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

Seventeen of 75 diabetic children without nephropathy had urinary calcium excretion of more than 4 mg/kg/day. Neither diurnal variation in calciuria, nor correlations between calcium excretion and glucose excretion as well as HbA1 levels were observed. The findings suggest that about one quarter of diabetic children is at risk for hypercalciuria and may be for renal damage due to hyperexcretion of calcium.
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PMID:Hypercalciuria in children with diabetes mellitus. 270 69

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

A 41-year-old man with acromegaly was suffering from chronic, progressive backache and aware of reduction in his body height. Endocrine studies revealed increased glucose non-suppressible serum growth hormone (GH) and serum prolactin (PRL). Pituitary microadenoma was detected by a computerized axial tomogram and subsequently resected by trans-sphenoidal adenomectomy. The tumor proved to be a mixed GH- and PRL-secreting adenoma by electron microscopy and immunoperoxidase staining. Concurrent investigation of backache and reduced height disclosed markedly reduced radiodensity of the spinal bones, bilateral nephrocalcinosis, and hypercalciuria, which were ascribed to renal tubular acidosis (RTA) demonstrated by reduced urinary excretion of acids and insufficient reduction of urinary pH following oral administration of ammonium chloride. From the analogy to certain endocrinopathies, it appears likely that enhanced calcium metabolism and resultant hypercalciuria due to excess GH and PRL have led to the development of RTA, which further enhanced calciuria. Such enhanced calcium metabolism and consequent hypercalicuria conceivably led to accelerated demineralization of the spine and resulted in the reduced height of this patient in his early forties.
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PMID:A case of active acromegaly with reduced height and type 1 renal tubular acidosis. 289 4

Poorly controlled type II diabetic patients with hypomagnesaemia, hypermagnesuria, and hypercalciuria were allocated to treatment with either metformin or glipizide, to determine the effects on some indices of mineral metabolism. Despite comparable improvement in glycaemic control, assessed by glucose and haemoglobin A1, there were significant differences between the two groups in the handling of magnesium. Patients receiving metformin showed a reduction in magnesium excretion but remained hypomagnesaemic and hypercalciuric. In contrast, patients receiving glipizide exhibited little change in either magnesium or calcium excretion but showed a significant rise in serum magnesium.
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PMID:Effects of improved glycaemic control on calcium and magnesium homeostasis in type II diabetes. 319 52

To define the degree of renal tubular involvement in idiopathic calcium nephrolithiasis, 18 patients (aged 23-60 years, 15 men and 3 women, with 1-30 years of renal stone history) with normal glomerular filtration rate (GFR) and effective renal plasma flow with no history of urinary tract infection and on no dietary or drug therapy underwent the following studies: measurement of proximal tubular maximum reabsorption of glucose (Tmglucose) and secretion of para-aminohippurate (TmPAH), urinary concentrating ability after 14 h of fluid deprivation, and urinary net acid excretion following an oral dose of ammonium chloride, 0.1 g/kg of body weight. Seventeen healthy subjects in the same age range served as control. Patients with calcium nephrolithiasis, with normal renal hemodynamic functions, have significantly lower proximal tubular maximum reabsorptive and secretory functions, diminished urinary concentrating mechanism, and reduced urinary net acid excretion following an oral acid load. These tubular functional abnormalities were observed in patients with or without hypercalciuria.
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PMID:Renal tubular dysfunctions in patients with idiopathic calcium nephrolithiasis. 369 99

Urinary calcium excretion is increased after the consumption of protein and carbohydrate by both the human and the rat due to a decreased efficiency in the renal reabsorption of calcium. We have previously shown that the magnitude of the postprandial change in urine calcium in human subjects fed a high protein meal was correlated with the protein-induced changes in serum insulin levels. The present study investigates further the relationship between plasma insulin and urinary calcium excretion. Renal calcium clearance studies were performed in rats infused with the insulin secretagogues glucose or arginine, in the presence and absence of mannoheptulose, a drug which suppresses insulin secretion. The hypercalciuretic effect of arginine was also examined in streptozotocin (SZ) diabetic rats. Arginine and glucose infusion increased urinary calcium excretion by 575 and 225%, respectively, by a mechanism which could be inhibited by mannoheptulose. A linear relationship (r = 0.86) was observed between plasma insulin and urinary calcium excretion. Arginine infusion had no effect on urinary calcium excretion in the SZ diabetic rat, in marked contrast to its effect on normal animals. We conclude that insulin is an important mediator of arginine- and glucose-induced hypercalciuria in the rat.
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PMID:Evidence for insulin involvement in arginine- and glucose-induced hypercalciuria in the rat. 634 22

