surgery rendered for renal hypercalciuria and absorptive hypercalciuria, respectively. Cases 3 and 4 had mild or intermittent hypercalcaemia. The correct diagnosis of primary hyperparathyroidism was made in Case 3 by parathyroid venous sampling and bone densitometry. In Case 4, the thiazide provocative test was used to establish the diagnosis of primary hyperparathyroidism.
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PMID:Pitfalls in parathyroid evaluation in patients with calcium urolithiasis. 50 80

A persistent hypercalciuria and normal serum levels of calcium were measured in a 5-year-old boy suffering from recurrent macro- and microhaematuria and bilateral nephrolithiasis (stone analysis was positive for calcium-oxalate). No growth retardation or any other relevant clinical parameters concerning hypercalciuria e.g. vitamin D-intoxication or renal tubular acidosis could be observed. A slight secondary hyperparathyroidism and increased calcium excretion during fasting or calcium depleted diet indicates a primary failure of calcium reabsorption as previously described by Bordier (hypercalciuria type 2). Treatment with a combination of hydrochlorothiazide (Esidrix) and sodium chloride depleted diet resulted in a long-lasting normalization of calcium excretion and thus disappearance of symptoms in the child.
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PMID:[Idiopathic hypercalciuria due to primary decrease in the renal tubular reabsorption of calcium. Hypercalciuria type 2 according to Bordier (author's transl)]. 51 92


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