Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microalbuminuria and proteinuria are strong independent predictors for increased cardiovascular mortality in non-insulin-dependent diabetic (NIDDM) patients. In such patients, angiotensin converting enzyme (ACE) inhibition improves the evolution of diabetic nephropathy; however, no data are currently available on the effects of such intervention on cardiovascular morbidity and mortality. The aim of the Diab-Hycar study is to test the hypothesis that ACE inhibition with a low daily dose of 1.25 mg ramipril, which has no significant effect on blood pressure, may reduce cardiovascular morbidity and/or mortality in normotensive or hypertensive NIDDM patients with persistent albuminuria. Selected and followed by general practitioners, 4000 patients will receive their usual oral antidiabetic treatment and if necessary antihypertensive treatment (ACE inhibitors excluded). In addition in a randomized, double-blind trial they will be given either a placebo or 1.25 mg ramipril daily. The follow-up is currently scheduled to last 3 years. The efficacy of ACE-inhibition will be assessed by the following major end-points: cardiovascular death, sudden death, myocardial infarction, stroke, renal replacement therapy. The Diab-Hycar study started on 3 February 1995. By 1 September 1995, 11,000 urine samples were tested. The prevalence of persistent albuminuria was 23%, 964 patients were initially included in the study, with 619 eligible patients included soon after. Different strategies have been developed to record cardiovascular events correctly and to minimize the number of patients lost to follow-up.
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PMID:The DIAB-HYCAR Study. 908 52

It is clear that angiotensin-converting enzyme (ACE) inhibitors slow progression of diabetic nephropathy to a greater extent than other antihypertensive agents when blood pressure (BP) is reduced to levels below 140/90 mm Hg. Recent studies also demonstrate that nondihydropyridine calcium channel blockers (NDCCBs) slow progression of diabetic nephropathy in people with pre-existing renal insufficiency secondary to non-insulin dependent diabetes mellitus. The combined effects of both a CCB and ACE inhibitor have recently been examined in both animal models of diabetes as well as patients with established diabetic nephropathy. These studies demonstrate the following points: (a) at comparable BP levels, a combination of an ACE inhibitor with a NDCCB result in a greater reduction in proteinuria when compared to either components alone; and (b) conversely, addition of an ACE inhibitor to a dihydropyridine CCB (DCCB) yields effects on proteinuria similar to the ACE inhibitor alone. Therefore, addition of an ACE inhibitor to a DCCB demonstrates protection against the effects of DCCB alone. Addition of an ACE inhibitor to a NDCCB does not potentiate the preservation of renal morphology associated with progression of diabetic nephropathy when compared to either of its components alone. Conversely, a DCCB/ACE inhibitor combination yields morphologic results similar to the ACE inhibitor alone. Taken together these results suggest that ACE inhibitors when combined with a NDCCB result in greater reductions in proteinuria, and similar preservation of renal morphology when compared to either of its components alone.
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PMID:Effects of an ACE inhibitor combined with a calcium channel blocker on progression of diabetic nephropathy. 911 Nov 55

We studied the immunohistochemical localization of advanced glycosylation end products (AGEs) in the progression of diabetic nephropathy. Fourteen NIDDM patients with diabetic nephropathy were evaluated: 2 patients with normoalbuminuria, 4 with microalbuminuria (MA) and 8 with overt proteinuria (OP). Three patients with minor glomerular abnormalities were used as nondiabetic controls. Immunoreactivity to a monoclonal anti-AGE antibody (6D12) was recognized on the internal elastic membranes of arterial walls in every diabetic group. Hyaline lesions of arterioles of the MA and OP groups demonstrated strong reactions with 6D12. A portion of the nodular and exudative lesions in glomeruli of OP group patients also revealed immunoreactivity to 6D12. No immunoreactivity to 6D12 was observed in nondiabetic control specimens. We confirm that the accumulation of AGEs began in arterial walls of the early stage and presented in glomerular lesions of the late stage of the progression of diabetic nephropathy.
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PMID:Histological localization of advanced glycosylation end products in the progression of diabetic nephropathy. 920 Apr 6

