Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 78 Chinese patients with clinically uncomplicated non-insulin-dependent diabetes (NIDDM) who had plasma creatinine concentrations of < 150 mumol/l were studied. Antihypertensive treatment was discontinued for at least six weeks prior to measurements of routine biochemistry, proteinuria, plasma atrial natriuretic peptide (ANP) concentrations and components of the renin-angiotensin-aldosterone system (RAAS). BP was measured on three occasions during the six weeks period prior to these measurements. At the end of the six week period, a total of 33 patients had definite hypertension (supine BP > or = 160/95 mmHg). The hypertensive patients had significantly higher plasma sodium (mean +/- SD): 140.3 +/- 1.9 vs. 138.5 +/- 2.0 mmol/l, P < 0.001) and lower plasma potassium (3.8 +/- 0.5 vs. 4.2 +/- 0.5 mmol/l, P < 0.01) concentrations. These were associated with reduced plasma aldosterone (median (range): 297 (98-1145) vs. 448.5 (93-1330) pmol/l, P < 0.01) and renin concentrations (16.8 (7.4-71.8) vs. 23.5 (7.4-83.7) ng/l, P = 0.06). The hypertensive patients also had significantly higher plasma ANP concentrations (36.5 (20.5-125.1) vs. 23.2 (11.7-63.0) pg/ml, P < 0.001), serum angiotensin converting enzyme (ACE) activity (65 (26-140.9) vs. 47 (22-106) units/l, P < 0.001) and urinary albumin excretion (UAE) (35.4 (1.6-4800) vs. 7.8 (1.8-310.4) mg/day, P < 0.001). Glycaemic control and renal function were similar between the two groups. Mean arterial pressure (MAP) correlated positively with plasma ANP concentration (r = 0.53, P < 0.001) and serum ACE activity (r = 0.37, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide and renin-angiotensin-aldosterone system in non-insulin-dependent diabetes mellitus. 808 30

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

The primary results of a three-year prospective, double-blind, placebo-controlled trial in non-insulin-dependent diabetic (NIDDM) patients show that an anti-hypertensive regimen, which includes the ACE inhibitor enalapril, preserves renal function to a greater extent than therapy with antihypertensive agents excluding ACE inhibitors (J Am Soc Nephrol 3:335, 1992). The influence of baseline urinary albumin excretion on the renal protective effects of enalapril treatment in these subjects was the objective of this further analysis. Adequate data were available in 121 patients of the 165 hypertensive NIDDM individuals studied [baseline glomerular filtration rate (GFR) 30 to 100 ml/min/1.73 m2]. Twenty-four hour urinary excretion of albumin (UAE), protein, urea nitrogen, creatinine and isotopically determined GFR were measured at baseline and six month intervals. Glycemic control and blood pressure regulation were assessed every three months. The rate of loss of GFR was significantly greater in patients with overt proteinuria at baseline (UAE > 300 mg/24 hr) as compared to patients with baseline sub-clinical proteinuria (UAE < or = 300 mg/24 hr). Antihypertensive treatment with enalapril preserved GFR significantly better (P < 0.01) in the patients with sub-clinical proteinuria at baseline (UAE < or = 300 mg/24 hr) than other antihypertensive treatments which excluded the ACE inhibitor. Furthermore, only 7% of the enalapril-treated group progressed to clinical albuminuria compared to 21% of control treated patients. Although the enalapril-treated group had a lower mean blood pressure during the maintenance period, no correlation between blood pressure (systolic, diastolic or mean arterial) and rate of change of GFR was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal protective effects of enalapril in hypertensive NIDDM: role of baseline albuminuria. 815 85

