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

Clinical diabetic nephropathy in man is the consequence of the development of a specific constellation of glomerular, tubular, vascular, and interstitial structural abnormalities accompanied by highly characteristic immunohistochemical alterations that, together, are unique to diabetes. Because changes resembling the specific pathology of diabetes do not develop in patients with conditions that lead to long-standing glomerular hyperfunction (such as unilateral nephrectomy), it is unlikely that glomerular hemodynamic abnormalities per se can be the cause of diabetic nephropathy. Whether hemodynamic abnormalities represent a risk factor that, in the presence of the diabetic state, can accelerate the rate of development of the basic lesions of diabetic nephropathy is currently unclear. However, there is considerable evidence that when the renal lesions of diabetes are far advanced, factors such as systemic hypertension can determine the rate of renal functional deterioration in diabetes as in other disorders. Although the diabetic rat may be a useful model for the study of aspects of the pathogenesis of diabetic nephropathy, much confusion has resulted from the inclusion of focal segmental glomerular sclerosis as a diabetic lesion. Similarly, the acceptance of all increases in urinary protein excretions in this model as resulting from or reflecting of diabetic nephropathology can be misleading. It is concluded that treatment aimed at manipulating renal hemodynamics in diabetic patients without evidence of renal disease should remain in the realm of clinical research.
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PMID:An overview of renal pathology in insulin-dependent diabetes mellitus in relationship to altered glomerular hemodynamics. 146 81

36 patients with insulin-dependent diabetes mellitus who had 'Albustix'-negative urine but raised urinary albumin excretion (30 to 300 mg/24 h) were randomly assigned to either remaining on conventional insulin treatment or continuous subcutaneous insulin infusion and followed up for 2 years. The insulin-infusion group showed a significant, sustained improvement in metabolic control, with a median glycosylated haemoglobin of 7.2% (range 5.9-8.8), but there was no change in the conventional-treatment group (median 8.6%, range 7.2-13.4) (p less than 0.001). Clinical diabetic nephropathy (a urinary albumin excretion rate above 300 mg/24 h in at least two of three 24 h urine collections) developed in 5 patients in the conventional-treatment group, but not in the insulin-infusion group (p less than 0.05, two-tailed). Fractional albumin clearance (mean and range X 10(7] increased in the conventional-treatment group from 160 (35-468) to 360 (29-1580) and was unchanged in the insulin-infusion group (170 [31-608] before to 160 [26-460] after) (p less than 0.05). Insulin infusion had an overall beneficial effect on the annual increase in urinary albumin excretion (p less than 0.05), and the mean glycosylated haemoglobin values correlated positively with annual change in albumin excretion (r = 0.57, p less than 0.0001). The diastolic blood pressure rose significantly in the conventional-treatment group (p less than 0.001), and annual change in mean blood pressure correlated with change in urinary albumin excretion (r = 0.49, p less than 0.001).
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PMID:Effect of two years of strict metabolic control on progression of incipient nephropathy in insulin-dependent diabetes. 287 75

A follow-up of 1475 Type 1 (insulin-dependent) diabetic patients diagnosed before 1953 (815 males, 660 females) and before the age of 31 years was conducted. All patients were seen at the Steno Memorial Hospital and were referred from all parts of Denmark; 91 (6%) could not be traced. The rest (94%) were followed until death or for at least 25 years; 249 (17%) were followed for greater than 40 years. Clinical diabetic nephropathy developed in 531 (41%) of the 1303 patients in whom sufficient information was available regarding proteinuria. Other causes of proteinuria were found in 3%, and 57% did not develop persistent proteinuria. The prevalence of diabetic nephropathy was 21% after 20-25 years of diabetes duration followed by a decline to 10% after 40 years. Two incidence peaks of the onset of proteinuria were seen, one after 16 and another after 32 years duration of diabetes and was low after 35 years duration. The cumulative incidence was 45% after 40 years of diabetes. A male preponderance was seen among patients with nephropathy. A significant difference in the pattern of annual incidence rates of diabetic nephropathy was seen, when groups with onset of diabetes before 1933, between 1933-1942, and 1943-1952, respectively, were compared. An association between daily insulin requirement and nephropathy incidence was found. Patients with nephropathy had a much poorer survival than those without proteinuria; 40 years after onset of diabetes, only 10% of patients who developed nephropathy were alive, whereas greater than 70% of patients who did not develop nephropathy survived.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic nephropathy in Type 1 (insulin-dependent) diabetes: an epidemiological study. 2269 35

Clinical diabetic nephropathy is a well-recognized cause of increased morbidity and mortality in patients with type 1 diabetes. The finding that microalbuminuria predicts progression to overt nephropathy has allowed early diagnosis and preventive interventions. Several studies have demonstrated that treatment with angiotensin-converting enzyme (ACE) inhibitors slows down the rate of decline of the glomerular filtration rate in type 1 diabetes patients with established proteinuria. The renoprotective properties of the ACE inhibitor captopril extend beyond its antihypertensive effects. ACE inhibitors represent the most appropriate class of antihypertensive drugs for treating type I diabetes patients because of their efficacy and safety. When microalbuminuria is detected and confirmed in a diabetic child or adolescent, and if it persists despite 6-12 months of improved metabolic control, treatment with ACE inhibitors should be started, even if the child is normotensive. Careful follow-up of renal function is essential.
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PMID:Diabetic nephropathy in children and adolescents: a critical review with particular reference to angiotensin-converting enzyme inhibitors. 982 93

Diabetic nephropathy is becoming an increasingly important cause of morbidity and mortality worldwide owing to the increasing prevalence of type 2 diabetes, largely driven by increasing obesity. There is considerable evidence that obesity, hypertension and other elements of the metabolic syndrome also contribute to the progression of renal disease independent of diabetes. How they interact and contribute to diabetic nephropathy, however, is not completely understood. Clinical diabetic nephropathy is preceded by an increase in glomerular filtration rate, microalbuminuria and glomerular hypertrophy. Poor glycemic control and elevated systolic blood pressure exacerbate proteinuria and renal injury that may culminate in end-stage renal disease. A similar sequence of events may lead to obesity-related renal disease even in the absence of diabetes. This chapter compares and contrasts factors involved in the development of glomerular hemodynamic and kidney pathological processes associated with diabetes and obesity.
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PMID:Obesity, metabolic syndrome and diabetic nephropathy. 2165 55