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)

The aim of this study was to determine the clinical significance of serum and urinary insulin-like growth factor I (IGF-I) in renal disease and diabetes mellitus. In renal portion, we measured their concentrations in patients with chronic renal disease (serum creatinine < 2.0 mg/dl) (CRD. n = 22) and those with chronic renal failure (serum creatinine > or = 2.0 mg/dl) (CRF, n = 26) and compared with normal healthy controls (C. n = 20). Serum concentrations growth hormone (GH) and IGF-I did not differ among these groups. Urinary IGF-I level was significantly increased in CRF (4.0 +/- 0.5 ng/mg creatinine) compared with CRD (2.8 +/- 0.6 ng/mg creatinine) and C (1.8 +/- 1.0 ng/mg) creatinine). Urinary IGF-I did not correlate with either serum GH or serum IGF-I. Urinary IGF-I, but not serum IGF-I, demonstrated a significant negative correlation with creatinine clearance. In diabetic portion, 29 patients with noninsulin dependent diabetes mellitus (NIDDM), whose serum creatinine were within normal range, and age-matched 12 subjects were enrolled. Serum IGF-I in NIDDM (130 +/- 11 ng/ml) was significantly lower than that in controls (201 +/- 11 pg/ml). In contrast, urinary IGF-I level in NIDDM (1.93 +/- 0.31 ng/mg creatinine) did not differ from that in controls (2.00 +/- 0.31 ng/mg creatinine). In NIDDM, urinary IGF-I had poor correlation with both serum IGF-I and albuminuria. The data in renal patients suggest the possible participation of renal IGF-I in the progression of renal disease, while in NIDDM with normal serum creatinine the role of renal IGF-I may be less in the early diabetic nephropathy.
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PMID:Serum and urinary levels of insulin-like growth factor I in patients with chronic renal disease and diabetes mellitus: its clinical implication. 879 28

A total of 168 patients with non-insulin dependent diabetes (NIDDM) followed over 10 years were recruited in this study. The patients were divided into two groups: Group 1 patients had a stable renal function (N = 96) and Group 2 had a declining renal function (N = 72). Group 1 included those whose serum creatinine was normal five years ago but had increased to > or = 2 mg/dl or those who has reached end-stage renal failure (requiring dialysis) by the time of study. All patients were genotyped for the insertion/deletion (I/D) polymorphism of the ACE gene, the M235T polymorphism of the angiotensinogen (Atg) gene and the A1166C polymorphism of the angiotensin II type 1 receptor (AT1) gene. The genotype frequency distributions of M235T Atg and the A116C AT1 gene polymorphisms were not different between Group 1 versus Group 2. While the frequency of the ACE DD genotype in Group 1 (7.3%) was comparable to that of the general population, the DD frequency was significantly higher in Group 2 (26.4%) than in Group 1 (odds ratio, 4.56; 95% confidence interval, 1.80 approximately 11.56, P < 0.001). Among all 168 patients studied, the renal survival rate was significantly lower among DD than ID (P < 0.005) or II patients (P < 0.001). In patients with a declining renal function (Group 2), those with the DD genotype had a significantly shorter time interval from onset of diabetes to the initiation of dialysis (13.4 +/- 1.4 years) than those with ID (20.7 +/- 1.2 years, P < 0.01) or II genotypes (17.5 +/- 1.1 year, P < 0.01). Analysis of the clinical course of the three ACE genotypes revealed that the majority (95%) of patients with the DD genotype who had albuminuria progressed to end-stage renal disease within 10 years of diagnosis of diabetes. Our analysis also revealed that initiation and continuation of dialysis are associated with a progressive decrease in the frequency of the DD genotype. These results indicate that, in NIDDM, the ACE DD genotype has a high prognostic value for progressive deterioration of renal function. Moreover, the DD genotype appears to increase the mortality once dialysis is initiated.
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PMID:Angiotensin I converting enzyme gene polymorphism in non-insulin dependent diabetes mellitus. 884 Feb 99

