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

To evaluate the cause of hypercalciuria, we carried out the oral calcium tolerance test before and after parathyroidectomy in a patient with primary hyperparathyroidism who had recurrent and multiple nephrolithiasis. Preoperative laboratory examination showed hypercalcemia, hypophosphetamia, hypercalciuria, decrease in % tubular reabsorption of phosphorus and strikingly elevated urinary cyclic AMP excretion. The oral calcium tolerance test indicated a significantly greater increase in serum calcium (delta serum calcium: 1.4 mg/dl vs 0.8 mg/dl) and a significantly greater suppression of urinary cyclic AMP excretion (delta U-cyclic AMP:-3.56 moles/gCre vs-1.17 moles/gCre) before parathyroidectomy than after. These results showed that hypercalciuria in this case was induced not only by the significant increase in the filtrated load of calcium but by the reduction in the resorption of calcium in the distal tubule caused by the significantly suppressed parathyroid hormone effect.
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PMID:[A case report: primary hyperparathyroidism--comparison before and after parathyroidectomy by oral calcium tolerance test]. 283 26

116 normocalcemic and 8 primary hyperparathyroid (PHPT) patients with calcium (Ca) nephrolithiasis and 10 normal controls underwent 1 g of oral Ca tolerance test following 4 days of Ca restricted diet (400 mg/day). On the basis of urinary Ca/creatinine (Cr) ratio obtained by the test, the 116 patients with normocalcemic nephrolithiasis were divided into 3 groups (normocalciuric nephrolithiasis; NN, absorptive hypercalciuria; AH, renal hypercalciuria; RH) according to our criteria which were slightly modified from Pak et al. Changes in urinary Ca/Cr ratio, and those in serum Ca and phosphorus (P), tubular maximum reabsorption of phosphate/glomerular filtration rate (TmPO4/GFR), nephrogenous adenosine 3',5'-monophosphate (NcAMP) and plasma immunoreactive parathyroid hormone (iPTH) were determined. As a result, the 116 patients were divided into 82NN, 13AH and 21RH. In general, a rise in serum Ca and fall in NcAMP were seen first, followed by rises in urinary Ca/Cr ratio, serum P and TmPO4/GFR although the changes were small. The group PHPT showed abnormality in the changes of TmPO4/GFR, NcAMP and plasma iPTH. The former one decreased constantly during the test and the latter two did not fall to within the normal range, suggesting parathyroid autonomy or abnormal suppressibility. Regarding the normal controls, all the changes were smallest among the 5 groups and clear parathyroid suppression was not observed while it was seen in the groups NN, AH and RH. In conclusion, oral Ca tolerance test is useful not only to separate NN, AH and RH, but also for the diagnosis of PHPT by demonstrating parathyroid autonomy or abnormal suppressibility assessed by NcAMP and/or TmPO4/GFR.
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PMID:Biochemical changes before and during oral calcium tolerance test in calcium stone formers. 284 10

To investigate whether overall tubular dysfunction is encountered in a particular subgroup of patients with urolithiasis, the following parameters of renal tubular function have been measured in fasting morning urine in 124 male stone formers: excretion of lysozyme and gamma-glutamyl transpeptidase (gamma-GT), fractional excretion (FE) or glucose, insulin, bicarbonate after an alkali load, and theoretical phosphate threshold (TmP/GFR). The following have been diagnosed: primary hyperparathyroidism (n = 3), medullary sponge kidneys (n = 5), hyperuricemia (n = 8), cystinuria (n = 1), struvite nephrolithiasis (n = 2), idiopathic hypercalciuria of the absorptive (n = 16), dietary (n = 46) or renal (n = 5) type, and normocalciuric idiopathic urolithiasis (n = 38). Urinary excretion of lysozyme and of gamma-GT were elevated in 14% and 21% of patients respectively; FE glucose and FE insulin were elevated in 6% and 8% of patients respectively. In 62% of the patients TmP/GFR was below 0.95 mmol/l and in 52% of the patients FE HCO3 after alkali load was above normal. The findings show that a large number of stone formers have signs of renal tubular dysfunction; apparent renal leaks of phosphate and of bicarbonate are the most frequently encountered defects; while they are not specific for a given etiologic group of patients, they have been found in each group. The latter observation suggests that nephrolithiasis itself can damage renal tubular function.
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PMID:[Tubular dysfunction in renal lithiasis: cause or consequence?]. 285 24

