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

The prevalence of microalbuminuria and persistent proteinuria was studied in a population of 801 diabetic patients (535 with type II and 266 with type I diabetes). Urinary albumin excretion rate (AER) was measured on morning samples by laser nephelometry. Normoalbuminuria, as defined, in the absence of contaminated urine, by an albumin: creatinine (A/C) ratio below 2, was found in 551 patients, microalbuminuria (NC greater than or equal to 2 with AER below 200 mg/l) in 190 patients and persistent proteinuria (AER greater than or equal to 200 mg/l) in 60 patients. Microalbuminuria was present in 48 (18 p. 100) IDDM patients and 142 NIDDM patients. In IDDM patients, AER increased with the duration of the disease with no apparent influence of age at the onset. The prevalence of hypertension was 25 p. 100 and 61 p. 100 in IDDM patients with microalbuminuria and macroproteinuria respectively versus 10 p. 100 in patients with normoalbuminuria. This prevalence increased in NIDDM patients from 39.3 p. 100 with normoalbuminuria to 40.8 p. 100 and 76.2 p. 100 with microalbuminuria or macroproteinuria respectively. Proliferative retinopathy in type I and type II patients with normal AER was 7.4 p. 100 and 1.2 p. 100 respectively increasing to 15.2 p. 100 and 8.9 p. 100 with microalbuminuria and 27.8 p. 100 and 23.1 p. 100 with macroproteinuria. The prevalence of coronary disease increased from 4 to 10.4 p. 100 in patients with type I diabetes and microalbuminuria. The prevalence of cardiac failure increased from 1.5 to 2.1 p. 100 in type I diabetics and from 3.2 to 7.8 p. 100 in type II diabetics in the presence of microalbuminuria. Patients with microalbuminuria had increased levels of glycosylated hemoglobin A 1C but statistical difference was only obtained for patients with type II diabetes. Routine analysis of AER in diabetics allows early detection of diabetic nephropathy and emphasizes the need for tight metabolic and blood pressure control. Hypertension can be detrimental to nephropathy but might also initiate renal lesions in NIDDM patients.
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PMID:[Microalbuminuria and diabetic nephropathy. Detection and correlation with other degenerative complications]. 214 8

Coagulation-fibrinolytic system is known to be one of the exacerbating factors in patients with diabetic nephropathy. The aim of the present study was to evaluate whether coagulation-fibrinolytic system in patients with diabetic nephropathy were significantly correlated with the development of this disease using new parameters of plasma thrombin antithrombin III complex (TAT) and plasmin alpha 2 plasmin inhibitor complex (alpha 2PIC). Fifty-six patients with NIDDM were examined. None of these patients showed more than 1.3 mg/dl of serum creatinine levels. These patients were divided into three groups according to the levels of albumin creatinine ratio (ACR) in urine as follows: 1) group I had ACR of less than 30 mg/g.Cr; 2) group II had ACR of greater than 30 mg/g.Cr and less than 100 mg/g.Cr; 3) group III had ACR of greater than 100 mg/g.Cr. Correlations of levels of plasma TAT and alpha 2PIC, levels of HbAlc, duration of diabetes, and presence of retinopathy were determined in these groups. The levels of plasma TAT and alpha 2PIC increased as the levels of urinary ACR increased regardless of presence of retinopathy. The levels of TAT and alpha 2PIC with retinopathy increased compared with those without retinopathy. There was a significantly positive correlation between plasma TAT and alpha 2PIC (r = 0.52, p less than 0.01). The levels of HbAlc and duration of diabetes did not significantly correlate to plasma TAT and alpha 2PIC. These data suggest that the existence of increase in coagulation-fibrinolytic system seem to be one of the exacerbating factors in patients with diabetic nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on coagulation-fibrinolytic system in diabetic nephropathy--with reference to plasma TAT and alpha 2PIC]. 214 99

The life expectancy and quality of life of diabetic patients are largely determined by the long-term complications. Convincing evidence exists to show that the complications are secondary to the altered internal milieu caused by inappropriate insulin action--insulin deficiency in type 1 diabetes and insulin resistance in type 2 diabetes. Genetic factors play only a minor role in the process with the exception of diabetic nephropathy. Of the many metabolic disturbances present in diabetes hyperglycaemia seems to be the most important in this respect. Long-term it has a cumulative effect on the development of background retinopathy in the whole diabetic population and a similar effect on diabetic nephropathy in a genetically predisposed subset. The role of hyperglycaemia in the pathogenesis of macroangiopathy is less clear. Since diabetic microangiopathy is not related to diabetes itself but is secondary to its metabolic consequences, it is--at least in principle--preventable. That this is true has been shown in animal experiments but it has not been proved in human diabetes. There is, however, much evidence suggesting that the incidence of diabetic complications may be diminished when diabetes is well controlled. When the known facts about the rise and fall of the diabetic complications are taken into account the treatment of hyperglycaemia remains as one of the most essential aspects of managing diabetic patients.
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PMID:Why should we treat hyperglycaemia? 239 56

