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

13 patients presenting with immobilization stones are reported. Young males with an infection of the urinary tract are most commonly affected. In the case of phosphate stones, the infection of the urinary tract with an alkaline shift of the pH and an idiopathic hyperuricosuria play a decisive part together with temporary hyperphosphaturia and hypercalciuria. The importance of urea splitting bacteria in the urine for stone formation is stressed. Applied in time increase of fluid intake, specific antibiotics and allopurinol can lead to litholysis. If the urine of immobilized patients were monitored closely from the beginning of the hospitalisation for the above factors, and treated appropriately, urine calculi should be largely prevented.
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PMID:Renal calculus dissolution in immobilized patients. 73 1

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.
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PMID:[Physiopathology, exploration and treatment of calcium lithiasis]. 178 95

To elucidate the pathophysiology of dietary calcium independent hypercalciuria, 42 calcium stone formers (Ca SF) were selected because they had on free diet a calciuria greater than 0.1 mmol/kg/day. For four days they were put on a diet restricted in calcium (Ca RD) by exclusion of the dairy products. They collected 24 hour urines on free diet and on day 4 of Ca RD as well as the two-hour fasting urines on the morning of the day 5 and the four-hour urines passed after an oral calcium load of 1 g, for measurement of creatinine, Ca, PO4, urea and total hydroxyprolinuria (THP). On day 5 fasting plasma concentrations of Ca, PO4, intact PTH, Gla protein, calcidiol and calcitriol were measured. The patients were firstly classified into dietary hypercalciuria (DH, 18 patients) and dietary calcium-independent hypercalciuria (IH, 24 patients) on the basis of the disappearance or not of hypercalciuria on Ca RD. Then the patients with IH were subclassified into absorptive hypercalciuria (AH) because of normal fasting calciuria (8 patients) and into fasting hypercalciuria (16 patients). Fasting hypercalciuric patients were subsequently divided according to the PTH levels into renal hypercalciuria (RH, 1 patient) with elevated fasting PTH becoming normal after the Ca load and undetermined hypercalciuria (UH, 15 patients) with normal PTH levels. Furthermore, their vertebral mineral density (VMD) was measured by quantitative computerized tomography which was normal in DH (91 +/- 6% of the normal mean for age and sex) but was decreased in IH to 69 +/- 4%. No difference in VMD was observed between AH and UH. Urinary excretions of urea, phosphate and THP was higher in IH than in DH and comparable in AH and UH. Sodium excretion Ca RD was the same in all groups and subgroups as well as the plasma parameters. Plasma calcitriol was increased in IH and DH comparatively to normal in spite of normal plasma calcidiol. Calciuria increase after oral calcium load, an index of Ca absorption, was higher in IH than in controls and comparable in IH and DH as well as in the three subgroups of IH. From these data and correlation studies in IH it is concluded: (1.) VMD is decreased in Ca stone formers with IH but not in those with DH, making the distinction of these two groups of hypercalciuria patients clinically relevant.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, vitamin D and vertebral mineral density in hypercalciuric calcium stone formers. 189 73

With the development of extracorporeal shock wave lithotripsy treatment, the duration of hospitalization for stone patients fortunately has become shorter. However, a detailed analysis of lithogenesis is not possible during such patients' short hospital stays. We prepared a standard diet to be eaten at home for investigation of lithogenesis at the out-patient clinic. This diet was nutritionally well-balanced and contained the following: energy: 2000 Kcal, total protein: 70-75 g, animal protein: 30-35 g, carbohydrate: 510 g, fat and oil: 50-60 g, calcium: 600-630 mg and magnesium: 320 mg. The urine of 24 male patients with stones on a free diet and the same patients after 3 days on the standard diet was analyzed for urea-nitrogen, uric acid, sodium, calcium, phosphorus, magnesium, citric acid and oxalic acid. The results were compared with those in 17 healthy male subjects who were eating the standard diet (controls). It was found that 66% of hypercalciuria (greater than = 300 mg/day) on a free diet became normocalciuria on the standard diet. The hypercalciuria was therefore thought to be of dietary origin. Moreover, urinary excretion of urea nitrogen, uric acid, sodium and phosphorus by patients remarkably decreased after 3 days on the standard diet, which was not different from that of controls. These results suggest that the standard diet at home is useful in the screening of hypercalciuria and also quite adequate for patients with stones.
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PMID:[Preparation of a standard diet for out-patients in the study of lithogenesis]. 207 1