To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.
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PMID:Tubulopathy in nephrolithiasis: consequence rather than cause. 287 Dec 16

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.
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PMID:Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis. 291 May 76

To elucidate the pathophysiology of mixed stone formation in cystinuria, 27 patients with documented cystine nephrolithiasis underwent an inpatient evaluation under a constant dietary regimen. All patients had homozygous cystinuria, since the daily urinary cystine excretion exceeded 250 mg. per gm. creatinine. Hypercalciuria was noted in 5 patients (18.5 per cent), 4 of whom had fasting hypercalciuria. Hyperuricosuria was found in 6 patients (22.2 per cent) and it was not caused by a consumption of a diet rich in animal proteins, since urinary pH was higher and urinary sulfate lower than in control subjects. Serum uric acid was slightly lower and uric acid clearance was higher in hyperuricosuric patients than in control subjects. Hypocitraturia was found in 12 patients (44.4 per cent) and it was associated with defective renal acidification in 4 of 5 patients in whom it was tested. Thus, hypercalciuria, hyperuricosuria and hypocitraturia frequently accompany cystinuria in patients with cystine nephrolithiasis. These conditions might be renal in origin, rather than a result of dietary or environmental aberrations. They may contribute to the formation of calcium and uric acid stones, which sometimes complicate cystine nephrolithiasis.
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PMID:The spectrum of metabolic abnormalities in patients with cystine nephrolithiasis. 292 71

Calcium-hydrogen-phosphate (CaHPO4) was considered as one of the main factors governing renal calculus formation. The degree of saturation (expressed as activity product) with respect to this phase was therefore calculated in urines of 36 hypercalciuric children (20 absorptive, 16 renal subtype) with isolated hematuria, 10 renal stone patients, and 30 healthy controls. On low calcium diet 12 children of the absorptive hypercalciuric-, 13 of the renal hypercalciuric and 7 of the renal stone forming children hat their urines in the saturated zone --irrespective of the evolution of hypercalciuria Ca/cr ratio. Thiazide normalised the activity product in all groups. The use of the Ca/cr ratio as the sole parameter in the investigation of children with isolated hematuria and hypercalciuria or calcium nephrolithiasis is therefore insufficient, simultaneous determinations of the state of saturation of urines is recommended. This technique should also allow a quantitative assessment of the various therapeutic regimens recommended.
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PMID:[Determination of the degree of saturation of calcium hydrogen phosphate in the urine]. 292 36

One hundred patients with recurrent calcium nephrolithiasis were submitted to the Pak test. At fasting state hypercalciuria was found in 27 cases, while a group of 16 further patients became hypercalciuric after oral calcium load. Only measurement of urinary cAMP excretion in both conditions made it possible to diagnose renal hypercalciuria in 9 out of 27 patients in the former group; according to test results 4 patients were expected to have primary hyperparathyroidism, but afterwards the disease was identified in only one case.
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PMID:Diagnostic value of urinary cyclic AMP measurement in patients with calcium nephrolithiasis. 301

