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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

The beneficial effects of conventional long treatment on declining renal function in diabetic nephropathy (non-insulin-dependent diabetes mellitus, NIDDM) were evaluated retrospectively. One hundred NIDDM patients with overt proteinuria were followed for more than three years. Clinical data before and after various regimens of treatment were compared statistically. Treatment included a calcium antagonist (CaA), alpha-methyl dopa (AMD), an alpha-blocker (ABL), angiotensin converting enzyme inhibitor (ACEI), anti-platelet agents (APL), essential amino acids (EAA), and an oral absorbent (AST-120). Changes in renal function were analyzed by comparing the degree of slopes of regression rate of the reciprocals of serum creatinine levels (R1/Cr). Administration of ACEI and EAA resulted in R1/Cr improvement after the initiation of treatment (p less than 0.05). It appears that the administration of EAA and ACEI are beneficial with regard to protection against renal failure in NIDDM patients with diabetic nephropathy.
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PMID:Ameliorating effects of conventional therapy on declining renal function in patients with diabetic nephropathy. 181 52

Geographic/population variation in the prevalence of diabetic nephropathy is well recognised. In a study of 'native' Indians, we screened 102 non-proteinuric diabetes mellitus patients (64 NIDDM, 38 IDDM; mean age and diabetic duration 48.7 and 6.5 years, 21.6 and 6.2 years, respectively) with blood pressure less than or equal to 170/105 and without congestive heart failure, ketonuria or urinary tract infection, for the presence of microalbuminuria (albumin excretion rate greater than 20 micrograms/min). Fifty-six patients (34 NIDDM, 22 IDDM) also underwent detailed fundus examination. Seventeen NIDDM (26.6%) and 3 IDDM (7.9%) patients had microalbuminuria. Glycated hemoglobin was significantly higher in microalbuminurics in the NIDDM group (P less than 0.05). Diabetic retinopathy tended to occur more frequently in microalbuminurics (NIDDM and IDDM).
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PMID:The prevalence of microalbuminuria in diabetes: a study from north India. 187 3

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

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

The pathophysiological basis of microalbuminuria is outlined. In a preliminary study (n = 71) and a comprehensive retrospective study over 4 years in type I diabetics (IDDM) (n = 1470) and type II diabetics (NIDDM) (n = 2112), clinical and anamnestic data were compared and the blood pressure, protein excretion, and albumin concentration in the urine were recorded. Early recognition of microalbuminuria in diabetic nephropathy permits successful therapeutic intervention and thus a significant postponement of terminal renal failure.
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PMID:[Microalbuminuria--an early marker of diabetic nephropathy]. 196 88

The pathophysiological connections between insulin resistance, hypertension and type 2 diabetes are discussed in this review article. Increased blood pressure levels are often found in type 2 diabetic patients long before the diabetes itself is diagnosed. By contrast, in type 1 diabetes hypertension is predominantly the consequence of diabetic glomerulopathy. Non-pharmacological strategies should be favoured in the treatment of hypertension in type 2 diabetic patients before specific pharmacological intervention is started. Antihypertensive treatment with beta-blocking agents and diuretics is criticized by many experts in the field of metabolic disorders, since these drugs induce a deterioration of glycaemic control and lipid metabolism in diabetic patients. Since calcium channel blockers, ACE inhibitors and alpha 1-specific blocking agents have no influence on metabolism, these drugs are recommended for the antihypertensive treatment of diabetic patients. Further studies should be undertaken to clarify, whether ACE-inhibitors have a specific nephroprotective effect. Since most type 2 diabetic patients do not develop diabetic nephropathy, a possible nephroprotective effect of ACE inhibitors is only relevant to the antihypertensive treatment of type 1 diabetic patients.
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PMID:[Hypertension, insulin resistance and diabetes mellitus: pathophysiological interactions and therapeutic consequences]. 198 Jul 67