In many renal diseases, glomerular thrombosis may play an important role in the development of glomerular sclerosis and progression of renal failure. The aim of this study was to assess the effect of antiplatelet agents on the evolution of patients with chronic glomerular disease. Twenty four patients aged 48 +/- 17 years (21 with idiopathic glomerulonephritis, one with systemic lupus erythematosus and two with type II diabetes mellitus) were treated with aspirin and dipyridamole or aspirin alone during 23.9 +/- 17.5 months. The patients were followed during 31.8 +/- 23 months; seven patients had a progressive deterioration of renal failure requiring dialysis or transplantation (Group A) and 17 had a stable or improving renal function (Group B). Initial serum creatinine was significantly higher in group A than in group B (3.6 +/- 1.6 vs 1.5 +/- 1.5 mg/dl respectively p = 0.003); no other significant differences in the initial assessment were observed between both groups. It is concluded that antiplatelet agents may delay the progression of renal disease when started in patients with normal or slightly deteriorated renal function.
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PMID:[Is it justifiable to use antiplatelet drugs as a universal protection in patients with chronic glomerular damage?]. 824 41

Recombinant human insulin-like growth factor I (rhIGF-I) lowers blood glucose, serum insulin, C-peptide, and lipid levels in healthy and diabetic animals and humans. We hypothesized that rhIGF-I might control blood glucose levels and concomitantly reduce pancreatic insulin secretion in patients with type II diabetes. If true, rhIGF-I might serve as a therapeutic agent that could mitigate some of the detrimental effects of hyperinsulinemia secondary to insulin resistance in these patients. In this study, we treated 12 patients with type II diabetes mellitus twice daily for 5 days with sc rhIGF-I in doses of 90, 120, or 160 micrograms/kg body weight. Metabolic parameters in the fasting and postprandial states were assessed during a 3-day baseline period, the rhIGF-I treatment period, and a 3-day follow-up period, respectively. Administration of rhIGF-I significantly reduced mean (+/- SD) concentrations of fasting blood glucose (12.3 +/- 4.5 to 9.1 +/- 2.6 mmol/L), serum insulin (98 +/- 52 to 56 +/- 27 pmol/L), and C-peptide (993 +/- 298 to 728 +/- 232 pmol/L). It also decreased postprandial (area under the curve) blood glucose (32.5 +/- 12.7 to 23.9 +/- 8.1 mmol/L.h), serum insulin (1102 +/- 707 to 467 +/- 332 pmol/L.h), and C-peptide (5958 +/- 2747 to 3442 +/- 1523 pmol/L.h). The administration of rhIGF-I was also associated with a small but significant reduction in serum triglycerides (6.76 +/- 3.45 to 5.32 +/- 2.59 mmol/L) and total cholesterol (6.13 +/- 1.25 to 5.66 +/- 1.20 mmol/L), 24-h creatinine clearance increased significantly (85 +/- 30 to 133 +/- 51 mL/min), and microalbuminuria was unchanged. Although rhIGF-I was reasonably well tolerated, side effects included low-grade edema, mild and mainly asymptomatic orthostatic hypotension, and bilateral temporomandibular tenderness. We conclude that short-term treatment of type II diabetic patients with rhIGF-I favorably affects metabolic control and enhances kidney function. An assessment of the risk/benefit ratio of rhIGF-I administration to this group of patients awaits extended experiments.
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PMID:Short-term effects of recombinant human insulin-like growth factor I on metabolic control of patients with type II diabetes mellitus. 826 42

Risk factors for contrast nephropathy were prospectively studied in 17 patients with non-insulin dependent diabetes mellitus undergoing cardioangiography. Contrast nephropathy, defined as a serum creatinine increase of greater than 25% at 3 day after angiography, occurred in 29.4% of diabetic patients. Patients who developed contrast nephropathy had significantly higher serum creatinine (Cr), fractional excretion of sodium (FENa), urinary albumin excretion rate (AER), and lower 24hr Ccr than patients who did not (Cr: 1.5 +/- 0.3 mg/dl vs. 0.8 +/- 0.1 mg/dl, FENa: 1.9 +/- 0.5% vs. 0.6 +/- 0.1%, AER: 522 +/- 335 micrograms/min vs. 27 +/- 13 micrograms/min, 24hr Ccr: 39.1 +/- 11.6 ml/min vs. 86.2 +/- 9.3 ml/min, P < 0.05). Contrast nephropathy developed in all of two patients with overt proteinuria (AER more than 200 micrograms/min), but none of eight patients with normoalbuminuria (AER below 15 micrograms/min). Three of seven patients with microalbuminuria developed contrast nephropathy, and two of them had advanced nephropathy. FENa obtained next day was significantly elevated over baseline in patients with contrast nephropathy (1.9 +/- 0.5% vs. 9.7 +/- 4.5%, P < 0.05), but unchanged in patients without contrast nephropathy. The rise in C beta 2-microglobulin/Ccr and enzymuria was noted in both group. Percentage decrease of Ccr on the next day was positively correlated with FENa before angiography (r = 0.645, p < 0.01). Of 24hr Ccr, AER, and FENa before angiography, FENa was revealed as a statistically significant discriminant factor for contrast nephropathy by stepwise discriminant analysis (p = 0.0008). These results suggest that contrast nephropathy develops predominantly in the stage not of incipient but of overt diabetic nephropathy indicated by a decline of glomerular filtration, overt proteinuria, and tubular dysfunction. Of them, tubular dysfunction may be the most important risk factor for contrast nephropathy.
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PMID:[Risk factors for contrast nephropathy in diabetic patients undergoing cardioangiography]. 831 79