Experience in the diagnosis and treatment of the renal form of primary hyperparathyroidism in 57 patients with bilateral nephrolithiasis was summed up. The main diagnostic criterion was the detection of biochemical changes in the blood and urine (hypercalcemia, hypophosphatemia, hypercalciuria) and the use of some tests (Howard's test and parathyroidin test). Parathyroidectomy was performed after establishing diagnosis. A new stage in therapy of such patients was a study of renal function and phosphocalcium metabolism after parathyroidectomy. The improvement of some indices (an increase in glomerular filtration, urea excretion with urine and relative urine density, and a decrease in hypercalciuria and hyperphosphaturia) indicated the effectiveness of surgical intervention for primary hyperparathyroidism in patients with bilateral nephrolithiasis. It was also confirmed by a decrease in lithogenic relapse after parathyroidectomy.
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PMID:[Primary hyperparathyroidism in patients with bilateral nephrolithiasis]. 258 27

In the Federal Republic of Germany the average daily protein intake exceeds the Recommended Dietary Allowances for adults (0.8 g protein/kg body weight) by about 100%. On the other hand calcium intake is below the recommendations for certain age groups. Protein-induced hypercalciuria involves the risk of depletion of skeletal calcium stores, especially for older people who have a decreased absorption capacity for calcium. As a result of our study we postulate, that an altered renal function probably is one inducing factor of hypercalciuria. While urea excretion and serum urea concentration increased with an elevated dietary protein content from 13 to 26 or 40 J%, glomerular filtration rate remained unchanged. Fractional tubular reabsorption of calcium was significantly reduced by about 3% with increased endogenous acid production and renal excretion of hydrogen ions (first part of the study), which were accompanying a higher protein intake of 40 J% compared to 13 J% protein in the control group. Increasing the phosphorus content of the diet improved the reabsorption of calcium and magnesium. The kidneys of rats fed diets high in protein and phosphorus were hypertrophied. Histology of the kidneys showed signs of glomerulonephrosis. While the calcium content of the femora was slightly reduced with a higher protein intake of 40 compared to 13 J%, the magnesium content was increased (after 61 weeks: calcium from 261.4 to 257.1 mg/g dry fat-free wt [p less than or equal to 0.05]; magnesium from 3.2 to 3.5 mg/g dry fat-free wt [p less than or equal to 0.001]). Calcium and magnesium metabolism depends not only on the level of protein intake, but also on its interrelation with the dietary phosphorus content. With continuous high protein intake higher intakes for calcium, phosphorus and magnesium should be recommended, especially for older people.
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PMID:[The effect of long-term increased protein administration on mineral metabolism and kidney function in the rat. II. Kidney function and bone mineralization]. 323 6

Kidney stones have an overall incidence of two to three percent in western countries. In many patients, the disease process is difficult to control and recurrence rates are high: 20 to 50 percent over the subsequent ten years. The pathogenesis and standard methods of treatment for the five major types of stones (i.e., calcium oxalate, struvite, calcium phosphate, uric acid, and cystine) are reviewed. Three new drugs are reviewed in the context of their roles in the selective treatment of kidney stones. Cellulose sodium phosphate (Calcibind) is a nonabsorbable ion-exchange resin with a limited indication for the treatment of calcium stones associated with absorptive hypercalciuria Type I. Acetohydroxamic acid (Lithostat) is an urease-inhibitor that is indicated as adjunctive therapy in patients with chronic urea-splitting urinary tract infections and struvite stones. Potassium citrate (Urocit) is an investigational agent that has clinical efficacy in patients with calcium oxalate and calcium phosphate stones who are hypocitraturic. In addition, potassium citrate is an alkalinizing agent that can be used in patients with uric acid stones.
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PMID:New drug therapy for kidney stones: a review of cellulose sodium phosphate, acetohydroxamic acid, and potassium citrate. 389 14

