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

Examination of glucose kinetics, pancreatic alpha and beta cell function, plasma lipids, urinary acidification and calcium excretion has been undertaken in a patient with hereditary fructose intolerance. This case was unusual as it was associated with insulin-requiring diabetes, type IV hyperlipemia, hypercalciuria and renal calculi. He also demonstrated the previously described fructose-induced defect of urine acidification. Glucagon and C-peptide assays showed that the pancreatic alpha cells were stimulated by fructose and that the beta cells did not respond to fructose. It is not known whether the latter was due to his diabetes or to the lack of a beta cell response to this sugar. Primed 14C-glucose infusions were used for the first time to study nonsteady state glucose kinetics in man. They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. However, after the administration of sorbitol the plasma glucose concentration decreased because glucose production decreased. After the administration of sorbitol there was no change in the metabolic clearance of glucose. This reflects the lack of a peripheral insulin effect and is consistent with the lack of any measurable C-peptide. Glucose utilization also decreased, but this decrease was less than the decrease in glucose production. Because the metabolic clearance of glucose remained unchanged, it was concluded that the change in glucose utilization was solely due to the decrease in glucose concentration. The absence of C-peptide in the plasma indicated that changes in glucose turnover were not related to any changes in endogenous plasma insulin. Furthermore, the plasma glucagon concentration increased and, hence, changes in this hormone could not account for the decrease in glucose production. Therefore, it was concluded that the sorbitol-induced decline in glucose production was due to a direct effect on hepatic metabolism.
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PMID:Studies of glucose turnover and renal function in an unusual case of hereditary fructose intolerance. 1 54

Calcium and phosphous metabolism was investigated in 20 patients with diabetes mellitus when their diabetes was under poor metabolic control and again once optimal glycaemic control was achieved with aggressive insulin therapy. Ten of the twenty uncontrolled diabetics had hypercalciuria; insulin therapy returned calcium excretion to normal in five. Twenty-four hour calcium excretion fell in all but two patients when optimal diabetic control was achieved and calcium excretion was positively correlated with glucose excretion. Urinary cyclic AMP excretion, which was in the high normal range during poor control, decreased significantly during optimal insulin therapy. These data suggest that the hypercalciuria of uncontrolled diabetes may be a form of renal hypercalciuria which could result in parathyroid stimulation which might contribute to the development of osteopenia in patients with diabetes mellitus.
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PMID:The hypercalciuria of diabetes mellitus: its amelioration with insulin. 21 58

The calciuric response to an oral glucose load (100 g) was determined in 16 patients with calcium oxalate urolithiasis (seven with renal hypercalciuria and nine with absorptive hypercalciuria) and seven normal subjects. The rates of renal calcium excretion increased significantly after glucose ingestion in all three groups. The calciuric response in patients with absorptive hypercalciuria and intestinal hyperabsorption of calcium was indistinguishable from that of normal subjects. However, the calcium excretions were significantly higher during 1 hr preceding and 3 hr after glucose ingestion in patients with renal hypercalciuria (with presumed "renal leak" of calcium) than in normal subjects. The increment in the calcium excretion rate was also higher in patients with renal hyperacalciuria, particularly during the 2nd hour of glucose ingestion. The results provide a further support for the concept of different etiologies of renal and absorptive hypercalciurias.
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PMID:An exaggerated augmentation of renal calcium excretion after oral glucose ingestion in patients with renal hypercalciuria. 34 35

Epidemiological studies indicate that renal stone disease is a rapidly increasing problem, already affecting around 10% of the entire adult male population. It has been suggested that environmental factors are responsible for this development, among them particularly disorders of carbohydrate metabolism. In the present study, therefore, 156 patients with active renal stone formation were investigated with respect to glucose tolerance and glucose-stimulated insulin response. Similar to other reports it was found that hypercalciuric subjects had evidence of an impaired glucose metabolism. However, this was mainly attributed to a tendency towards overweight in this group of patients and there were no firm indications of a true disorder of carbohydrate metabolism connected with hypercalciuria or the process of stone formation.
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PMID:Glucose metabolism in renal stone formers. 74 6

During the past 5 years, we have identified idiopathic hypercalciuria in five of seven patients referred for evaluation of renal glycosuria between 1985 and 1991. The children, all boys, ranged in age from 6 to 12 years. Endocrine function was normal, and none of the patients had hyperparathyroidism, hypercalcemia, renal tubular acidosis, or other secondary causes of hypercalciuria. The calcium/creatinine ratio in a fasting urine specimen was elevated in all five children who had hypercalciuria, with a mean value (+/- SD) of 0.34 +/- 0.06 (normal, < 0.2). In one child who had renal colic with spontaneous passage of gravel-like material, the idiopathic hypercalciuria persisted after 1 week on a diet containing 2000 mg of sodium and 300 mg of calcium. On the basis of studies that examined the site along the nephron responsible for hypercalciuria in rats with streptozocin-induced diabetes, we speculate that in children with renal glycosuria, there is defective reabsorption of glucose and calcium in the straight portion of the proximal tubule or in the collecting duct. It is likely that a similar mechanism accounts for the idiopathic hypercalciuria in children with diabetes mellitus.
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PMID:Hypercalciuria in children with renal glycosuria: evidence of dual renal tubular reabsorptive defects. 841 May 29