In order to gain insight into the potential role of endothelin, a 21 amino acid peptide produced by endothelial cells, in the development of complications of diabetes mellitus, basal plasma endothelin levels were measured in 152 patients with diabetes mellitus (83 patients with type 1 diabetes mellitus, 69 patients with type 2 diabetes mellitus) and compared to those in 50 healthy controls. Blood was drawn at 8.00 a.m. under resting conditions and endothelin was determined after prior extraction by a sensitive radioimmunoassay. Endothelin levels were increased in patients with diabetes mellitus in comparison to controls (controls 0.9 +/- 0.1 pg/ml, type 1 diabetes mellitus 1.7 +/- 0.1, type-2-diabetes mellitus 2.0 +/- 0.1 pg/ml, p < 0.01 vs controls). 60% of patients with type 1 diabetes mellitus and elevated endothelin levels > 2.5 pg/ml (highest value measured in a control subject) had arterial hypertension with blood pressure > 140/90 mm Hg (p < 0.05 vs patients with normal endothelin levels). A reduced creatinine clearance (< 60 ml/min) was detected in 30% of patients with type 1 diabetes mellitus with elevated endothelin levels > 2.5 pg/ml, but only in 7% of patients with endothelin levels < 2.5 pg/ml (p < 0.05). In patients with type 1 diabetes mellitus and elevated endothelin levels diabetic retinopathy and peripheral neuropathy (p < 0.05) were more prevalent than in patients with normal endothelin values. 62% of patients with elevated endothelin levels had insufficient metabolic control (HbA1 concentrations above 10%). Positive correlations were found between endothelin and human atrial natriuretic peptide levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Significance of increased endothelin level for development of sequelae of diabetes mellitus]. 832 15

OBJECTIVE--To evaluate the frequency and correlates of glomerular hyperfiltration in NIDDM patients without overt proteinuria. RESEARCH DESIGN AND METHODS--A cross-sectional study was conducted. Seventy-one consecutive NIDDM patients attending an outpatient clinic, with Albustix-tested negative urine and a 24-h AER < 200 micrograms/min, were examined for long-term complications of diabetes. We measured their GFR (51Cr-EDTA single-injection method), 24-h AER (RIA), plasma creatinine, HbA1c, total cholesterol, triglycerides, urinary glucose, and urea. RESULTS--GFR above the upper limit of the normal range for age-matched control subjects (137.1 ml.min-1 x 1.73 m2) was present in 15 of 71 (21%) NIDDM patients. Subjects with normal and hyperfiltration did not differ in terms of age, sex distribution, BMI, duration of NIDDM, BP, AER, or frequency of long-term complications. Plasma glucose was significantly higher in subjects with hyperfiltration (mean [range]: 12.8 [4.3-18.7] vs. 8.7 [2.6-17.5] mM). HbA1c failed to reach statistical significance, although it tended to be higher in the group with hyperfiltration (10.4 [6.7-13.9] vs. 9.4 [4.2-16.5]%, P = 0.10). Age (rS -0.37, P = 0.002), FPG (rS 0.45, P < 0.0005), total cholesterol (rS -0.31, P = 0.008), and glycosuria (rS 0.40, P = 0.001) correlated significantly with GFR. In a stepwise multiple regression analysis, FPG, age, and total cholesterol emerged as significant correlates of the dependent variable GFR. CONCLUSIONS--Hyperfiltration occurred in 21% of NIDDM patients without overt proteinuria. FPG and age significant correlates of the GFR in these patients. Cholesterol is significantly (although only modestly) correlated with the GFR.
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PMID:Glomerular hyperfiltration in NIDDM patients without overt proteinuria. 842 64

