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

Reports of renal replacement therapy in diabetes usually refer to patients with insulin-dependent diabetes mellitus (IDDM) only, and little is known about renal failure in non-insulin-dependent diabetics (NIDDM). A high proportion, 46/141 (32%), of the diabetics treated at our unit since 1974 had NIDDM. They were older at treatment (56 +/- 9 years, mean +/- SD) compared to the IDDM patients (39 +/- 10 years, p less than 0.001), and had a shorter duration of diabetes (13 +/- 8 years versus 23 +/- 8 years, p less than 0.001). Asians and Afro-Caribbeans accounted for 48% of the NIDDM patients (22/46) compared to only 7% of those having IDDM (6/95, p less than 0.0001). Non-diabetic renal disease accounted for the renal failure in 32% (15/46) of the NIDDM patients but only in 10.5% (10/95) of the IDDMs (p less than 0.001). Despite these differences the prevalence of other diabetic complications (retinopathy, neuropathy, and cardiovascular disease) was similar. Patient survival after transplantation was poorer in NIDDM than IDDM (23% and 57%, respectively, at 2 years). Survival on dialysis was equally poor in NIDDM and IDDM. Thus, NIDDM patients treated for renal failure are more commonly non-European and more often have non-diabetic renal disease. Yet other diabetic complications occur to the same extent in both IDDM and NIDDM patients with diabetic nephropathy.
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PMID:Non-insulin-dependent diabetes and renal replacement therapy. 296 85

Diabetic nephropathy, a rarely listed cause of end-stage renal failure (ESRF) among patients starting renal replacement therapy (RRT) in the early seventies, has progressively gained in importance and become one of the major reasons for the continuous growth of the patient population on RRT in most European countries. Amongst new patients commencing RRT in 1985, the acceptance rate varied between 3 and 12 per million population for type I diabetes mellitus and between one and four per million population for type II diabetes mellitus. Nordic countries, particularly Sweden and Finland, had the highest acceptance rate of young patients with type I diabetes mellitus whose median ages were 38-42 years. In most central and southern European countries the median age of patients with type I diabetes mellitus varied between 50 and 58 years. The high number of young patients with type I diabetes mellitus and ESRF in Nordic countries point to a different natural history of this disease. It cannot be excluded, however, that the higher median age in other countries might result from doctors mistakenly diagnosing type I disease in patients with type II disease who need insulin treatment. Patients with type II diabetes mellitus had a similar age distribution at start of RRT throughout Europe and their median ages clustered around 60 years in most countries. The contribution of haemodialysis, peritoneal dialysis and renal transplantation was analysed for diabetic compared to non-diabetic ESRF. Despite large geographical differences in the proportional use of methods of treatment, a general trend to apply CAPD more frequently in diabetic as compared to non-diabetic patients was observed, and this was true for countries with both predominant haemodialysis and predominant transplant programmes. Transplantation without prior dialysis was performed in 17% of Swedish and 30% of Norwegian patients with type I diabetes mellitus. In order to better explain the mortality of patients with diabetic ESRF, the proportional distribution of causes of death was analysed. Myocardial ischaemia and infarction was confirmed to be the leading cause of death in patients with diabetes mellitus on RRT. The coronary death rate was estimated to be 10 times greater in young patients with type I diabetes mellitus as compared to their non-diabetic counterparts. Other cardiovascular as well as infectious causes were recorded in a similar proportion of deaths in diabetics as in non-diabetics. Cancer deaths, however, appeared to be definitely less frequent in patients on RRT due to diabetic nephropathy.
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PMID:Renal replacement therapy in patients with diabetic nephropathy, 1980-1985. Report from the European Dialysis and Transplant Association Registry. 314 13

An epidemic of renal disease is occurring among the Zuni Indians in western New Mexico. In 1985, 1.6% of Zunis had clinically recognized renal disease and 1% had renal insufficiency. The incidence of end-stage renal disease (ESRD) in 1984 and 1985 was 14 times the rate for US whites, and three times the rates of other Indians in ESRD network 6. One third of the cases of renal disease and ESRD is due to type 2 diabetes, but the etiology of disease in most of the remainder is unknown. Affected subjects range from early childhood to old age. Early signs are hematuria, mild to moderate proteinuria, normal BP, and low total hemolytic complement, normal or low C3 and C4 levels, in about 40% of the cases. The clinical course varies from benign to rapidly progressive renal failure. Biopsies usually reflect an immune-complex mediated mesangiopathic glomerulonephritis, with IgA, IgG, IgM, and C3 variably present in the mesangium. In some cases, there is a very strong familial pattern suggesting autosomal dominant inheritance or a marked communal exposure effect. This may be a genetic disease educed by the consanguinity in the ethnically homogeneous Zuni population. Mesangiopathic renal disease is common in some Oriental populations, and this phenomenon may reflect the American Indians' Oriental ancestry. This disease may also be due to toxic exposures related to jewelry-making, potting, Zuni water, Zuni salt, or herbal or other products used for medicinal or religious purposes. This epidemic is much morbidity and generating huge costs for ESRD treatment. Further study is needed to better understand its etiology.
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PMID:Epidemic renal disease of unknown etiology in the Zuni Indians. 359 94