In-vivo microperfusion was used to localize the reabsorptive defect responsible for the hypercalciuria of diabetes mellitus and to investigate possible causative factors. Unidirectional proximal calcium absorption was not significantly different in rats made diabetic with streptozotocin compared with controls, providing evidence against the involvement of this nephron segment in the phenomenon. Calcium absorption by the loop of Henle, was however, significantly (P less than 0.01) lower in diabetic animals (32.1 +/- 1.2 vs 40.4 +/- 0.6 pmol/min). Based on our knowledge of calcium movements within the loop, it is likely that the reabsorptive defect residues within the thick ascending limb. The calcium lesion was found to be independent of acute changes in intraluminal glucose concentration and could not be corrected by acute insulin treatment. The study also provides new information on the relationship between intratubular glucose and fluid movements in the rat nephron. In diabetic rats a proximal perfusate containing 30 mmol glucose/l resulted in fluid absorption comparable with that seen in control rats perfused with 5 mmol glucose/l. However, intraluminal glucose had a stimulatory effect on fluid absorption in the loop of Henle of diabetic rats (10.7 +/- 0.5 vs 7.9 +/- 0.4 nl/min; P less than 0.01).
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PMID:Calcium transport in the proximal convoluted tubule and loop of Henle of rats made diabetic with streptozotocin. 178 84

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.
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PMID:Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet. 183 14

Renal calcifications have been described in very low birth weight (VLBW) infants, and diuretic drug-associated hypercalciuria is believed to play a role in the pathogenesis of this lesion. Hyperoxaluria is an important cause of renal stone formation in children and adults. Because parenteral nutrition solutions contain the oxalate precursors ascorbate and glycine, the relationship between total parenteral nutrition administration and oxalate excretion in VLBW infants was examined. Administration of approximately 0.5 g of total parenteral nutrition protein per kilogram per day to VLBW infants was associated with an increased urinary oxalate concentration and an increased urinary oxalate to creatinine ratio, when compared with VLBW infants receiving a glucose and electrolyte solution. A further increase in urinary oxalate concentration and oxalate to creatinine ratio was noted when total parenteral nutrition protein was increased to approximately 1.5 g of protein per kilogram per day. In VLBW infants who receive total parenteral nutrition, elevated urinary oxalate concentrations may develop and may be a factor in the pathogenesis of nephrocalcinosis in these infants.
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PMID:Urinary oxalate excretion by very low birth weight infants receiving parenteral nutrition. 250 54

Male patients with recurrent calcium (Ca) urolithiasis (RCU) with idiopathic hypercalciuria (I-HC, n = 12) or normocalciuria (NC, n = 12), and age, sex, and weight-matched controls (C, n = 12) were evaluated before and after a carbohydrate-rich synthetic meal for blood glucose, free fatty acids (FFA), alpha-amino-nitrogen, several glucometabolic hormones and parathyroid hormone (PTH), and urine Ca, phosphate, oxalate, and cyclic adenosine monophosphate (cAMP) levels as well as saturation. Fasting serum Ca was significantly higher and PTH significantly lower in I-HC than in controls, whereas in fasting urine cAMP and phosphate were unchanged. There were only minor differences between fasting blood glucose levels and postprandial glucose tolerance of RCU patients and controls. However, serum insulin was significantly elevated in I-HC versus C, but serum C-peptide, plasma glucagon, and somatostatin levels were comparable in RCU and C. FFA were significantly lower in RCU than C. Postprandial phosphaturia and urinary saturation with Ca-phosphates were significantly higher in RCU versus C, whereas urinary cAMP, pH, and oxalate were similar. We conclude that: (1) in RCU patients some postabsorptive steps in glucose metabolism may be abnormal; (2) those with I-HC have enhanced postprandial Ca and phosphate excretion concomitantly with disordered insulin metabolism; and (3) RCU patients may suffer from a postprandial renal phosphate leak, which may make their urine more lithogenic.
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PMID:Blood levels of glucometabolic hormones and urinary saturation with stone forming phases after an oral test meal in male patients with recurrent idiopathic calcium urolithiasis and in healthy controls. 257 28

The study was aimed at the evaluation of changes in the urinary excretion of calcium in patients with diabetes of type I and II. The investigations were carried out in 34 patients with type I diabetes, 28 patients with type II diabetes and 30 control subjects having the normal glucose tolerance. The oral calcium tolerance test according to Pak was performed in all the patients and the controls. Besides normocalciuria, also hypercalciuria of renal origin, as well as hipercalciuria resulting from an elevated intestinal absorption of calcium have been found in diabetic patients. These disturbances occurred much more frequently in patients with type I diabetes, especially in those of age below 40.
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PMID:[Hypercalciuria in patients with diabetes mellitus type 1 and 2--studies of its pathogenesis using the oral calcium tolerance test]. 262 18


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