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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic nephropathy, clinically defined by overt albuminuria, hypertension and declining GFR, affects 25-35% of IDDM patients. The risk of nephropathy peaks during the second decade of IDDM and declines thereafter, suggesting that only a subset of IDDM patients is at risk for nephropathy. A role for hypertension in the progression of established renal damage in IDDM is now accepted; however the role of hypertension in the genesis of diabetic nephropathy is not yet clear. Mesangial expansion is a characteristic lesion of diabetic nephropathology and correlates with renal function. Functional studies are not indicative of underlying renal pathology except relatively late, when glomerular injury is advanced. Microalbuminuria in the 'predictive' range (greater than 30 micrograms/min) and associated with hypertension and/or declining GFR is a marker of established diabetic glomerulopathy. Only carefully designed longitudinal studies of renal morphology and function with accurate blood pressure monitoring beginning early in the course of IDDM will clarify the relationships between blood pressure and renal damage in IDDM. In NIDDM the frequent presence of non-diabetic renal lesions, of hypertension at or before the onset of diabetes, and the relative paucity of clinical-pathological correlations currently make it difficult to understand the role of hypertension in the genesis and progression of nephropathy. Again, longitudinal studies of blood pressure and renal structure and function are required in NIDDM patients. Finally, animal models of hypertension and diabetes may aid progress in these areas.
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PMID:Hypertension and diabetic renal disease. 179 13

In a study over one year, it was observed that mortality amongst hospitalised patients with non insulin dependent diabetes mellitus (NIBDM) was nearly 20%. Those dying within 24 hr were classified as group A, between one day and one week as B, between one week and one month as C, and those after one month as D. There were 31 patients each in groups A and B, 14 in C, and 4 in D. The mean age at death was 61 years in the first three groups. The prevalence of cerebro-vascular accident as a terminal event was similar i.e. 32.2, 35.5 and 35.7 per cent in groups A, B and C respectively; 48% of patients in group A suffered from ischaemic heart disease. Diabetic ketoacidosis was equally prevalent amongst groups A, B and C. Infection was significantly more common in group B (45.2%) than A (P less than 0.05). Nephropathy was observed in 57% of patients in group C as compared to 22.5% in A (P less than 0.02). Cerebrovascular accident and infection were the major causes of mortality in groups B and C (80.7% and 71.4%), whereas ischaemic heart disease and cerebrovascular accident accounted for 80% of deaths in group A.
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PMID:Mortality events amongst non insulin dependent diabetes mellitus patients in Orissa. 180 Apr 90

In type 2 diabetes elevated glomerular filtration rate (GFR) and increased renal volume (RV), often accompanied to normo or microalbuminuria, were demonstrated. This condition is considered a pathogenetic factor for clinical nephropathy. As this topic is little studied in type 2 diabetes, we have investigated 73 type 2 diabetic patients (34 normo and 39 microalbuminuric), looking for a correlation between GFR, RV, hypertension, duration of diabetes and indexes of metabolic control. GFR was measured by a scintigraphy, after infusion of 99Tc-DTPA. Renal volume was determined by ultrasound scanning. Between the groups GFR and RV weren't different; elevated GFR was demonstrated in 3 patients; increased RV in 1 patient. In the hypertensive group GFR was lower than in normotensive group and in controls. Multivariate analysis in stepwise demonstrated that GFR presents a negative correlation to systolic blood pressure as in normo as in microalbuminuric patients. In the normotensive group GFR didn't correlate to the other variables. The present data suggest that in type 2 diabetes there is a little prevalence of glomerular hyperfiltration and increased renal volume and that hypertension plays a role on GFR of hypertensive diabetic patients.
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PMID:[Glomerular filtration and renal volume in type II diabetes (non-insulin-dependent): study in normal and microalbuminuria patients]. 180 4