Diabetic renal disease is a major source of morbidity and mortality in Pima Indians. Excess mortality in NIDDM occurs principally in those with proteinuria regardless of whether death is due to cardiovascular or renal disease. Diabetes duration is a strong predictor of diabetic renal disease. Additional predictors include blood pressure, severity of diabetes, and, most likely, genetic or shared environmental determinants. The incidence rate of diabetic renal disease in Pima Indians with NIDDM is similar to that reported for subjects with IDDM with equivalent durations of diabetes. These observations suggest that clinical proteinuria and renal failure may occur in patients with NIDDM just as frequently as in those with IDDM. This finding has important implications and suggests that the variations in the frequency and age of onset of NIDDM among different populations and ethnic groups may be primarily responsible for the apparent variations in the frequency of ESRD associated with diabetes in different populations. Furthermore, diabetic renal disease appears to account for virtually all of the excess mortality associated with diabetes among Pima Indians and may perhaps do so in other populations. Improved survival of persons with NIDDM, an increasing incidence of this disease, and a relatively early age of onset in many populations could lead to a dramatic increase in the incidence of ESRD in the future. On the other hand, if diabetic renal disease and its consequences could be prevented, a profound improvement in the longevity and quality of life of those afflicted with diabetes might be possible.
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PMID:Diabetic renal disease in Pima Indians. 260 4

Many areas of information in the epidemiology of diabetic nephropathy are lacking, but multiple studies designed specifically to answer these questions are currently being conducted. In the next 5-10 years, our current understanding of the epidemiology of diabetic nephropathy may either be confirmed or discredited. In the meantime, clinicians should use the data available to make decisions about treatment and should focus on the modifiable factors of glucose and blood pressure control in both IDDM and NIDDM, especially in patients with low-level albuminuria or clinical proteinuria.
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PMID:The epidemiology of diabetic nephropathy. 268 17

Both early onset and late onset type II diabetes were present in one family of nine siblings. The three early onset type II diabetic siblings showed severe microvascular complications: proliferative retinopathy, diabetic nephropathy, and peripheral neuropathy. Early onset type II diabetes was not associated with any particular HLA haplotype. Early onset type II diabetes could be considered a clinical and genetic disease entity different from MODY type diabetes.
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PMID:Severe microvascular disease in type II diabetes of early onset. A family study. 275 Apr 46

We studied the profile of nephropathy in 250 patients, 177 males and 73 females, with type 2 diabetes mellitus. The mean age was 55.9 +/- 8.8 years. Therapy for control of diabetes included diet alone in 1.6%, oral hypoglycaemic agents in 90.6% and insulin in 7.8%. Glycaemic control was satisfactory in 4.8%, fair in 41.2% and poor in 54.0%. Blood sugar values were normal without any therapy in 33 out of the 206 patients (16%) after the onset of renal insufficiency. The mean interval between the onset of diabetes and the appearance of proteinuria was 9.5 +/- 7.05 years. Proteinuria appeared within one year in 23 patients (9.2%), 1-5 years in 32 (12.8%), 6-10 years in 86 (34.4%) and more than 10 years in the remaining 109 patients (43.6%). Proteinuria was of nephrotic range in 17.6% of patients. Renal insufficiency was present in 206 (82.4%) patients and occurred 10.5 +/- 7.5 years after the detection of diabetes. Hypertension was present in 61.2% and was first detected 7.5 +/- 7.4 years after onset of diabetes. Endstage renal disease occurred 11.8 +/- 6.8 years after the onset of diabetes mellitus. Thus, clinical evidence of diabetic nephropathy is present in most patients with type 2 diabetes mellitus within a decade after the detection of diabetes. Subsequent progression to end-stage renal failure is rapid in the face of poorly controlled hypertension and hyperglycemia in the economically poor countries.
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PMID:Nephropathy in type 2 diabetes mellitus in Third World countries--Chandigarh study. 278 52

The purpose of this study was to determine the occurrence and severity of diabetic retinopathy and to clarify its association with the duration of diabetes and several other factors in an outpatient diabetic population. The material consisted of 328 diabetics, mainly (77%) C-peptide negative, type 1 diabetics. The mean age of the patients was 45 years, and the mean duration of diabetes was 15 years. Retinal changes were assessed by ophthalmoscopy and widefield fundus photography. All retinopathy was confirmed in 59% and proliferative retinopathy (PR) in 20% of the patients. The frequency of diabetic retinopathy was 15% in patients with diabetes for less than five years but 100% in those with diabetes for 30 or more years. In type 1 diabetics PR was seen only after 10 or more years' duration but, after 20 years' duration it was seen in half of the patients with type 1 and in one-third of the patients with type 2 diabetes. The patients with diabetic nephropathy often had PR. In type 1 diabetics with onset of the disease less than 30 years peripheral sensory neuropathy, coronary disease, hypertension and leg-vessel disease were also often associated with PR. Because one reason for visual handicapping in diabetes is the delay of the diagnosing of vision-threatening lesions screening for treatable retinopathy should be intensive after 10 years' duration and in poorly-controlled diabetics even earlier.
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PMID:Predicting diabetic retinopathy. 283 48

We examined clinical and laboratory features retrospectively in 402 patients at the start of chronic hemodialysis in order to define better the "uremic syndrome" in the dialysis era. The information gathered included demographic data, renal diagnoses, uremic symptoms, biochemical values, and prevalences of hypertension (69%), diabetes mellitus (23%) and ischemic heart disease (16%). Unexpected findings were the wide ranges of serum creatinine levels (3.5 to 35 mg/dl) and blood urea nitrogen levels (35 to 345 mg/dl), and the frequency of hyponatremia (27%), hypoalbuminemia (52%), and anion gaps above 25 mg/dl (5%). There were higher hematocrits in males and diabetics, lower serum creatinine levels in females, diabetics and older patients, and lower blood urea nitrogen levels in blacks. The time interval from diagnosis of diabetes mellitus to initiation of dialysis in patients with diabetic nephropathy due to juvenile-onset diabetes mellitus (20.6 +/- 6.8 years) was twice that in adult onset diabetes mellitus (10.3 +/- 8.3 years).
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PMID:Clinical and laboratory features of patients with chronic renal disease at the start of dialysis. 292 Apr 71

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


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