European guidelines recommend annual screening for microalbuminuria in patients with Type 1 (insulin-dependent) diabetes mellitus (IDDM) of greater than 5 years' duration and in those with Type 2 (non-insulin-dependent) diabetes mellitus (NIDDM) from diagnosis. To determine the current provision of screening for microalbuminuria we performed a postal survey of all diabetologists in the United Kingdom. Of 556 questionnaires sent, 326 (59%) were returned (246 adult, 57 paediatric, 3 adolescent clinics) and of these 306 (55%) were suitable for analysis. Screening programmes have been established by 210 (69%) diabetologists: 70 of these in the last 2 years. 46 more plan to screen patients with IDDM within 2 years. 155 (92%) of 169 adult programmes perform annual screening in IDDM, 74% according to European guidelines (39% in NIDDM). Other clinics use age, type of diabetes or criteria such as blood pressure to target screening. An albumin/creatinine ratio (52%) on an early morning urine (56%) or random (29%) urine sample is most commonly requested. Financial constraint was the principal reason given in 32 (33%) of 96 clinics that do not currently screen. Other reasons included implementation of other developments with a higher priority (24%) and doubts about the medical value of screening (46%). Assuming respondents are representative of current UK practice, we conclude that microalbuminuria screening is available to patients in many clinics, but is neither universal nor always performed according to European guidelines.
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PMID:Microalbuminuria screening in the UK: are we meeting European standards? 886 54

Treatment of hypertension with ACE inhibitors in diabetic patients reduces proteinuria and slows progression of nephropathy compared with agents that do not maintain declines in proteinuria. Calcium channel blockers (CCBs) have variable effects on proteinuria; their long-term effects on progression of diabetic nephropathy are not known. The current study examines the hypothesis that CCBs that maintain reductions in proteinuria slow progression of nephropathy associated with non-insulin dependent diabetes mellitus (NIDDM) by a degree comparable to ACE inhibitors, given similar levels of blood pressure control. To test this hypothesis we randomized 52 patients with NIDDM associated nephropathy and hypertension, mean age of 63 +/- 8 years, to either the ACE inhibitor, lisinopril (N = 18), nondihydropyridine CCBs (NDCCBs), verapamil SR (N = 8) or diltiazem SR (N = 10), or the beta blocker, atenolol (N = 16). Goal blood pressure was < or = 140/90 mm Hg. Patients were followed for a mean period of 63 +/- 7 months. The primary end point was change in creatinine clearance (CCr) slope in each group. There was no significant difference in mean arterial pressure reduction among the groups over the study period (P = 0.14). The mean rate of decline in CCr was greatest in the atenolol group (-3.48 ml/min/year/1.73 m2; P < 0.0001). There was no difference in the CCr slopes between lisinopril and NDCCBs groups (P = 0.36). Proteinuria was reduced to a similar extent in the lisinopril and NDCCBs groups (P > 0.99). Therefore, in persons with renal insufficiency secondary to NIDDM, similar levels of blood pressure control with either lisinopril or NDCCBs slowed progression of renal disease to a greater extent than atenolol. Moreover, this enhanced slowing of renal disease progression correlated with sustained and significant reductions in proteinuria, findings not observed in the atenolol group.
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PMID:Calcium channel blockers versus other antihypertensive therapies on progression of NIDDM associated nephropathy. 891 31

According to extensive autopsy studies, non-diabetic renal disease seems to be rare in diabetes mellitus, but recent publications suggest a significant prevalence of non-diabetic renal disease in non-insulin-dependent diabetic (NIDDM) patients, especially in the absence of retinopathy. The purpose of this study was to evaluate the prevalence of non-diabetic renal disease in NIDDM patients in renal biopsies from clinical practice, in patients suspected of having non-diabetic renal disease. In addition we systematically reviewed the literature. Biopsies were evaluated at the University Department of Pathology, Aarhus, Denmark, but had been collected at several departments of nephrology. In total 33 consecutive biopsies were available from 1988-1995 (mean age of patients: 62 years (range 39-75) (mean known diabetes duration 8 years (range 1-25); the main clinical reason for a biopsy was proteinuria. Renal function changes ranged from slight elevation of serum creatinine to uraemia. In addition 9 original papers, including our own material 580 patients were examined. On the basis of careful morphological evaluation according to international criteria, no patient exhibited an unequivocal sign of non-diabetic glomerular disease. Two patients had strongly but not completely convincing evidence of glomerulonephritis. One patient had some evidence of glomerulonephritis. These 3 patients also exhibited diabetic lesions. One patient with end-stage renal disease showed evidence of interstitial nephropathy without glomerular lesions. Thus, in 4 patients evidence of non-diabetic lesions was found. In the remaining 29 patients typical diffuse (n = 9) or nodular (n = 20) diabetic lesions were found. Twenty patients showed evidence of diabetic retinopathy. One of the patients with evidence of non-diabetic renal disease had simplex retinopathy. In the literature a considerable bias exists towards including patients with non-diabetic renal disease. In non-biased materials with proteinuria the prevalence of non-diabetic renal disease is very similar to our series. In microalbuminuric patients non-diabetic renal disease seems to be very rare. It can be concluded that in our material non-diabetic renal disease is uncommon in NIDDM patients, even if a clinician has suggested renal disease of other origin. A considerable bias towards including non-diabetic renal disease in NIDDM patients exists in the literature. The indication for biopsy should be evaluated carefully, and biopsy should by no means be routinely performed in NIDDM patients with proteinuria.
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PMID:How often is NIDDM complicated with non-diabetic renal disease? An analysis of renal biopsies and the literature. 896 Aug 56

