Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cadmium is an inessential trace metal which accumulates in human tissues from contamination of food, water or air. The kidney is the critical organ following long-term, low-level absorption either by inhalation or ingestion; accumulation occurring in tubular epithelium in the form of a cadmium-metallothionein complex, giving rise to tubular dysfunction. In a group of 12 cadmium workers some of whom were followed for up to 16 years, tubular proteinuria, renal glycosuria, aminoaciduria, hypercalciuria and defects of concentration and acidification have been observed. Two men became recurrent renal stone formers and 1 man, who had nephrocalcinosis when first seen, later developed vitamin D-resistant osteomalacia. Renal tubular dysfunction following cadmium exposure may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may eventually develop.
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PMID:Cadmium nephropathy. 22 11

FActors predisposing to renal stone formation have been studied in 309 patients. Dehydration before diagnosis of urolithiasis was due in 12% of the cases to frequent diarrhea and in 36% to bad working conditions. Daily fluid intake was less than 1 liter in 25% of the patients before stone formation and was persistently low in 11% after stone discovery. 41% of the patients drank irregularly over the day, before stone formation, and 11% continued to do so after its detection. Immobilization was present in the patient's history in over 20% of the cases. Normocalcemic hypercalciuria was found in 26% of the patients. 24% of the patients drank water with a calcium concentration of 100--500 mg/l before the lithiasis was diagnosed; 21% continued to do so after stone discovery or paradoxically even drank harder water than before stone detection.
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PMID:High fluid-low calcium intake: not all renal stone formers adhere to this simple treatment. 42 10

Eighty-eight urinary tract stone formers (74 men) with idiopathic hypercalciuria were treated by dietary calcium restriction alone. Short-term control of hypercalciuria was achieved in only 27 patients and all but 12 eventually escaped control. Failure of control was twice as likely in patients with severe hypercalciuria. Almost all patients lived in a hard water area. In such areas at least, attempts to control hypercalciuria by diet alone are likely to fail and early introduction of additional treatment is advisable. In most severe hypercalciurics, such treatment should be introduced from the start.
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PMID:Dietary treatment of idiopathic hypercalciuria. 46 84

Hypercalcaemia would seem to be rare during immobilisation, whilst osteoporosis and hypercalciuria are constant. In fact, it often goes unnoticed. The case presented here confirms its predominance in the adolescent male. The reason for immobilisation seems to be irrelevant. The clinical symptoms are very variable: polydipsia, nausea, headache, apathy, anorexia. Blood calcium levels are raised, up to 14 mg%. This hypercalcaemia is due to very marked bone loss in adolescents, secondary to hyper-resorption and a temporary stoppage in osseous formation. The differential diagnosis from primary hyperparathyroidism is sometimes difficult but is aided by laboratory and histological findings. The essential is to consider the possibility of immobilisation hypercalcaemia in the presence of any suggestive symptoms in an immobilised adolescent. Treatment includes a return to weight bearing, adequate water intake and the administration of phosphorus, calcitonin, furosemide, and corticosteroids.
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PMID:[Immobilisation hypercalcaemia (author's transl)]. 59 68

The effects of phosphate depletion on magnesium (Mg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell significantly (P < 0.01) from 10.1+/-0.27 (SE) to 5.0+/-0.54 mg/100 ml within 1 day and continued to fall gradually to a level of 1.2+/-0.21 mg/100 ml by the end of the 8th wk. A significant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46+/-2.7 to 126+/-24 mueq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300+/-24 mueq/24 h by the 3rd day and remained high ranging between 150-300 mueq/24 h, thereafter. The magnitude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2+/-0.02 to 0.79+/-0.10 meq/liter by the 1st day of the study and remained low throughout.Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which became evident by the 3rd wk of phosphate depletion. Mg content of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral content because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 mueq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or weight of the animals. Our results indicate that phosphate depletion is associated with (a) magnesuria due to a decrease in the net renal tubular reabsorption of Mg with the main source of the urinary losses being bone Mg; (b) hypomagnesemia secondary to the renal leak of Mg; (c) negative Mg balance; and (d) increase in the intestinal fractional absorption of Mg. The latter was not adequate to compensate for the urinary losses of Mg.
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PMID:Effect of phosphate depletion on magnesium homeostasis in rats. 64 Nov 38