Diabetic nephropathy is a progressive renal disease and represents a serious late complication of diabetes. There are familial clustering and huge ethnic differences in the occurrence of diabetic nephropathy, which point to a genetic predisposition. Diabetic nephropathy is defined by persistent albuminuria (albumin excretion rate [AER] > 300 mg/day), declining glomerular filtration rate and rising blood pressure. Several years of incipient nephropathy, characterized by worsening microalbuminuria (AER 30 to 300 mg/day or 20 to 200 micrograms/min), which is Albustix-negative and detectable by special assays only, are followed by established nephropathy. The natural history of nephropathy differs between insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. In IDDM, nephropathy develops in 30 to 40% of cases. The incidence peaks after 15 to 16 years of diabetes. In NIDDM, estimates of prevalence range from 15 to 20%, and nephropathy often supervenes after a shorter known duration of diabetes than in IDDM. GFR is often increased above normal (hyperfiltration) from the onset of IDDM due to increased renal blood flow, glomerular capillary hypertension and increased filtration surface. The glomeruli are hypertrophied and the kidneys enlarged. In both IDDM and NIDDM, GFR begins to decline irreversibly, when AER has risen to 100 to 300 mg/day at an average rate of 10 ml/min. per year. This is due to progressive reduction of the filtration surface area through mesangial expansion. Serum creatinine levels begin to rise when GFR falls below 50 ml/min, and then end-stage renal failure follows after an average of five years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic nephropathy: significance of microalbuminuria and proteinuria in Type I and Type II diabetes mellitus]. 749 50

At present we are able to disclose diabetic nephropathy in the very early stages, i.e. when urinary albumin excretion is only slightly increased (20-200 micrograms/min = microalbuminuria). Good blood glucose control and active antihypertensive treatment may stop or retard the further development towards renal failure. Angiotensin-converting-enzyme (ACE)-inhibitors seem to have a renoprotective effect. In this article we suggest guidelines for the use of ACE-inhibitors in patients with type 1 diabetes and early diabetic nephropathy. Special concerns are included in respect of adolescents, pregnant women and persons with type 2 diabetes.
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PMID:[ACE inhibitors and early diabetic nephropathy]. 757 May 36

Islet amyloid polypeptide (IAPP) is the main proteinaceous component of pancreatic islet amyloid, which is a characteristic feature of type 2 diabetes. The factors responsible for amyloid deposition are unclear. Patients with end-stage renal failure (ESRF) on dialysis treatment have increased insulin resistance which is associated with hypersecretion of beta-cell products. Furthermore, elevated concentrations of circulating IAPP are found in these patients due to reduced renal clearance of IAPP. To determine the prevalence of islet amyloid in this group of patients, pancreas was examined from 23 non-diabetic [aged 62 (29-79) years, median and range] and four type 2 diabetic [aged 67 (56-72) years] patients with ESRF on dialysis treatment. Pancreatic specimens from 30 non-diabetic control subjects [aged 67.5 (56-86) years] and 14 type 2 diabetic subjects without renal disease [aged 69 (48-86) years] were used as control groups. Islet amyloid was present in all type 2 diabetic patients with ESRF and in 12 out of 14 type 2 diabetic control subjects (86 per cent). Amyloid deposits were found in 8 out of 23 non-diabetic patients with ESRF (35 per cent), which was a higher prevalence than that found in non-diabetic control subjects (3 per cent) (P < 0.01). This may be related to undiagnosed (pre)diabetes. Elevated secretion rates of IAPP due to insulin resistance and high circulating IAPP concentrations as a result of severely reduced renal clearance of IAPP will cause high pericellular concentrations of IAPP. This condition is likely to enhance amyloid fibril formation in pancreatic islets similar to that observed in type 2 diabetes.
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PMID:High prevalence of pancreatic islet amyloid in patients with end-stage renal failure on dialysis treatment. 773 22

Insulin resistance is the major pathogenetic link of atherosclerosis development and progression. The clinical diagnosis is made on the basis of analysis of glycemic and insulinemic response during the oral glucose tolerance test. Insulin resistance prevalence is constant in NIDDM and advanced renal failure, and almost 50% in early stages of essential hypertension and kidney diseases. Its prevention and therapy are effective. The increase of free Ca and decrease of free Mg concentrations participate both in insulin resistance and hemodynamic changes in diseases of the Reaven's syndrome. The intracellular mineral dysbalance is caused by the alteration of Na+,H(+)-antiporter. (Fig. 1, Tab. 4, Ref. 51.).
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PMID:[Insulin resistance: its clinical importance and trends in modern research]. 781 48

