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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes mellitus and hypertension constitute two powerful independent risk factors for cardiovascular, renal and atherosclerotic disease. The frequent occurrence of the two diseases in the same individual doubles the risk of cardiovascular death, as well as substantially increasing the frequency of transient ischemic attacks, strokes, peripheral vascular disease with lower extremity amputations, as well as end-stage renal disease and blindness. Although hypertension usually occurs in IDDM in association with renal disease, in NIDDM the evolution of hypertension appears to be multifactorial and independent of renal disease. Obesity appears to be dissociable from hypertension and NIDDM with a common link between obesity, hypertension and NIDDM appearing to be hyperinsulinism and insulin resistance. It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Further, insulin itself may have a direct effect upon the atherosclerotic process in the hypertensive diabetic patient. These considerations have been taken into account in the structuring of antihypertensive therapy in Type I and Type II Diabetes Mellitus.
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PMID:Diabetes and hypertension. 207 56

Urinary excretion of calcium, inorganic phosphorus, magnesium, glucose, and creatinine was measured in first-void spot urine samples collected 4 days apart in 220 insulin-dependent diabetic (IDDM) children (mean age 11.9 yr) attending a summer camp. A single control urine sample was obtained from 33 healthy nondiabetic siblings (mean age 11.2 yr). Mean +/- SD urinary calcium-creatinine ratios (UCa/Cr) did not significantly differ between IDDM and control subjects (0.14 +/- 0.09 vs. 0.12 +/- 0.09, respectively, P = 0.156). Mean urinary magnesium-creatinine ratios (UMg/Cr) were elevated in IDDM compared with control subjects (0.15 +/- 0.06 vs. 0.08 +/- 0.03, respectively, P = 0.0001). Similarly, mean urinary phosphorus-creatinine ratios (UP/Cr) were significantly increased over those in control subjects (1.12 +/- 0.33 vs. 0.40 +/- 0.22, respectively, P = 0.0001). UCa/Cr, UMg/Cr, and UP/Cr were correlated with increasing mean urine glucose content (P = 0.0001). No correlations were found when UCa/Cr, UMg/Cr, or UP/Cr were compared with patient age, duration of diabetes, glycosylated hemoglobin, or insulin dosage. Urine losses of phosphorus and magnesium were present even when glycemic control was considered good by several methods (glycosylated hemoglobin, short-term glycemic index, or urinary glucose content). Glomerular hyperfiltration was unable to account for increased urinary mineral content. In conclusion, the data indicate that urinary excretion of phosphorus and magnesium is elevated in children with IDDM, regardless of glycemic control. In the presence of glucosuria, this loss is further enhanced. Urinary calcium excretion is significantly higher only during periods of glucosuria. The data suggest that children with IDDM could be at risk for mineral deficiencies in the absence of intensive insulin management.
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PMID:Hyperphosphaturia and hypermagnesuria in children with IDDM. 218 Jun 62

Nephron loss is a common progression of a diverse range of kidney diseases. Recent experimental models of chronic renal disease have suggested that hemodynamic and nonhemodynamic mechanisms play key roles in progressive renal injury. Extensive renal ablation in the rat was followed by development of altered glomerular hemodynamics. Albuminuria and histologic damage leading to focal glomerulosclerosis were preceded by the development of increased glomerular pressures and were prevented by interventions such as severe dietary protein restriction and angiotensin-converting enzyme (ACE) inhibitor therapy. Both experimental interventions ameliorated glomerular hypertension. It was therefore concluded that these interventions ameliorated injury by glomerular hemodynamic effect. Similar findings were obtained in a rat model of type I diabetes mellitus induced by streptozotocin in which glomerular hemodynamic factors appeared important to the development of progressive renal disease. Recent studies have suggested that nonhemodynamic factors have important roles in the progression of glomerular injury. For example, although the predominant effects of ACE inhibitor therapy appear to be hemodynamically mediated, data are emerging which suggest that these agents may also influence growth/proliferation of glomerular cells. Because hyperplasia/hypertrophy may influence glomerular susceptibility to injury, this may also be a potential mechanism whereby ACE inhibitor therapy influences glomerular damage. In addition, a variety of studies have suggested that hyperlipidemia, which is frequent accompaniment of glomerular disease, is an important modulator of glomerular injury independent of glomerular hemodynamic effects. Coagulation factors, calcium phosphorus balance, as well as the genetic susceptibility of the glomerulus to injury, all appear to contribute to progressive nephron destruction.
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PMID:Renal protective effects of angiotensin-converting enzyme inhibition. 218 11