The effects of chronic phosphate depletion on renal tubular function were evaluated by micropuncture and free water clearance studies in the dog. Proximal tubular punctures demonstrated that chronic hypophosphatemia led to a reduction in ratio of tubular fluid to plasma inulin in late superficial tubular from 1.59+/-0.08 in control animals to 1.29+/-0.06 in phosphate-depleted dogs, with proportional inhibition of calcium and sodium reabsorption. The chronic decrease in proximal tubular fluid reabsorption was confirmed by the analysis of sustained water diuresis in conscious, phosphate-depleted dogs, before and after repletion of body PO4 stores, and in control animals. Urine flow rate/100 ml glomerular filtration rate (V/GFR) was significantly higher in PO4 DEPLETION THAN CONTROL (15.8+/-1.1 VS. 10.7+/-0.82). In addition, acetazolamide infusion did not increase V/GFR in phosphate-depleted dogs (15.8+/-1.1 vs. 17.16+/-0.9), supporting the conclusion that inhibition of proximal tubular fluid reabsorption was responsible for the elevated urine flow rate. PO4 repletion over 5 days reduced V/GFR to 9.2+/-0.7 despite no change in urine osmolality and no change in GFR, further suggesting a specific reversible alteration in proximal tubular reabsorption in phosphate depletion. Although hypercalciuria was a constant finding in phosphate depletion (fractional excretion of calcium of 2.04+/-0.4% vs. 0.47+/-0.13% in controls), the enhanced distal delivery of calcium was not a crucial factor; acute phosphate infusion reduced urinary calcium excretion to control values without affecting the reduced proximal tubular reabsorption in either intact or thyroparathyroidectomized phosphate-depleted dogs the change in distal nephron calcium reabsorption was independent of parathyroid hormone (PTH) levels since infusion of PTH failed to alter urinary calcium excretion. We conclude that chronic phosphate depletion leads to a reversible, sustained inhibition in proximal tubular reabsorptive fuction as well as a specific decrease in distal nephron calcium reabsorption. This latter reabsorptive defect is sensitive to phosplate infusion but not corrected by PTH.
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PMID:Renal tubular effects of chronic phosphate depletion. 85 68

Sham-operated and parathyroidectomized (PTX) rats were divided into two pair-fed groups, one on a normal mineral intake (0.5% Ca, 0.3% P), the other on a regimen low in phosphorus (0.5% Ca, 0.03% P). P depletion led to a drop in plasma P and urine P, a rise in plasma Ca and a marked rise in urine Ca, a drop in serum magnesium and a rise in urine Mg. The changes were more pronounced in the PTX animals, but final values were the same in both groups. Parallel bone-seeking isotope (85Sr, 177Lu, 237Np) studies in nonablated animals revealed an increase in the urinary nuclide output and in the urine/tibia ratio in P-deficient animals. Normal and primary bone osteocytes decreased and enlarged osteocytes increased as a result of P deficiency; osteoclasts and osteoblasts also increased. Bone composition showed a drop in ash content and a rise in water, with a light decrease in both Ca and P, and a corresponding rise in hydroxyproline and nitrogen in the P-deficient animals. The results are interpreted to mean that P-deficiency in the young growing rat leads to an increase in bone resorption which occurs also in the absence of parathyroid hormone (PTH). The fact that final values were similar in the control and PTX P-deficient animals suggests that steady-state regulation can also occur without PTH. Because P-deficiency leads to rapid hypercalcemia and rapid marked hypercalciuria, there may exist a mechanism for phosphate regulation which would then supersede Ca homeostasis. The change in serum and urine Mg levels may reflect a decrease in tubular Ca and Mg reabsorption associated with P-deficiency.
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PMID:Phosphorus deficiency, parathyroid hormone and bone resorption in the growing rat. 95 82

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P less than 0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean +/- SEM) was 11.62 +/- 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 +/- 0.48 nmol/day in the control subjects (P = 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.
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PMID:Increased urinary excretion of prostaglandin E2 in patients with idiopathic hypercalciuria is a primary phenomenon. 132 25

The addition of sucrose to drinking water of rats at the rate of 2.5 or 5 grams per 100 ml, for one month, induced hypercalciuria which appeared to be dependent on the degree of supplementation. In spite of these disorders, calcium deposits were not observed in treated animals. This protection against renal calculi was probably due to high urinary excretions of magnesium, phosphorus, zinc and copper. These lithogenesis inhibitors varied, like oxaluria and calciuria, in parallel with dietary sucrose intake.
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PMID:[Is sucrose a risk factor in calculus formation?]. 174 29

We have studied urinary sodium and magnesium excretion in 30 normal subjects (15 women and 15 men, mean age 43 +/- 14 years, mean weight 74 +/- 18 Kg) and in 60 hypercalciuric stone-forming patients, 30 with renal hypercalciuria (HR) (15 women and 15 men, mean age 39 +/- 10 years, mean weight 71 +/- 16 Kg) and 30 with absorptive hypercalciuria (HA), (15 women and 15 men, mean age 41 +/- 13 years, mean weight 69 +/- 12 Kg). The diagnosis of hypercalciuria and the classification in HA and HR was made with our ambulatory study protocol. Hypercalciuria was defined by a daily calcium excretion above 300 mg (men) or 220 mg (women), and patients with fasting calcium to creatinine ratio, and calcium per 100 ml of glomerular filtrate average value above 0.11 were considered to have HR. Control subjects and hypercalciuric patients were maintained on a diet containing 1200 mg Ca, 800 mg P, 200 mg Mg and 100 mmol Na per day for a 7-day period. Two 24-hour urine samples were collected on days 6 and 7 of this diet. On the morning of day 8, following a 12-hour fast, 300 ml of distilled water was drunk and a 2-hour urine sample was collected. A blood sample was taken halfway this time. In all blood and urine samples, calcium, magnesium, sodium, phosphorus and creatinine were quantified. Creatinine clearance and calcium, sodium and magnesium per 100 ml of glomerular filtrate were calculated from these determinations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary excretion of sodium and magnesium in idiopathic hypercalciuria]. 182 17


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