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

Patients with hypercalciuria have been reported to have an exaggerated response to hydrochlorothiazide (HCTZ), implying a renal tubular defect in solute reabsorption. To determine whether this disturbance is generalized or unique to a particular pathogenetic type of hypercalciuria, we measured the increments in urinary sodium (delta Na), calcium (delta Ca), and magnesium after a 100-mg dose of oral HCTZ in 10 normal subjects and 31 patients with different types of hypercalciuric nephrolithiasis. Eleven patients with renal hypercalciuria had significantly greater delta Na (P less than 0.005) and delta Ca (P less than 0.005) than the normal subjects. Ten patients with absorptive hypercalciuria and 10 patients with fasting hypercalciuria without parathyroid stimulation had delta Na and delta Ca indistinguishable from those of normal subjects. In all groups, urinary HCTZ and basal 24-h urinary Na did not differ. The results suggest that the unique natriuretic and calciuric responses to HCTZ occur only in renal hypercalciuric patients with secondary hyperparathyroidism. The data support a renal tubular defect in renal hypercalciuric in contrast to other diagnostic categories of hypercalciuric nephrolithiasis.
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PMID:Exaggerated natriuretic and calciuric responses to hydrochlorothiazide in renal hypercalciuria but not in absorptive hypercalciuria. 404 75

A 26-year-old woman was admitted to the Institute of Endocrinology in Bucharest for evaluation of primary hyperparathyroidism (P-HPT). Anamnesis revealed a 10-year history of nephrolithiasis; peptic ulcer, chronic pancreatitis, cholelithiasis. Eight months previously, she had given birth to a child who had neonatal hypocalcaemic tetany. Investigations revealed the presence of moderate hypercalcaemia, hypercalciuria, hypo-phosphoremia; serum chloride level was above 100 mEq/1, and the chloride phosphate ratio was greater than 33. X-ray films of the abdomen revealed the presence of nephrolithiasis and right nephrocalcinosis. Selenium methyonine scanning, ultrasonography and computerized tomography were negative. On surgical exploration a 2-3 cm parathyroid adenoma was removed from between the trachea and the esophagus.
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PMID:Primary hyperparathyroidism. Report of a clinical case without bone lesions. 404 20

The frequency of renal tubular acidosis was evaluated in 28 adult patients with recurrent calcium nephrolithiasis (19 with 'renal' hypercalciuria, 9 with normocalciuria and no metabolic abnormality) and no evidence of obstruction or infection of the urinary tract. Eight patients with hypercalciuria (42%) had a defective renal reabsorption of bicarbonate, based on a fractional excretion of bicarbonate higher than 7% and a TmHCO3/GFR lower than 2.2 mEq/dl; 2 of them had an associated distal defect of acidification, as judged by a U-B pCO2 lower than 18 mm Hg in maximally alkaline urine. One patient with hypercalciuria had distal tubular acidosis, based on a urine pH higher than 5.3 during acidosis. Only 1 patient with normocalciuria had associated proximal and distal acidification defects. The remaining 8 patients displayed a normal renal acidifying capacity. The bicarbonate wastage was independent of serum PTH levels, vitamin D status and hypercalciuria and was associated with a defective tubular reabsorption of phosphate, increased random urinary pH and more active nephrolithiasis, with a prevalence of mixed calcium oxalate and phosphate stones. Our study shows a high incidence of defective tubular reabsorption of bicarbonate in patients with calcium nephrolithiasis and 'renal' hypercalciuria and suggests that the proximal acidification defect plays a pathogenetic role in promoting calcium nephrolithiasis.
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PMID:Renal acidification defects in patients with recurrent calcium nephrolithiasis. 406 1

Calcium phosphate metabolism was thoroughly investigated in twenty-four patients with calcium nephrolithiasis and hypercalciuria. Increased absorption was demonstrated in twelve cases. In two patients findings suggested normocalcemic hyperparathyroidism. Results were normal in the remaining ten cases. Metabolic investigations failed to noticeably improve the specificity of therapeutic indications over the conventional prevention by adequate fluid intake and an appropriate diet. Nevertheless continuing metabolic investigations are needed as they allow more accurate designing of studies on renal lithiasis.
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PMID:[Calcium stones: are current metabolic studies warranted in everyday practice?]. 408 38