Certain acute and chronic metabolic effects of nicardipine have been studied in 20 patients with non-insulin dependent diabetes (NIDD). An intravenous glucose tolerance test (i.v. GTT, glucose 0.33 g/kg as a bolus) and the corresponding insulin response were assessed at the end of a 4 week placebo period, after the first dose and on administration for 12 weeks of nicardipine 20 mg t.i.d. The glucose and insulin responses to the i.v.GTT, evaluated as incremental AUCs, did not change significantly (glucose 30.5 mg/dl.90 min on placebo, 33.1 mg/dl.90 min acutely and 31.4 mg/dl.90 min on chronic administration of nicardipine; insulin 2.08 microU/ml.90 min on placebo, 1.87 microU/ml.90 min acutely and 1.93 microU/ml.90 min after chronic nicardipine). Glucose removal rate (KG) following the i.v.GTT was 0.73%/min on placebo 0.75%/min on acute administration and 0.8%.min-1 with chronic nicardipine. Active treatment produced a significant reduction of blood pressure (from 187/96 mm Hg on placebo to 166/89 mm Hg acutely and 152/83 mm Hg after 12 weeks of nicardipine treatment). It is concluded that the calcium antagonist nicardipine was an effective antihypertensive drug, and that it did not cause deterioration of metabolic control in hypertensive patients with NIDD.
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PMID:Effect of nicardipine on insulin secretion, glucose and lipid metabolism in hypertensive, non-insulin dependent diabetics. 264 44

Serum concentrations of prealbumin, albumin, orosomucoid, magnesium, zinc and calcium were studied in 30 children with newly diagnosed IDDM aged 3-15 years, during the first two years of the disease, and in 44 healthy control children. On admission serum prealbumin was significantly lower in IDDM children (149 +/- 48 mg/l) (M +/- SD) than in healthy controls (194 +/- 39 mg/l) (p less than 0.001). During the two years follow-up prealbumin increased significantly, but did not reach the level of healthy controls. Serum albumin was slightly increased at diagnosis (p less than 0.01), but later decreased significantly (p less than 0.01). Orosomucoid concentrations did not differ between diabetics and controls. Serum magnesium was initially within the reference interval but later decreased, and after 2 years of IDDM it was highly significantly reduced (p less than 0.001). Serum zinc was significantly reduced in IDDM children at diagnosis (p less than 0.001), but was within the reference interval after one and 2 years. Serum calcium was increased in the IDDM group at diagnosis (p less than 0.01), but later normalized. It is concluded that in early IDDM there is a decrease in serum prealbumin and albumin, and serum magnesium decreases progressively, while serum zinc is only transiently reduced.
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PMID:Early changes of some serum proteins and metals in diabetic children. 305 55

Persistent proteinuria is strongly associated with increased mortality in insulin dependent diabetes, and risk of this condition can be predicted many years in advance by subclinical increases in albumin excretion rate (microalbuminuria). Eight normotensive insulin dependent diabetics with microalbuminuria who had overnight albumin excretion rates of between 15 and 200 micrograms/min underwent a three week randomised crossover study of their normal protein diet (median 92 (range 55-117) g/day) and a low protein diet (47 (38-57) g/day). Both diets were isoenergetic, and the low protein diet was supplemented with calcium and phosphate. Median overnight albumin excretion rate fell from 23.0 (15.0-170.1) micrograms/min during the normal diet to 15.4 (4.1-97.8) micrograms/min during the low protein diet. No consistent change was found in urinary excretion of beta 2 microglobulin during the two diets. The reduction in albumin excretion rate was accompanied by a significant fall in median glomerular filtration rate and fractional renal clearance of albumin. Kidney volume remained unchanged. There were no significant changes in glycaemic control or arterial blood pressure. In these few patients restriction of dietary protein had a beneficial effect on microalbuminuria, independent of changes in glucose concentrations and arterial blood pressure.
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PMID:Effect of protein restriction in insulin dependent diabetics at risk of nephropathy. 310 47