A cohort of 6792 NIDDM patients attending a diabetes centre at Madras in South India was screened using a combination of retinal photography and clinical examination by retinal specialists. A total of 2319 patients (34.1%) had evidence of retinopathy. This included 2090 patients (30.8%) with non-proliferative diabetic retinopathy including 435 patients (6.4%) with maculopathy and 229 patients (3.4%) with proliferative diabetic retinopathy. Multiple logistic regression analyses showed that duration of diabetes, glycosylated haemoglobin, type of treatment (insulin treatment versus non-insulin treatment), systolic and diastolic blood pressures and serum creatinine, showed a positive association with retinopathy while body mass index (BMI) showed an inverse association. The prevalence rates of retinopathy in Southern Indians are comparable to those seen in Europeans. However in view of the high prevalence of diabetes in the Indian sub-continent, diabetic retinopathy could become a formidable challenge in the future.
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PMID:Prevalence of retinopathy in non insulin dependent diabetes mellitus at a diabetes centre in southern India. 896 88

This study aimed to investigate the relationship between microalbuminuria and office blood pressure (BP) as compared with ambulatory BP in patients with diabetes mellitus under everyday practice conditions. It was also undertaken to assess the effect of the angiotensin converting enzyme inhibitor cilazapril on diabetes-associated albuminuria. Ambulatory BP was recorded during daytime in 54 patients with type II diabetes mellitus at the end of a 4-week period during which they received no vasoactive drug. The difference between office and ambulatory BP was unpredictable in the individual patient. There was no significant correlation between either ambulatory or office BP and urinary albumin/p5eatinine ratio. Fifty-one patients underwent a 40-week treatment with 5 mg/day of cilazapril. There was, in the absence of satisfactory BP control, the possibility of adding the calcium antagonist amlodipine (5 mg/day) from the 10th week onward and 12.5 mg/day of hydrochlorothiazide from the 20th week onward. Office mean BP was significantly reduced after 30 to 40 weeks of therapy in patients with normoalbuminuria (n = 19, -14%, P < .001), in those with microalbuminuria (n = 22, -6.6%, P < .01), as well as in those with clinical proteinuria (n = 9, -11.4%, P < .01). During the same time, the urinary albumin/creatinine ratio was not modified in normoalbuminuric patients (n = 19, +24.6%, P = .72) as well as in those with clinical proteinuria (n = 9, -29.4%, P = .09). On the other hand this value was significantly reduced for the group with microalbuminuria (n = 23, -24.3%, P < .05). In the overall population, as well as in hyperalbuminuric patients (patients with microalbuminuria + patients with clinical proteinuria), the reduction of the albumin/ creatinine ratio was also significant (n = 51, -7%, P < .01 and n = 32, -25,7%, P < .01, respectively). In conclusion, the findings of this study performed by practicing physicians show that ambulatory BP may differ greatly from office BP in diabetic patients. They also indicate that urinary albumin excretion is poorly correlated with office and ambulatory BP in type II diabetics. Finally, they demonstrate the antiproteinuric action of prolonged treatment with the angiotensin converting enzyme inhibitor cilazapril, whether given alone or combined with amlodipine.
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PMID:Albuminuria in diabetes mellitus: relation to ambulatory versus office blood pressure and effects of cilazapril. 897 94

