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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed the recommendations and outcomes for all patients with diabetes mellitus and end-stage renal disease referred to the Medical Center Hospital of Vermont from 1971 through December 1983. During this period, we recommended transplantation in 53 of 73 patients evaluated. Thirty-two transplants were performed in 30 patients. Of the 30 patients, 10 had clinical vascular disease prior to transplantation, i.e., claudication, amputation, active angina, myocardial infarction, or stroke. Seven of the 10 had only claudication or amputation. These 10 patients showed a clear excess in graft failure and mortality. One- and 2-year graft survival was 37 and 13%; patient survival was 48 and 24%. By comparison, the 20 patients without evident vascular disease had 1- and 2-year graft survival rates of 83 and 75% and patient survival rates of 85% at both 1 and 2 years. The incidence of cardiovascular death in the group with vascular disease was 45% at 1 year and 63% at 2 years, as compared with none in the group without vascular disease. The high graft loss and mortality in this group after transplantation should be a major consideration when therapeutic alternatives are considered in diabetics with end-stage renal disease.
Nephron 1986
PMID:Renal transplantation in diabetes mellitus. Influence of preexisting vascular disease on outcome. 351 20

Cerebrovascular accidents, often secondary to severe atherosclerotic disease, are very common in uremic patients on long-term hemodialysis. The aim of the present study is to assess asymptomatic carotid artery atherosclerotic disease (CAAD) in hemodialyzed normotensive and hypertensive patients in comparison with age-matched controls, by the use of Doppler ultrasound flow velocity wave form analysis (FVWFA), recorded from the common carotid artery. This study was performed on 47 subjects divided into four groups: 10 young and 10 middle-aged normals were considered in groups I and II, respectively, 5 young uremic normotensive, 6 young uremic hypertensive and 16 middle-aged uremic normotensive patients in groups III, IV and V, respectively. All the examined patients were nonsmokers, without diabetes or cardiopathy. The five wave form dimensions most capable of separating different degrees of atherosclerotic disease were determined on every common carotid tracing and used in a single best fit discriminant equation; the resultant discriminant score (DS) classified each carotid tracing and consequently every group's range. DS of groups I and III were not different, but significantly higher compared to the other three groups; besides DS was statistically not different in groups II, IV and V. In conclusion, FVWFA did not detect a different degree of CAAD between normotensive dialyzed patients and age-matched normals, whereas the blood pressure pharmacological control did not affect the velocity findings of advanced CAAD in young uremic hypertensive patients.
Nephron 1986
PMID:Carotid artery atherosclerotic disease assessed by flow velocity wave form analysis in hemodialyzed normotensive and hypertensive patients. 353 16

Norepinephrine, isoproterenol, insulin, and glucagon increase the type II (low Km) iodothyronine 5'-deiodinase (5'-D) in the brown adipose tissue (BAT) of intact rats. Cycloheximide or actinomycin D blocks the increase after norepinephrine, suggesting new mRNA synthesis is required for this effect. The 3- to 10-fold increase in BAT 5'-D after insulin administration was also blocked by cycloheximide. The effects of all stimulators are blunted by fasting or streptozotocin-induced diabetes. While all these hormones have the potential for stimulating BAT 5'-D, the dose-response relationships suggest that norepinephrine and insulin are the most potent. These and our earlier studies showing additional effects of thyroid and growth hormones on BAT 5'-D point to the complex regulation of this enzyme, suggesting that the triiodothyronine produced from its action has an important role in the thermogenic response of this tissue.
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PMID:Hormonal regulation of iodothyronine 5'-deiodinase in rat brown adipose tissue. 353 96

An unusual case of diabetes secondary to acute pancreatitis in a boy with end-stage renal failure receiving continuous ambulatory peritoneal dialysis (CAPD) is described. A hyperglycaemic, hyperosmolar pre-coma developed, aggravated by associated hypercalcaemia. The glucose content of the dialysis fluid contributed to the hyperglycaemia, which settled as the pancreatitis resolved and lower glucose concentration dialysis fluid was used. Our experience suggests that pancreatic dysfunction should be considered where significant hyperglycaemia occurs during peritoneal dialysis.
Nephron 1986
PMID:Non-ketotic hyperosmolar diabetic pre-coma due to pancreatitis in a boy on continuous ambulatory peritoneal dialysis. 354 Jun 93