In order to better understand the role of diet in etiology of urolithiasis, 84 oxalo-phospho-calcic-lithiasic patients (52 men, 32 women) have been studied by a nutritional week-interview and by urinary and blood testing. Diet data were compared to an ideal standard. Total caloric intake was 2428 +/- 651 calories/d; this intake is high in 7% women and 40% men. 79% out of patients are fat. Protidic intake is 87 +/- 21 g/d higher than 1 g/kg/d in 84.5% of patients. Lipids are high in 38.9 +/- 7%, glucid are low in 45.3 +/- 7%. Calcium intake is 934 +/- 406 mg/d, sodium intake is 12.9 + 3 g/d. Water intake is 2305 +/- 759 ml/d. Different groups of patients are studied: a) 21 patients with mean age of 43 +/- 12 years have recurrent lithiasis (R). This group is compared to 48 patients with 37 +/- 44 years who have a single lithiasis. Half of (R) patients have hypercalciuria, hyperphosphaturia and hyperoxaluria. Diet study is no different between these two groups. b) Other groups are studied: 21 have hyperophosphaturia (HPU) without hypophosphoremia and they have hypercalciuria, hyperuraturia and high urinary urea; diet shows higher glucicid and potassium intake than group with normal phosphaturia; 23 have hypercalciuria (HCU) and high uraturia and phosphaturia: diet study shows no difference with a group with normal calciuria. 21 have hyperoxaluria (HOU): diet study of a normal oxaluric group shows higher lipid intake, lower glucidic and calcium intake; 22 have hyperuraturia (HAU) and higher urinary urea, sodium and potassium than normouraturia group: in this group potassium intake is higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of dietary evaluation during calcium oxalate and calcium phosphate lithiasis]. 814 88

Hypercalciuria has long been considered a common abnormality in stone formers, and familial predisposition to renal stone formation has also been reported. Renal stone formers, their spouses and first-degree blood relatives (the latter two groups of subjects had no previous or present history of stone disease) were investigated for their response to an oral load of 2 g calcium (as di-calcium phosphate). Serum calcium, phosphorus, uric acid, creatinine and urea were within the normal range in all the subjects initially as well as 4 h after the load. After the oral calcium load, 66.6% of the stone formers, 25% of the first-degree relatives and none of the spouses were hypercalciuric. Administration of 2 g calcium produced a significantly greater urinary excretion of calcium in stone formers (123.8 +/- 43 mg/8 h, p < 0.001) and their first-degree blood relatives (89.8 +/- 26 mg/8 h, p < 0.01) as compared to the spouses of stone formers (65.5 +/- 12.8 mg/8 h). A significant increase in urinary calcium excretion after calcium loading was also found among the stone formers (p < 0.01) as compared to their first-degree blood relatives. A significantly higher mean rise in calcium excretion (over the basal excretion) in calcium stone formers (p < 0.001) and their first-degree blood relatives (p < 0.01), as compared to the spouses of stone formers suggests a greater predisposition to renal stone disease in first-degree blood relatives than the spouses of the stone patients.
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PMID:Study of urinary calcium excretion after oral calcium load in stone formers, their spouses and first-degree blood relatives. 817 84

A high prevalence of hypercalciuria has been reported in patients with essential hypertension. Nevertheless, the clinical and therapeutic implications of this finding have scarcely been studied. This study was designed to determine the prevalence of hypercalciuria in an unselected population with essential hypertension and to analyze the relationship between the urinary calcium and the clinical and therapeutic status of these patients. This article presents a prospective study of 112 patients with essential hypertension and 49 healthy normotensive control subjects. Urinary excretion rates of calcium, sodium, chloride, potassium, urinary calcium/creatinine index, the fractional excretion of sodium, potassium and uric acid, the creatinine clearance and serum values of creatinine, urea, uric acid, electrolytes, total proteins, parathormone (intact molecule), plasma renin activity, aldosterone, glucose, and insulin (fasting and after an oral glucose load) were performed in every patient and control subject. Untreated hypertensive patients had a higher prevalence of hypercalciuria (35% had a urinary calcium/creatinine ratio > 0.20 versus 20% of treated hypertensives and 2% of control subjects; P < 0.001). Patients on thiazide or beta-blocker monotherapy had lower urinary excretion rates of calcium and urate than patients on calcium-antagonist monotherapy or untreated patients. Urinary calcium, sodium, and urate correlated positively both in treated and untreated essential hypertension patients. Patients with the higher urinary calcium levels also had higher excretion rates of sodium and urate, higher creatinine clearance rates, and lower serum creatinine and serum uric acid levels. It was concluded that hypercalciuria is a frequent finding of untreated essential hypertension. The association of high urinary calcium levels with high urinary urate excretion rates in the same patient may predispose to development of lithiasis in patients with essential hypertension. Antihypertensive drugs have a variable effect on calciuria-uricosuria, which may constitute an additional criterion in the selection and individualization of therapy. Thiazides and beta-blockers can decrease calciuria and uricosuria and, therefore, the lithogenic risk in these patients.
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PMID:Urinary calcium excretion in treated and untreated essential hypertension. 882 22


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