For the early diagnosis of diabetic nephropathy, it is best to use the albumin excretion rate (AER). However, it is a complicated test to perform in the outpatient setting, and it is sometimes affected by inaccurate urine collection. Therefore, we have used the albumin/creatinine ratio, which is measured simply with randomly collected urine, for evaluation of microalbuminuria and found it to be of equal diagnostic value to the AER. The AER, albumin/creatinine ratio, and creatinine excretion rate were measured in 86 patients with NIDDN who were negative for proteinuria. Urine was obtained after bed rest and in the outpatients department (without rest). 1) The reproducibility of time-restricted urine sampling was investigated using the rate of creatinine excretion. The mean coefficient of variation was found to be 42%, and inaccurate urine sampling appeared to cause variation in the AER. 2) The AER and albumin/creatinine ratio obtained in the outpatient setting were higher than those after bed rest, and urine collection at the time of outpatient examination was considered to be more useful than that after bed rest. To check variations in urine collection at the time of outpatient examination, the albumin/creatinine ratio in random urine samples was superior on the basis of the correlation coefficients to urine obtained after bed rest. 3) The urinary creatinine excretion rate showed a significant sex difference (males: 0.823 +/- 0.152 mg/g. creat., females: 0.577 +/- 0.194 mg/g. creat) (p less than 0.001), but there was no significant difference for BMI and age. The relationship between each level of microalbuminuria and the creatinine excretion rate did not change significantly. 4) The following formula was used to calculate the albumin/creatinine ratio corresponding to the AER. Albumin/creatinine ratio formula; (see text) An AER of 30 micrograms/min thus corresponds to an albumin/creatinine ratio of 36 mg/g. creat. for males and 51 mg/g. creat. for females. 5) The percentage of positive results for microalbuminuria in patients with NIDDM showed that the albumin/creatinine ratio and the AER were equal as diagnostic criteria, when the sex difference was taken into consideration. Thus, the albumin/creatinine ratio is equal to the AER for evaluation of microalbuminuria, and it is a simple and convenient test to use in daily clinical practice.
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PMID:[Clinical evaluation of the albumin/creatinine ratio in outpatients with diabetes]. 206 14

Renal involvement was studied in 538 consecutive NIDDM subjects (271 males and 267 females). The mean (SD) age of males was 55.4 (11.0) and of females 51.0 (10.5). Diabetic nephropathy was present in 8.9 per cent of the patients (urinary albumin excretion greater than 200 micrograms/min) and another 19.7 per cent had microalbuminuria (20-200 micrograms/min). Male predominance was striking in the macroalbuminuric group (P less than 0.001). The age of the patients and duration of diabetes in patients with micro and macroalbuminuria were significantly higher as compared to those in normoalbuminuric group (P less than 0.001). Patients with micro and macroalbuminuria had significantly elevated blood sugars and blood pressures (P less than 0.01). The prevalence of vascular complications were found to be higher in the macroalbuminuric group (P less than 0.01). Male sex, older age, longer duration of diabetes, poor glycaemic control and raised blood pressure were significant risk factors in the development of diabetic nephropathy.
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PMID:Prevalence of diabetic nephropathy in non-insulin dependent diabetics. 207 Nov 80

We have studied the long term effects of captopril therapy on proteinuria in ten patients with non-insulin-dependent diabetes mellitus with hypertension and nephropathy. There were 7 males and 3 females, with a mean age of 53.3 +/- 10.6 years. After a run-in period of two weeks, therapy with captopril was started. The following parameters were studied: serum glucose, sodium, potassium, cholesterol and triglycerides, glycosylated haemoglobin, renal function and 24 hour urine protein excretion before and at six month intervals for up to 24 months. Average BP fell significantly from 182.5 +/- 28/95 +/- 7.1 to 146 +/- 16.7/76 +/- 18.1 mmHg although no significant changes were seen in the biochemical parameters studied, except a reduction in 24 hour urine protein excretion from 3.86 +/- 2.85 to 0.88 +/- 1.08 g/24 h after 24 months of treatment (P less than 0.01). No correlation was observed between the reduction in proteinuria and any other parameters studied. Our results confirm the reduction of proteinuria in patients with type II diabetes mellitus and stable diabetic nephropathy treated with captopril. This effect was maintained for a period of 24 months.
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PMID:Long term follow-up of the effect of captopril on severe proteinuria in hypertensive diabetic patients. 209 9


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