Total parenteral nutrition (TPN) is known to cause hypercalciuria and negative calcium balance in some patients. We have now shown that the administration of TPN to rats causes marked increases in urinary calcium losses. Moreover, urinary calcium excretion in the TPN rat responds to changes in the infusate concentration of calcium and amino acids similarly to what has been observed in TPN patients. For any given increase in the amount of calcium infused 130% more calcium was excreted in the urine by rats receiving TPN compared to rats receiving saline alone. At a fixed level of calcium infused, urinary calcium increased linearly when the amino acid content of the infusate was increased from 0 to 2.75 to 4.25%. However, a reduction in the glucose load, via isocaloric substitution with lipid by 60%, had no effect on urinary calcium excretion. The TPN rat appears to be a promising animal model in which to investigate the hypercalciuretic effect of intravenous nutrition, particularly as calcium homeostasis may be affected by various nutritional components of the TPN solution.
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PMID:Calciuria in total parenteral nutrition: effects of amino acids and glucose in rats. 643 58

To investigate the pathogenesis of the alterations in bone and mineral metabolism that are found in young insulin-dependent diabetics (IDDs), we performed a standard oral calcium load in 26 IDDs, 7-18 yr of age, and in 17 normal children, 9-18 yr of age. Eighty-five percent of the IDDs had second metacarpal cortical bone widths below the mean for matched controls. Calcium excretion in the IDDs fell along a continuous spectrum, ranging from normal to values consistent with renal hypercalciuria. Immunoreactive PTH was significantly (P less than 0.03) lower in the IDDs compared to that in the controls, and 24,25-dihydroxyvitamin D was significantly elevated (P less than 0.001). We were not able to document a significantly lower concentration of 1,25-dihydroxyvitamin D in the IDDs. Serum calcium, phosphate, and PRL levels were normal, as were creatinine (Cr) clearance and 24-hr urinary cortisol excretion. There was no apparent correlation between the fasting and postload urinary Ca to Cr and glucose to Cr concentration ratios. The accumulated data suggest that in many young IDDs, there is a component of intestinal calcium hyperabsorption which results in appropriate feedback responses by the parathyroid gland and vitamin D metabolic pathway(s). This imbalance between circulating PTH and vitamin D metabolites could result in defective bone remodeling and decreased cortical thickness.
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PMID:Use of oral calcium loading to characterize the hypercalciuria of young insulin-dependent diabetics. 685 83

Serum immunoreactive parathyroid hormone (iPTH) and indices of mineral and glucose metabolism were determined in 58 insulin treated diabetic patients (duration of disease 1-11 years). The mean serum iPTH level in all diabetic patients, measured simultaneously with sera from normal subjects, was 55% of normal mean (P < 0.01). The diabetic patients had hypomagnesaemia (P < 0.001), hypercalciuria (P < 0.001) and a 9.6% decrease in bone mass (P < 0.001). Low serum iPTH values were correlated with high glycosuria (R = -0.28, P < 0.05) and with long duration of diabetes (R = -0.31, P < 0.02). Patients with both high glycosuria and long diabetes duration had especially low iPTH values (mean 16 ng/l, n = 16) compared with patients with both low glycosuria and short diabetes duration (mean 32 ng/l, n = 15, P < 0.005) and with normal subjects (mean 37 ng/l, n = 28, P < 0.001). The 16 patients with low serum iPTH values also had higher urinary calcium excretion rate (P < 0.05) than the 15 patients with low glycosuria and short duration of diabetes. The diabetic hypoparathyroidism may be secondary to a primary disturbance of bone metabolism, with a negative net calcium balance.
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PMID:Hypoparathyroidism in diabetes mellitus. 745 85


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