109 patients with calcium-containing nephrolithiasis and 10 normal controls underwent oral calcium load test. After thorough examination, 6 of the 109 patients were diagnosed as having primary hyperparathyroidism (PHPT) and the remainder as having normocalcemic nephrolithiasis without PHPT. Following the oral calcium load test, the latter were operationally divided into 3 groups - normocalciuric nephrolithiasis (NN), n = 78; absorptive hypercalciuria (AH), n = 10, and renal hypercalciuria (RH), n = 15 - according to the criteria reported by Pak et al. Before the oral calcium load test, nephrogenous adenosine 3',5'-monophosphate (NcAMP), urinary adenosine 3'-5'-monophosphate (urinary cAMP), and plasma immunoreactive parathyroid hormone (iPTH) were determined to evaluate parathyroid function. This function, as assessed by mean basal NcAMP in the NN, AH and RH groups as well as the PHPT group, was significantly increased as compared with that in the normal controls. Within the NcAMP-elevated 4 groups, the mean basal NcAMP was highest in the PHPT group followed by the RH, AH and NN groups. In view of the mean basal NcAMP, disregarding the PHPT group, the NN and AH groups seemed to be intermediate types between the normal controls and the RH groups. Similar, but less distinctive results were obtained in the determination of urinary cAMP and plasma iPTH. On the other hand, when leaving the PHPT group out, the mean basal urinary calcium creatinine ratio (Ca/Cr) was highest in the RH group followed by the AH and NN groups, and lowest in normal controls, suggesting that the NN and AH groups were intermediate between normal controls and the RH group. The mean basal urinary Ca/Cr ratio in the PHPT group was moderately elevated but not remarkable. Almost similar tendencies were observed in 24-hour urinary calcium excretions on a calcium-restricted diet. A weakly positive correlation (r = 0.232, p less than 0.05) between basal NcAMP and basal urinary Ca/Cr ratio was observed in accumulated cases of the NN, AH and RH groups, whereas a negative correlation (r = -0.664, p less than 0.05) was obtained in normal controls. It is concluded that a possible abnormal calcium metabolism is suggested in stone formers without PHPT. Additionally, it is speculated that 'relative hypercalciuria' in NN and hypercalciuria in AH and RH might be accounted for in a single line of a primary renal leak of calcium.
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PMID:Possibility of elevated parathyroid function in patients with calcium-containing nephrolithiasis as compared with normal controls. 303 19

The clinical and laboratory findings in 14 infants, 2 children and 42 adults with RTA-1 have been retrospectively analyzed and the patients classified as having the hereditary (14%), acquired (31%), or idiopathic (55%) form. In 7 of the 8 hereditary cases, RTA-1 appeared to be a complication of hereditary hypercalciuria. The majority of acquired cases (61%) were secondary to immune-mediated diseases. All of the 14 infants with RTA-1 were classified as idiopathic. All of the idiopathic cases in children and adults were associated with nephrolithiasis and/or nephrocalcinosis, 33% of which had a family history of nephrolithiasis. The 14 infants presented with failure to thrive. Seventy-seven percent of children and adults with RTA-1 had nephrolithiasis and/or nephrocalcinosis and usually presented with symptoms related to this problem. Adults without nephrolithiasis or nephrocalcinosis usually presented with electrolyte disturbances or acidosis. Hypokalemia, the most common electrolyte disturbance, was present in 28% of the entire series. Acidosis was present in all infants and in 70% of children and adults. Clinically apparent bone disease was observed in 3 infants, and in 1 adult with nephrolithiasis. Glomerular function was normal in infants and in the 2 children, but depressed in 40% of adults. Recurrent urinary tract infection was a contributing factor but was not the sole cause of renal failure. Surprisingly, kidney stone number, the number of surgical procedures, and the presence of nephrocalcinosis had no apparent effect on the development of renal failure. Glomerular filtration rate was significantly higher in patients with incomplete RTA-1, and serum total CO2 was significantly correlated with creatinine clearance and minimum urinary pH. Hypercalciuria was present in 32% of patients with nephrolithiasis and/or nephrocalcinosis, and urinary citrate excretion was low in all of 16 patients in whom it was measured. Hypocitraturia appeared to be due in most cases to potassium depletion and renal failure, but may have occurred as a primary defect in 1 patient with hereditary RTA. Urinary uric acid excretion was elevated in 23% of patients with stones in whom it was measured. The mean number of stone-forming events was 51 +/- 14. Although a weak correlation between urinary calcium excretion and stone number was observed, the cause for prodigious stone formation could not be explained. This series emphasizes the variable degree to which the common clinical manifestations of RTA-1 (metabolic acidosis, hypercalciuria, nephrolithiasis, nephrocalcinosis, and potassium depletion) are expressed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The syndrome of distal (type 1) renal tubular acidosis. Clinical and laboratory findings in 58 cases. 312 50


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