Diabetic nephropathy is the only increasing cause of renal failure in the Western world. It affects a large proportion of both insulin-dependent (IDDM) and non-insulin-dependent diabetic (NIDDM) patients. A critical stage in the development of diabetic renal disease is the onset of microalbuminuria, defined as an albumin excretion rate of 30 to 300 mg/day. Microalbuminuria predicts progression to renal failure and early cardiovascular mortality in both IDDM and NIDDM patients. Microalbuminuria is associated with a constellation of other risk factors for small and large vessel damage which include raised blood pressure, poor glycemic control, plasma lipid and clotting factor abnormalities, left ventricular hypertrophy, and insulin resistance. Treatment with angiotensin-converting enzyme inhibitors corrects microalbuminuria and prevents progression to persistent proteinuria. Good blood glucose control significantly reduces the risk of progression from normoalbuminuria to microalbuminuria. The treatment of microalbuminuria appears highly cost-beneficial and substantially increases life expectancy. The development of microalbuminuria, for which all diabetic patients aged 12 to 70 years should be screened, should alert the physician to set in motion a program of assessment, monitoring, and correction of all risk factors for renal and cardiovascular disease.
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PMID:Prognostic significance of microalbuminuria. 781 38

The association of apolipoprotein E (apo E) genetic polymorphism, particularly apo E2, with renal failure (plasma creatinine > or = 1.4 mg/dl, and urinary albumin excretion index > or = 300 mg/g.creatinine and/or persistent proteinuria) was investigated in 57 non-insulin-dependent diabetic (NIDDM) patients. Apo E2 allele frequency was significantly higher in diabetic patients with renal failure (9.6%) than in diabetic patients without renal failure (3.2%) and in the general Japanese population (3.7%). This finding suggests that apo E2 is associated with renal failure in NIDDM. In addition, to elucidate the association of apo E2 with lipid abnormalities, plasma lipid and lipoprotein levels were compared among the apo E2 (E2/2 and E3/2) and E3/3 groups of NIDDM with renal failure (n = 27) and the apo E2 (E3/2) and E3/3 groups of NIDDM with normoalbuminuria (n = 34). In diabetic patients, the apo E2 group with renal failure had significantly higher levels of plasma total cholesterol (T-chol), very-low-density lipoprotein (VLDL)-chol, triglyceride (TG), VLDL-TG and apo E than the apo E3/3 group with renal failure, and had significantly higher levels of plasma T-chol, VLDL-chol, TG and VLDL-TG than the apo E2 and E3/3 groups with normoalbuminuria. Furthermore, the apo E2 group with renal failure had significantly higher ratios of VLDL-(chol/TG) and VLDL-chol/TG (an index of remnants in plasma) than the apo E3/3 group with renal failure and the apo E2 and E3/3 groups with normoalbuminuria. These results suggest that apo E2 leads to the accumulation of TG-rich lipoprotein and remnants in plasma. It is concluded that apo E2 is associated with renal insufficiency in NIDDM and that apo E2 may be a factor that aggravates lipid abnormalities in NIDDM with renal failure.
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PMID:Apolipoprotein E2, renal failure and lipid abnormalities in non-insulin-dependent diabetes mellitus. 798 Jun 94

1. Renal involvement in non-insulin dependent diabetes mellitus patients is the single most important cause of renal failure. The aim of this study was to evaluate the clinical features and to assess the risk factors for the development of proteinuria by non-insulin dependent diabetic patients. 2. Risk factors (expressed as an odds ratio) were calculated by multiple logistic regression analysis taking into account age, sex, body mass index, known duration of diabetes, presence of arterial hypertension, fasting plasma glucose, cholesterol and triglycerides as independent variables and proteinuria as the dependent variable. Sixty-four normoalbuminuric (24-h albumin excretion rate < 30 micrograms/min, 27 females, mean age 53.7 years) and 53 proteinuric (24-h proteinuria > 0.5 g, 31 females, mean age 59.3 years) were studied. 3. Proteinuric patients were older, with a longer mean known duration of diabetes (12.4 vs 5.6 years), higher mean fasting plasma glucose (214 vs 168 mg/dl) and plasma creatinine (1.5 vs 1.1 mg/dl) and more frequently presented diabetic retinopathy (94% vs 23%), peripheral neuropathy (94% vs 23%) and arterial hypertension (73% vs 16%) than normoalbuminuric patients. Age > 50 years, body mass index > 28.6 kg/m2, known duration of diabetes > 10 years, presence of arterial hypertension, and fasting plasma glucose > 160 mg/dl were significantly and independently associated with development of proteinuria.
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PMID:Risk factors for development of proteinuria by type II (non-insulin dependent) diabetic patients. 813 28


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