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

Dietary and drug treatments of calcium nephrolithiasis depend mainly on the mineral composition of renal stones: calcium oxalate, phosphate or mixed stones. The association with an hypercalciuria is an important factor which must be taken into account because oxalates and phosphates precipitate as calcium crystals in case of urinnary oversaturation. Despite many therapies have been proposed, their efficiency seems to be rather small when they are used alone. Usually, it is necessary to act on several factors with a combination of therapeutic methods. Absorptive hypercalciuria are improved with both low calcium diets and inhibitors of calcium absorption. In renal hypercalciuria, the treatment is based on the administration of thiazide diuretics which enhance calcium renal tubular reabsorption. The other therapeutic methods depend on the nature of renal stones: urinary acidification for calcium phosphate; administration of succinimide, oral phosphate or organic phosphonates for calcium oxalate stones; association with purine biosynthesis inhibitors in case of the presence of urates in renal calculi.
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PMID:[Dietary and drug treatments of calcium nephrolithiasis (author's transl)]. 3 18

Studies were performed on 12 patients with idiopathic hypercalciuria to evaluate the hypothesis that the acid load accompanying potassium acid phosphate would adversely affect renal calcium reabsorption and citrate excretion compared to the neutral form of the phosphate salt. During acute clearance studies, neutral phosphate (NP) led to a fall in FECa (2.2 +/- 0.6% to 0.8 +/- 0.1%, P less than 0.02) and no change in titratable acidity (TA) or net acid excretion (NAE). Acid phosphate (AP) did not reduce FECa acutely, and led to a rise in TA (22 +/- 4 to 62 +/- 6 muEq/min, P less than 0.02) and NAE (46 +/- 6 to 6 89 +/- 7 muEq/min, P less than 0.02). During chronic administration, AP resulted in higher urinary calcium excretion in both absorptive (187 +/- 29 vs. 141 +/- 18 mg/day, P less than 0.02) and renal hypercalciuric patients (233 +/- 24 vs. 173 +/- 190.02 mg/day, P less than 0.02). Also, TA and NAE were higher following AP, whereas citrate excretion was lower (375.4 +/- 64.6 vs. 633.4 +/- 28.8 mg/day, P less than 0.01). These data suggest that the reported ineffectiveness of AP in the therapy of nephrolithiasis may be related to the deleterious effects of the acid load on calcium and citrate metabolism.
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PMID:Differing effects of acid versus neutral phosphate therapy of hypercalciuria. 4 88

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69

States of hypersecretion of PTH may occur primarily, or in response to other physiologic abnormalities. Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease. The clinical manifestations of this disease have become more subtle with improved detection. The serum calcium level is almost always elevated, and when it it accompanied by relatively high serum PTH levels or increased urinary cAMP excretion, the diagnosis is usually secure. Findings of hypophosphatemia, decreased renal tubular reabsorption of phosphorus, hypercalciuria, and characteristic roentgenographic changes support the diagnosis of hyperparathyroidism, but are not prerequisites for that diagnosis. Most cases will come to operation, and experienced intraoperative assessment is necessary for the correct distinction between multiglandular disease and that involving only a single gland. We expect that a clearer understanding of the histopathologic features of these diseases, and improvement in the methods for measurement of PTH will be the main areas of advancement in the diagnosis of hyperparathyroidism in the next few years.
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PMID:Diagnosis of hyperparathyroidism. 19 30