Insulin-dependent diabetes mellitus (IDDM) in humans is accompanied by an attenuation of the response of glucagon to hypoglycemia. To identify an animal model of IDDM with alpha-cell unresponsiveness to glucopenia in which to pursue morphologic and in vitro functional investigation of the lesion, pancreases isolated from rats with IDDM induced by streptozocin (STZ) or occurring spontaneously in BB/W rats were perfused with buffer containing 150, 25, and 150 mg/dl of glucose. In both forms of IDDM the normal glucagon rise during glucopenia was markedly impaired, suggesting an abnormality comparable to that of human IDDM. Studies of the insular sympathetic apparatus were conducted in these rat models. Electron-microscopic examination of peri-insular nerve endings disclosed no discernible abnormality in either form of rat IDDM. However, morphometric analysis of contacts between [3H]norepinephrine-labeled sympathetic nerve terminals and alpha-cells in pancreases from STZ-induced diabetic (STZ-D) rats revealed a 65-70% reduction in direct contacts. An 80% reduction in the number of nerve endings (not labeled) in direct contact with alpha-cells was also noted in the BB/W diabetic rats. Norepinephrine reuptake, studied only in the STZ-D group, was not impaired. The availability of local endogenous norepinephrine to alpha-cells and their sensitivity to exogenous norepinephrine was determined by perfusing 2, 5, or 10 micrograms/ml of tyramine, a releaser of endogenous norepinephrine, and norepinephrine at a concentration that in pancreases from nondiabetic rats gave a quantitatively similar glucagon response.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1987 Mar
PMID:Morphologic and functional changes in sympathetic nerve relationships with pancreatic alpha-cells after destruction of beta-cells in rats. 354 58

A child developed steroid-responsive nephrotic syndrome at the age of 3 years. 6 years later, he developed insulin-dependent diabetes mellitus. At this time renal biopsy disclosed minimal-change disease. After multiple relapses requiring cyclophosphamide or repeated courses of steroid therapy, a second renal biopsy, 5 years after the first, revealed early diabetic changes with associated exudative lesions. The nephrotic syndrome remains responsive to steroids and cyclophosphamide, and the patient maintains an increased glomerular filtration rate and normal blood pressure 3.5 years afterwards. His HLA typing showed DR4 and DR7. Since DR4 and DR7 are associated with diabetes and minimal-change disease, respectively, we speculate that he could carry the genetic predisposition for the development of both diseases.
Nephron 1987
PMID:Steroid-responsive relapsing nephrotic syndrome associated with early diabetic glomerulopathy in a child. 360 Sep 16

To elucidate the nature of the abnormality of elastin metabolism in arteriosclerosis, we determined the elastase-type activity in the human radial artery of patients with chronic renal failure due to glomerular disease and diabetes. Elastase-type activity was determined by HPLC analysis of the hydrolyzed products of succinyl-trialanine-4-nitroanilide, a sensitive synthetic substrate for elastase. Three kinds of hydrolyzed products, (L-Ala)2-NA, L-Ala-NA and NA, were found after incubation of the substrate with human radial artery in the presence of amastatin (an inhibitor of aminopeptidases). We assumed the activity that liberates NA to be an elastase-type activity because purified human aorta elastase liberates NA from the substrate. The pH optima of the human artery and rat aorta activities were 6.0 and 6.8, respectively. The elastase activity in human radial artery and rat aorta was inhibited by diisopropyl phosphofluoridate, a serine protease inhibitor, and by elastatinal, an elastase inhibitor. The elastase-type activity in the radial artery of patients with chronic renal failure was significantly lower than that of the control group, and the decrease was especially marked in the patients with juvenile onset diabetes. These results suggest that the elastin metabolism is abnormal in the radial artery in diseases that tend to cause atherosclerosis.
Nephron 1986
PMID:Elastase-type activity in human radial artery in patients with chronic renal failure. 363 13