A prospective study to determine if subcutaneous edema interferes with insulin absorption was performed. Forty-six patients entered the study. Three groups were formed. Twenty patients with generalized edema (Group 1), ten of them with non-insulin dependent diabetes mellitus (NIDDM). Twenty patients without edema (Group II). 10 of them with NIDDM; and six patients with mild edema (Group III). The disappearance of I125-insulin was measured throughout 360 minutes. The rate of absorption in group I was significantly lower and delayed than in group II. The amount of insulin absorbed at 360 minutes was 3 to 4 fold lower in group I than in group II (p 0.001). Group III had intermediate values. The peak of plasma I125-insulin level was 3 to 4 fold lower in group I than group II. The impairment of insulin absorption in subjects with edema was more evident in those with NIDDM. In conclusion, this study demonstrates that subcutaneous edema impairs insulin absorption. Insulin absorption from subcutaneous tissue varies due to several conditions, resulting in a difficult glycemic control. Previous studies have shown that insulin absorption is affected by several factors as the site of injection, room and skin temperature, physical exercise, the thickness of adipose tissue, local massage, and local degradation of insulin. Edema due to chronic complications such as nephropathy and cardiopathy often occurs in long-standing diabetic subjects. However, the effects of edema of the skin and subcutaneous tissue on insulin absorption has not been previously examined. The aim of this study was to assess if edema affects the absorption of insulin.
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PMID:Delayed insulin absorption due to subcutaneous edema. 181 99

To determine the effectiveness of dietary protein restriction on proteinuria in patients with non-insulin dependent diabetes (NIDDM), 14 diabetic patients with overt nephropathy were placed on either a low protein diet (N = 7) or conventional protein diet (N = 7) for one month. After the study period, daily urinary protein excretion rates decreased significantly, from 3.2 +/- 0.4 to 1.9 +/- 0.4 g/day, and serum albumin levels increased from 3.3 +/- 0.2 to 3.7 +/- 0.5 g/dl only in the low protein diet group, without any significant changes in either serum creatinine levels or creatinine clearance. These findings suggest that dietary protein restriction has a beneficial role in the treatment of NIDDM patients with overt nephropathy.
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PMID:Effect of dietary protein restriction on proteinuria in non-insulin-dependent diabetic patients with nephropathy. 182 Apr 50

Albumin excretion rate measured by new immunoassays and semiquantitative tests is advocated as a means for early detection of diabetic nephropathy. We determined albumin excretion rate in 276 patients. Albumin excretion rate was normal in 66%, within the microalbuminuric range in 27%, and within the macroproteinuric range in 7%. Significant predictors of albumin excretion rate included presence of hypertension and glycosylated hemoglobin level in type I diabetes mellitus, and years since diagnosis in type II diabetes mellitus. A semiquantitative test was deemed to be of limited diagnostic value. We conclude that testing for early diabetic nephropathy in routine clinical practice gives valuable information and that determination by a quantitative immunoassay based on a single 24-hour urine sample is preferable. The optimal frequency of screening and the levels that determine progressive renal disease have yet to be established.
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PMID:Microalbuminuria in clinical practice. 188 40

Treatment of hypertension in patients with NIDDM should be administered with special attention not to increase insulin resistance nor to impair insulin secretion capacity. The coexisting risk for coronary artery disease and myocardial infarction should not be increased by undesired drug effects on the plasma lipoprotein profile. Late lesions of diabetes mellitus (nephropathy, neuropathy) have also to be taken into account. Consequently angiotensin converting enzyme inhibitors, if necessary combined with calcium channel blockers, should be administered first. If blood pressure is thus not sufficiently controlled, alpha-adrenergic blockers, vasodilating agents or sympatholytics may be added. Once insulin treatment is installed, or if required for other reasons (nephropathy, congestive heart failure, cardiac arrhythmia), also diuretics and beta-adrenergic blockers are indicated in antihypertensive treatment of diabetic patients.
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PMID:[Hypertension in type II diabetes mellitus]. 195 Mar 78