A total of 412 Hong Kong Chinese diabetic patients were studied on at least two occasions 8-16 weeks apart. Although 28% were insulin-treated, only 3.6% had insulin-dependent diabetes (IDDM). In the remaining 397 patients with non-insulin-dependent diabetes (NIDDM), the mean (s.d.) body mass index (BMI) was 24.4 +/- 3.2 kg/m2 in females and 24.2 +/- 3.2 kg/m2 in males. Obesity was present in 17% of males (BMI > 27 kg/m2) and 40% of females (BMI > 25 kg/m2). Established hypertension was present in 49%. Abnormal albuminuria, defined as a mean urinary albumin/creatinine (UA/Cr) ratio greater than 5.4 mg/mmol based on two random spot urine samples, was present in 47%. On stepwise multiple regression analysis, UA/Cr ratio (R2 = 0.34, F = 65.4, P < 0.001) showed significant associations with systolic blood pressure (standardized regression coefficient beta = 0.40, P < 0.001), plasma creatinine concentration (beta = 0.27, P < 0.001) and glycosylated haemoglobin (beta = 0.20, P < 0.001). While the prevalence of hypertension increased with increasing severity of proteinuria, 40% of normoalbuminuric patients had hypertension. Among patients diagnosed before the age of 35 (n = 67), 52% were insulin-treated although only 10% were insulin-dependent. Among these NIDDM patients of young onset (n = 59), obesity was present in 25% of males and 56% of females. Overall, 18% of these patients had a blood pressure greater than 140/90 mmHg and 27% had abnormal albuminuria. In Hong Kong Chinese, diabetes mellitus is predominantly non-insulin-dependent even in the young. Obesity is more prevalent among females. Abnormal albuminuria is relatively common and is closely associated with hypertension and glycaemic control. In the light of increasing prevalence of diabetes among overseas Chinese, our findings may have important implications in the management of Chinese diabetic patients.
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PMID:Obesity, albuminuria and hypertension among Hong Kong Chinese with non-insulin-dependent diabetes mellitus (NIDDM). 849 35

We evaluated 725 diabetic haemodialysis (HD) patients, inducted into HD from 1967 to 1993 in Niigata University Hospital and its affiliated hospitals, to clarify the relationships among the clinical course and features including diabetes mellitus treatment. The glucose metabolism was also studied during HD with dialysis fluids containing different glucose concentration. At the time of HD induction, diabetic patients showed lower serum creatinine and more frequent overhydration, compared with those with glomerulonephritis. Heart failure was the leading cause of (53%) among the symptoms as the direct cause of HD induction. The survival rate in Japan, particularly in our group, was more prolonged than that in USA and Europe. The rate was lower in patients with cardiac complications than in those with gastrointestinal problems, and also lower in older patients (more than 70 years old) than in younger patients. Among the patients less than 70 years old, the survival period was longer in patients with serum HbA1c values of less than 7.5%, compared to those with greater than 7.5% Cerebro- and cardio-vascular involvements and infectious diseases were three major causes of death, and cerebro- and cardio-vascular disorders and diabetic gangrene were three major complications. Serum HbA1c was not different among patients with or without these causes of death or complications. In 18.1% of non-insulin-treated NIDDM patients insulin was needed one year after HD induction, while 32.1% of insulin-treated NIDDM patients before HD induction became free from insulin, who showed body weight loss on average of 10 kg. In 33.6% of insulin-treated patients, insulin doses increased from 2 to 20 units/day on the non-dialysis day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The treatment of the uraemic diabetic. Are we doing enough? A view from Japan. Fumitake Gejyo and Collaborate Study Group. 857 79


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