Renal biopsies were obtained from 164 patients with diabetes mellitus. Their histological changes were evaluated together with clinical findings and prognosis. In 36 patients, various types of glomerulonephritis were complicated: mesangial proliferative glomerulonephritis (17 patients), membranous glomerulonephritis (8), endocapillary proliferative glomerulonephritis (5), membranoproliferative glomerulonephritis (4) and minimal change nephrotic syndrome (2). Superimposed glomerulonephritis was suspected in diabetic patients with a short history of less than 5 years, persistent proteinuria, occasional hematuria and no retinopathy. They may, however, produce little effects on the long-term prognosis of diabetic patients except membranoproliferative glomerulonephritis.
Nephron 1986
PMID:Glomerulonephritis in diabetic patients and its effect on the prognosis. 370 65

It is proposed that stiffened red cells can interfere with normal microvascular and glomerular function. In diabetics intrinsic stiffening of red cells is intensified during poor metabolic control when plasma osmolarity is increased. Hypoxia, acidosis, catecholamines and other changes in red cell environment also increase red cell stiffness. Exercise proteinuria may help to identify individuals with the greatest intrinsic stiffening of red cells which appears to be due to the disposition of spectrin molecules rather than to changes in the lipid bilayer. Stiffened red cells may impede blood flow in the microcirculation and stimulate an autoregulated vasodilation which increases perfusion pressure, enhancing transudation. In the absence of vasodilation, stasis will lead to vascular occlusion and localised ischaemic necrosis. If diabetic microangiopathy is caused by abnormal haemorheology then the possibility exists that the complications of diabetes might be alleviated or prevented by agents which enhance red cell flexibility and improve blood rheology.
Nephron 1985
PMID:Intrinsic stiffening of red blood cells as the fundamental cause of diabetic nephropathy and microangiopathy: a new hypothesis. 388 63

The effects on ketogenesis and lipolysis of a norepinephrine (0.04 microgram/kg-min), epinephrine (0.04 microgram/kg-min), or saline infusion were examined in the overnight-fasted, conscious dog. Plasma insulin and glucagon levels were maintained constant by means of a somatostatin infusion (0.8 microgram/kg-min) and intraportal replacement infusions of insulin and glucagon. In saline-infused dogs, plasma epinephrine (62 +/- 8 pg/ml), norepinephrine (92 +/- 29 pg/ml), blood glycerol (87 +/- 10 microM), and plasma nonesterified fatty acid (NEFA) (0.82 +/- 0.17 mM) levels did not change. Total blood ketone body levels tended to rise (62 +/- 10 to 83 +/- 11 microM) by 3 h as did total ketone body production (1.5 +/- 0.4 to 2.2 +/- 0.4 mumol/kg-min) over the same time interval. Norepinephrine infusion to produce plasma levels of 447 +/- 86 pg/ml caused a sustained 50% rise in glycerol levels (66 +/- 17 to 99 +/- 15 mumol/L, P less than 0.05) and 53% rise in nonesterified fatty acids (0.53 +/- 0.07 to 0.81 +/- 0.15 mumol/L, P less than 0.05). Total ketone body levels rose by 43% (51 +/- 8 to 73 +/- 10 mumol/L) and ketone body production rose by a similar proportion (1.5 +/- 0.2 to 2.2 +/- 0.3 mumol/kg-min), changes that did not differ significantly from control animals. A similar increment in plasma epinephrine levels (75 +/- 15 to 475 +/- 60 pg/ml) caused glycerol levels to rise by 82% (105 +/- 23 to 191 +/- 26 mumol/L) in 30 min, but this rise was not sustained and the level fell to 146 +/- 14 mumol/L by 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 May
PMID:Regulation of ketogenesis by epinephrine and norepinephrine in the overnight-fasted, conscious dog. 388 59


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