Microalbuminuria has been reported to precede the development of NIDDM and to be a risk marker for cardiovascular disease. Therefore, the present study investigated the relationship between urinary albumin excretion rate (UAER) and the degree of insulin resistance in Japanese subjects with impaired glucose tolerance (IGT). Thirty-three normotensive IGT subjects were divided into three groups and twenty hypertensive IGT subjects were divided into two groups according to the degree of insulin resistance (GIR value) estimated by the euglycemic hyperinsulinemic clamp method. UAER was significantly higher in the lower GIR group in normotensive subjects (highest GIR group, 6.6 +/- 0.9 mg/24 h; intermediate group, 10.5 +/- 3.0 mg/24 h; lowest group, 21.3 +/- 3.8 mg/24 h; P<0.01 between highest and both of the other groups), but not in hypertensive subjects. The lowest GIR was associated with higher fasting plasma insulin, increased insulin response to glucose, higher plasma triglyceride and uric acid, and lower high-density-lipoprotein cholesterol, but not with increased creatinine clearance rate in normotensive subjects. A similar tendency was also found in hypertensive subjects. It is concluded that UAER is related to insulin resistance in normotensive subjects with IGT through a mechanism other than glomerular hyperfiltration.
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PMID:Urinary albumin excretion rate is related to insulin resistance in normotensive subjects with impaired glucose tolerance. 906 67

In order to detect the prevalence of microalbuminuria, a screening procedure was carried out in 1016 adult (age > 14 years) diabetic patients registered in primary health care system at the 17st district of the capital. The clinical characteristics of patients were investigated and microalbuminuria was measured by immunoturbidimetric method using first void morning urinary samples. In this way, the urinary albumin/creatinine ratio was calculated (abnormal value in men > or = 2.5 mg/mmol, in women > or = 3.5 mg/mmol). Moreover, serum creatinine, blood glucose, serum cholesterol and triglycerides were measured in fasting blood samples. After applying exclusion criteria data of 933 diabetic patients [129 insulin-dependent (IDDM) and 804 non-insulin-dependent (NIDDM) patients; 424 men, 509 women] were analysed. Abnormal urinary albumin/creatinine ratio was found in 315 (33.8%) patients. Microalbuminuria was detected in 32 (24.8%) IDDM and in 201 (25.0%) NIDDM patients. Macroalbuminuria was found in 13 (10.1%) IDDM and in 69 (8.6%) NIDDM patients. Abnormal urinary albumin/creatinine ratio was more often found in men than in women (IDDM men 41.3%, IDDM women 28.8%; NIDDM men 38.0%, NIDDM women 30.0%). Significant difference was found between diabetic patients with (n = 315) and without (n = 618) abnormal urinary albumin/creatinine ratio regarding age (64.3 +/- 0.7 years vs. 61.4 +/- 0.5 years; p < 0.001), duration of diabetes (10.3 +/- 0.5 years vs 7.9 +/- 0.3 years; p < 0.001) systolic blood pressure (151 +/- 1 mmHg vs 146 +/- 1 mmHg; p < 0.01), serum creatinine (99 +/- 2 mumol/l vs 88 +/- 1 mumol/l; p < 0.001) and blood glucose (10.4 +/- 0.2 mmol/l vs 9.4 +/- 0.1 mmol/l; p < 0.001). One third (33.8%) of diabetic patients in primary health care setting exhibited signs or were at risk of renal involvement of diabetes. Diabetic patients with micro- or macroalbuminuria should be carefully controlled in order to prevent or to decrease deterioration of renal function due to diabetic nephropathy.
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PMID:[Screening for microalbuminuria in diabetic patients in the primary health care system]. 913 49

In Jamaica, malnutrition related diabetes mellitus (MRDM) presents the clinical picture of phasic insulin dependence. This study was undertaken to investigate nephropathic changes associated with this group of patients. Fourteen phasic insulin dependent diabetes mellitus (PIDDM) patients were compared with 10 insulin dependent (IDDM) and 10 non-insulin dependent (NIDDM) diabetes mellitus patients, and 10 normal controls. Each group was matched for age, sex, body mass index (BMI) and, in the case of the diabetic patient controls, duration of diabetes. Urinary microalbumin concentration was significantly (p < 0.05) higher in the PIDDM group (mean +/- SD: 153 +/- 48.3 mg/dl) than in the groups of NIDDM (35.7 +/- 9.6 mg/dl) or IDDM (38.6 +/- 15.8 mg/dl) patients. Serum urea and creatinine concentrations (mean +/- SE 7.6 +/- 1.0 mmol/l and 130.0 +/- 20.3 mumol/l, respectively) were higher in the PIDDM patients than in the NIDDM and IDDM groups. Confounding factors such as hypertension and urinary tract infections were excluded as causes for these differences. We conclude that PIDDM patients have more severe renal dysfunction than NIDDM patients and, since glycosylated haemoglobin concentrations are comparable in these groups, we attribute this to a renal insult due to malnutrition predating the onset of the PIDDM.
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PMID:Kidney function in phasic insulin dependent diabetes mellitus in Jamaica. 914 47


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