Blood pressure is generally normal in insulin-dependent diabetic patients in the absence of nephropathy. Despite this, exchangeable sodium is increased. Blood pressure rises with the development of incipient nephropathy, and hypertension is common in patients with overt nephropathy. Exchangeable sodium is then markedly increased, but plasma renin is not suppressed. Raised BP in diabetic nephropathy is probably sustained, in part at least, by sodium retention and inappropriate activity of the renin-angiotensin system. There is an increased prevalence of hypertension among patients with non-insulin-dependent diabetes (NIDDM). In normotensive patients, exchangeable sodium is elevated and plasma renin is suppressed. In hypertensive patients, exchangeable sodium is less markedly increased, while plasma renin is again suppressed. These findings are in contrast with those in diabetic nephropathy, and are in keeping with the hypothesis that hypertension in NIDDM is usually due to coexisting essential hypertension. Also in keeping with this suggestion is an increased prevalence of raised BP among the siblings of NIDDM patients. Prolonged hyperinsulinaemia precedes the diagnosis of NIDDM, and hypertension is often present at the time of diagnosis. Insulin resistance and compensatory hyperinsulinaemia might lead to an increase in BP by a number of putative mechanisms, such as enhancing renal sodium retention, by an effect on cell membrane ion exchange mechanisms or by enhancing activity of the sympathetic nervous system. This seems a fertile area for further research, although a causal link between insulin resistance and hyperinsulinaemia on the one hand, and raised BP on the other, remains to be proved.
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PMID:The causes of raised blood pressure in insulin-dependent and non-insulin-dependent diabetes. 195 22

NIDDM and hypertension are both characterized by insulin resistance and/or hyperinsulinemia. In IDDM, factors associated with nephropathy produce hypertension. To avoid exacerbation of the metabolic condition, and to prevent further deterioration in glycemic control, treatment of hypertension in the diabetic patient should include the administration of medication with the fewest adverse effects on glucose homeostasis. If diuretics are to be used, it appears that loop diuretics may be preferable to the thiazides or potassium-sparing compounds. Among the remaining classes of antihypertensive drugs, ACE inhibitors may be the agents of choice because of their potential positive effects on insulin sensitivity and renal function, and their lack of severe adverse side-effects.
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PMID:Insulin sensitivity and blood lipids during antihypertensive treatment with special reference to ACE inhibition. 197 44

Non-insulin-dependent diabetes mellitus (NIDDM) is a common disorder occurring in 3-6% of adults in most western populations. In the United States, 29% of patients with diabetes take insulin; of these, 76% have NIDDM. Insulin therapy is usually required at some time in NIDDM. Insulin therapy improves the abnormalities of NIDDM (reduced beta-cell function, increased hepatic glucose production, reduced peripheral glucose disposal, lipid abnormalities). Insulin and sulfonylurea agents have comparable effects on mild forms of NIDDM, but for more severe forms, insulin is usually superior. Combination insulin-sulfonylurea treatment may improve the response to sulfonylureas, although long-term well-controlled trials have not been conducted. Short-term insulin treatment may restore response to sulfonylureas. Other promising treatments (human proinsulin, nasal insulin, somatostatin) have not shown any advantage over conventional insulin therapy. Insulin causes hypoglycemia and peripheral hyperinsulinemia. The hazards of hyperinsulinemia, e.g., weight gain and hypoglycemia, have been overstated, and questions about its atherogenic effects remain to be resolved. The effect of glycemic control on macro- and microvascular complications has not been established; however, maintaining fasting blood glucose levels of less than 6.7 mM may protect against progression of retinopathy, neuropathy, and nephropathy and reduce the severity of ischemic stroke. Dosage algorithms generally use intermediate- or long-acting insulin to control basal glycemia, with regular insulin added before meals if needed to control postprandial glycemia. Effective therapy depends on the patient being informed, cooperative, and willing to self-monitor blood glucose. Insulin treatment intermittency increases the risk for immune complications (resistance and allergy). Overall, patients with NIDDM can benefit from insulin therapy.
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PMID:Treatment of NIDDM with insulin agonists or substitutes. 198 Apr 53


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