The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+/-3.63 SD mumol/g creatinine; normal, 4.02+/-0.70 mumol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (Ca(A)), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by (125)I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their Ca(A) exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion of Ca and a suppression of cAMP excretion. The urinary Ca of 453+/-154 SD mg/day was significantly higher than the control group's 211+/-42 mg/day. The urinary cAMP of 2.26+/-0.56 mumol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hypercalciuria was corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since Ca(A) was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their Ca(A) exceeded urinary Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.
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PMID:The hypercalciurias. Causes, parathyroid functions, and diagnostic criteria. 436 91

Brushite (CaHPO(4).2H(2)O) was considered to govern the formation of renal calculus of calcium phosphate origin. The degree of saturation of urine with respect to this phase was therefore calculated. This value was obtained from the ratio of the activity product of Ca(++) and HPO(4) (m) (K(sp)) before and after incubation of urine with brushite. The errors in the calculation of K(sp) were largely eliminated by this procedure.The urine of patients with idiopathic hypercalciuria and recurrent calcium-containing renal calculi was supersaturated with respect to brushit largely because of the high urinary concentration of Ca(++). The urine of normocalciuric subjects was undersaturated except at high urinary pH. This technique of estimating the degree of saturation of urine should allow a quantitative assessment of the various therapeutic regimens recommended for patients with nephrolithiasis.
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PMID:Physicochemical basis for formation of renal stones of calcium phosphate origin: calculation of the degree of saturation of urine with respect to brushite. 582 95

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

Protected phosphate therapy was used in 65 cases of recurrent calcium nephrolithiasis. Mean duration treatment was 2 years and 1 month (more than 3 years in 17 cases). Mean lithiasis episodes by year-patients were 1,55 renal colics and 0.34 stone formation before phosphate treatment, versus 0.66 renal colics and 0.10 stone formation (more than 60% reduction), during treatment. There was simultaneously decrease of hypercalciuria (24 cases out of 42), of asthenia (16 cases out of 19), of signs of spasmophilia (12 cases out of 18) and disappearing of bone pains (4 cases out of 6). Side effects were rare. Minor digestive troubles were observed in 11 cases: diarrhea (3 cases) or gastralgias (9 cases). These side-effects necessitated discontinuation of thiazide therapy in only two cases and reduction of doses in 6 other cases. From our data, phosphate therapy appears an efficient drug in recurrent calcium nephrolithiasis. It acts in reducing levels of calciuria and enhancing urinary pyrophosphates excretion, inhibitors of calcium crystallization.
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PMID:[Calcium nephrolithiasis and phosphate therapy. Long term study (65 cases) (author's transl)]. 624 82

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.
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PMID:[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)]. 625 Jul 84

Patients with idiopathic recurrent calcium nephrolithiasis (n = 57) and controls (n = 16) were investigated regarding the relationship between renal phosphate handling, other renal tubular functions and calcium metabolism. Incomplete renal tubular acidosis (RTA) was disclosed in 13 patients. RTA patients together with stone formers with normal renal acidification capacity (SF) exhibited low values for serum phosphate and renal threshold phosphate concentration (TmP/GFR) compared with controls. TmP/GFR was lower in RTA patients than in stone formers with normal renal acidification. Hypercalciuria of the absorptive type with normal serum PTH and urinary cAMP concentrations was a common finding in both stone patient groups, whereas no patient displayed unequivocal evidence of parathyroid hyperfunction. Fractional excretion of sodium was raised in both SF and RTA patients compared with controls. There was a positive relationship between the fractional excretion of phosphate and sodium in all subjects as a group. TmP/GFR was negatively correlated to fractional excretion of sodium. Twenty-three percent of RTA patients and 8% of SF displayed tubular proteinuria which often was associated with low TmP/GFR levels and enhanced natriuresis. It is concluded that a defective renal tubular phosphate handling is common in calcium stone formers and often associated with signs of other tubular dysfunctions. The altered phosphate handling seems to be unrelated to hypercalciuria.
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PMID:Phosphate metabolism in renal stone formers. (II): Relation to renal tubular functions and calcium metabolism. 627 2


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