Many authors have described abnormalities of calcium homeostasis in type I diabetes mellitus, but data in the literature are conflicting. Consequently we studied calcium, phosphorus and magnesium (in serum and urine), parathyroid hormone, calcitonin and 25-hydroxyvitamin D (25-OHD) levels in 21 prepubertal diabetic patients and in 21 sex- and age-matched controls. We did not find any significant difference of all the aforementioned parameters between diabetics and controls. Also the value of 25-OHD was similar in diabetic and healthy subjects (24.33 +/- 6.04 vs 22.09 +/- 5.01 ng/ml). The results suggest that the principal parameters of calcium metabolism are normal in prepubertal diabetic children.
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PMID:Calcium homeostasis in prepubertal diabetic children. 322 92

Hematuria of unknown origin occurs in 30% of patients with diabetic nephropathy. In nondiabetic persons, hematuria may be caused by hypercalciuria with or without nephrolithiasis. Eight children with type I diabetes mellitus, hematuria, and hypercalciuria were observed in our clinic during a 1-year period. Two of these also had evidence of renal papillary necrosis. To assess the importance of hypercalciuria in the pathogenesis of hematuria in children with diabetes mellitus, we measured urinary calcium excretion in a large population of such patients. The calcium to creatinine ratio in the urine of diabetic children (0.21 +/- 0.01) was greater than that of nondiabetic children (0.12 +/- 0.01). A calcium to creatinine ratio of 0.28 was established as the upper limit of normal in our nondiabetic population, and 27% of the diabetic children were hypercalciuric on this basis. The diabetic children with hypercalciuria also had hyperphosphaturia and a urinary CaHPO4 X 2H2O molar ion product three times that found in the nondiabetic control population. These data suggest that many children with diabetes are at risk for renal damage due to hypercalciuria. Because hypercalciuria is more common in diabetic than nondiabetic children, it may play a previously unrecognized role in the renal disease associated with diabetes mellitus.
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PMID:Hematuria and hypercalciuria in children with diabetes mellitus. 357 34

Sixty-nine patients with type I diabetes mellitus were followed for from 1-4 yr (mean, 3 yr). Their overall growth, as measured by height and weight, was normal; however, repeated measurements of their bone mass using photon absorptiometry and radiogrammetry showed that, relative to normal subjects, the patients had a persistent bone deficit throughout the course of the study. This deficit was not attributable to bone width, which was normal. On the average, the magnitude of the deficit did not change with time; furthermore, an individual's rate of change in bone mass deficit during the study was not correlated with the patient's glucose control, as measured by hemoglobin A-1 or fasting blood glucose levels. Initial levels of serum ionized calcium and magnesium were decreased in the patients with diabetes. During the study, the mean level of ionized calcium increased, but that of magnesium decreased further, compared to the initial values. In a group of 19 patients with newly diagnosed diabetes, bone mass was found to be significantly below normal among the girls, but not among the boys.
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PMID:A prospective study of bone mass in patients with type I diabetes. 396 95

A 38-year-old man with brittle, juvenile onset diabetes mellitus and bilateral severe dry eyes with recurrent corneal ulcers developed atypical band-shaped calcifications of both corneas during a 24-hour period. Serum calcium, phosphate, and carbon dioxide levels all were within normal limits. The patient was mildly uremic but was not in renal failure. When EDTA chelation failed to clear the deposits, partial keratectomies were performed in both eyes and the specimens were examined by light and electron microscopy, including energy dispersive x-ray analysis. Microscopic studies revealed an atypical calcific keratopathy which involved neither Bowman's layer nor the most superficial stromal lamellae. The deposits were confined to deeper lamellae in the anterior stroma and by electron microscopy were composed of extracellular crystalline aggregates. Energy dispersive x-ray analysis of these aggregates confirmed the presence of calcium and phosphate. Corneal dessication appeared to be a major contributing factor in the rapid formation of these deposits.
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PMID:Bilateral acute corneal calcification. 400 Jun 45


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