Twenty-one unselected patients with recurrent nephrolithiasis and normocalcemic hypercalciuria with or without hypophosphatemia and 18 normal subjects were studied with an oral calcium tolerance test and for 3- to 5-day periods while consuming a low normal (400 mg) and high-normal (1000 mg) calcium intake. The oral calcium tolerance test consisted of the measurement of the calcemic, calciuric, and parathyroid (assessed by determinations of serum immunoreactive parathyroid hormone and nephrogenous cAMP) responses to acute 1000- or 350-mg doses of calcium. Nineteen patients displayed normal results for basal serum calcium, parathyroid function, and fasting calcium excretion, and striking calcemic (mean increase in serum calcium, 0.9 vs. 0.2 mg/dl in the normal subjects) and calciuric (mean increase in urinary calcium, 0.33 vs. 0.15 mg calcium/100 ml GF in the normal subjects) responses to the 1000-mg calcium tolerance test, associated with a mean 54% suppression in nephrogenous cAMP. These patients were operationally defined as having "absorptive" hypercalciuria. The variable occurrence of hypophosphatemia in this group suggested that the pathogenesis of "absorptive" hypercalciuria may be complex and/or multifactorial. There were strong positive correlations between the calciuric response to the calcium tolerance test and fractional isotopic calcium absorption (r = 0.75, P less than 0.00), the calcemic responses to the test (r = 0.71, P less than 0.001) and the calciuric responses noted on the 1000- vs. the 400-mg daily calcium intake (r = 0.78, P less than 0.001). Two patients displayed low or low normal basal serum calcium, increased parathyroid function, increased fasting calcium excretion, and a striking calciuric but minimal calcemic response to the 1000-mg calcium tolerance test, associated with a moderate suppression in nephrogenous cAMP. These patients were operationally defined as having "renal" hypercalciuria. Several lines of evidence indicated that the hyperparathyroidism in these patients was physiological or secondary, including the near normalization of parathyroid function on the daily 1000-mg calcium intake. A steep slope of calcium excretion on calcium intake (due to increased calcium absorption) was noted in all hypercalciuric patients and accounted for the significantly improved diagnostic accuracy of screening patients for hypercalciuria on the high-normal calcium intake. The simple measurement of total cAMP excretion (nanomoles per 100 ml GF) and urinary calcium on the 1000-mg daily calcium intake seemed to provide reliable separation of patients with "renal" from those with "absorptive" hypercalciuria. A physiological (350 mg) dose of oral calcium produced a 30% suppression of nephrogenous cAMP in normal subjects; this suggests that dietary calcium exerts an important control of parathyroid function under physiological circumstances.
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PMID:Pathophysiological studies in idiopathic hypercalciuria: use of an oral calcium tolerance test to characterize distinctive hypercalciuric subgroups. 23 82

Urinary saturation with respect to calcium oxalate monohydrate was measured in 111 consecutive patients with calcium nephrolithiasis. Each patient also was evaluated by a detailed conventional metabolic protocol. Patients with idiopathic hypercalciuria produced abnormally oversaturated urine more frequently than normal subjects and normocalciuric patients, but normocalciuric patients had unexpectedly high levels of urine saturation. Measuring levels of calcium concentration, oxalate concentration, or the chemical concentration product of calcium and oxalate in urine did not predict oversaturation. During thiazide treatment, saturation level tended to fall if it was initially elevated, whether the patient was hypercalciuric or not. Patients whose urine was not remarkably oversaturated showed no tendency to elaborate even less saturated urine during thiazide treatment; instead, the average calcium oxalate saturation level remained constant. Direct urine saturation measurements can detect a small but significant number of normocalciuric patients who have marked oversaturation with respect to calcium oxalate and appear to benefit from treatment.
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PMID:Urinary saturation measurements in calcium nephrolithiasis. 44 49

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

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

Three patients with nephrolithiasis were found to have both medullary sponge kidney (MSK) and primary hyperparathyroidism. In all cases, urine calcium excretion returned to normal after parathyroidectomy. The passage of stones was abolished for more than 20 years in one case and for more than 12 years in another. The available data suggest that many patients with MSK are asymptomatic and that the risk of stone formation is increased by an associated metabolic abnormality such as hypercalciuria or hyperparathyroidism.
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PMID:Primary hyperparathyroidism. A cause of hypercalciuria and renal stones in patients with medullary sponge kidney. 57 83

In the group of 1635 patients with nephorolithiasis the authors found 16% with idiopathic hypercalciuria. They administered thiazide diuretics for 8 days as a test for the detection of masked hyperparathyroidism in idiopathic hypercalciuria. In 6 cases which were diagnosed in this manner, the existence of a parathyroidadenoma could be demonstrated by surgical operation. The hypercalciuria persisted after exstirpation of the tumor, in some cases the nephrolithiasis also remained active. the various pathogenetic mechanisms connected with these common diseases are discussed in relation to these results.
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PMID:[Nephrolithiasis in hypercalciuria and hyperparathyroidism]. 81 7


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