Proteinuria and nephropathy have been found to cluster in families of non-insulin-dependent diabetic (NIDDM) Pima Indian, and in Caucasian insulin-dependent diabetic (IDDM) patients. No information is at present available for Caucasian NIDDM patients. The aim of the present study was to determine whether micro-macroalbuminuria (AER+) is associated with albumin excretion rate abnormalities in diabetic and non-diabetic siblings of probands with NIDDM and AER+. We identified 169 Caucasian families with one NIDDM proband (the patient with longest known NIDDM duration) (101 families with only NIDDM siblings, 33 families with both NIDDM and non-NIDDM siblings and 35 families with only non-NIDDM siblings). Of the probands 56 had AER+ [Prob-NIDDM-(AER+)], 78 had AER-[Prob-NIDDM-(AER-)], 74 siblings of Prob-NIDDM-(AER+), and 113 siblings of Prob-NIDDM-(AER-) also had NIDDM. Data on albuminuria and retinopathy from multiple sibling pairs when the size of the sibship was more than two was adjusted according to a weighting factor. The odds ratio for AER+, in siblings of Prob-NIDDM-(AER+) adjusted for age, hypertension, glycated haemoglobin A1c and other confounding variables was 3.94 (95% confidence intervals: 1.93-9.01) as compared to siblings of Prob-NIDDM-(AER-). The 74 siblings of Prob-NIDDM-(AER+) had higher prevalence of proliferative retinopathy than siblings of Prob-NIDDM-(AER-) (14 vs 2%; p < 0.01). We also identified 66 non-diabetic siblings of 41 NIDDM probands with AER+ and 36 non-diabetic siblings of 27 NIDDM probands with AER-. Albumin excretion was two times higher, although still within the normal range, in the non-diabetic siblings of Prob-NIDDM-(AER+) than in siblings of Prob-NIDDM-(AER-) [median = 13.5 (range 0.5-148) vs 6.6 (range 1-17) micrograms/min (p < 0.05)]. In conclusion higher rates of albumin excretion aggregate in Caucasian families with NIDDM. Proliferative retinopathy is more frequently observed in families showing a clustering of AER+ and NIDDM. These findings suggest that familial factors play a role in the pathogenesis of renal and retinal complications in NIDDM.
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PMID:Clustering of albumin excretion rate abnormalities in Caucasian patients with NIDDM. The Italian NIDDM Nephropathy Study Group. 924 3

To investigate the association between insulin resistance and diabetic nephropathy, peripheral insulin sensitivity indices (M/I values) were evaluated via euglycemic-hyperinsulinemic clamp in 45 non-obese, non-insulin-dependent diabetic (NIDDM) subjects. The patients were divided into four groups: 18 with normoalbuminuria (urinary albumin excretion rate [AER] < 30 mg/24 h, stage I), 10 with microalbuminuria (30 < or = AER < or = 300 mg/24 h, stage II), seven with overt proteinuria (AER > 300 mg/24 h, stage III), and 10 with uremia (serum creatinine levels > 2.0 mg/dL, stage IV). There were no significant differences in age, body mass index (BMI), fasting plasma glucose, or hemoglobin A1c (HbA1c) among the four groups. No significant difference in M/I values was seen between stage I and stage II (6.30 +/- 0.73 and 5.95 +/- 0.85 mg/kg/(min per microU/mL) x 100, respectively). M/I values in the stage I and stage II groups were strongly correlated with BMI (r = -.790, P = .0001 and r = -.785, P = .007, respectively). M/I values in the stage III group (4.53 +/- 0.51) were lower than in the stage I group, although not significantly so. M/I values in the stage IV group (3.16 +/- 0.37) were significantly lower than in the stage I group (P = .025). In multiple regression analysis with a model in which age, sex, BMI, HbA1c, and creatinine clearance (Ccr) were included as independent variables, BMI and Ccr were demonstrated to be significant and independent contributors to insulin sensitivity indices as the dependent variable (beta = -0.716 and beta = 0.272, respectively, R2 = .564, P < .0001). In conclusion, the present cross-sectional study demonstrated in non-obese NIDDM patients with nephropathy that microalbuminuria did not affect peripheral insulin resistance, but uremia did, as in nondiabetic patients, and that the peripheral insulin resistance was significantly contributed to by the degree of obesity and uremia.
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PMID:Insulin resistance in non-obese, non-insulin-dependent diabetic patients with diabetic nephropathy. 928 89

To gain current data about epidemiology of diabetic retinopathy in a population of type 2 diabetics a long-term prospective study was started. The study included 1334 patients with type 2 diabetes mellitus registered in Warsaw regional Diabetes Center. The prevalence of any form of diabetic retinopathy in this group was 31.4% and proliferative retinopathy-1.3%. It was found that the patients with retinopathy had diabetes mellitus of longer duration, higher fasting and postprandial levels of glycemia and higher daily proteinuria in comparison with diabetics without retinopathy. Apart from that, a frequency of ischemic heart disease and lower extremity ischemic disease was higher in diabetics with retinopathy. 109 new cases of retinopathy were diagnosed during 3-year follow-up. The study allowed us to determine the current epidemiological parameters concerning diabetic retinopathy in type 2 diabetics and a set of parameters characterizing people at highest risk of a development of retinopathy.
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PMID:[Prospective studies of diabetic retinopathy in a cohort of patients with type II diabetes mellitus]. 929 90

Cigarette smoking was known to promote the progression of diabetic nephropathy in patients with type 1 diabetes, but its influence on the course of diabetic nephropathy in patients with type 2 diabetes had not been previously established. In a prospective follow-up study we therefore compared the progression of nephropathy in type 2 diabetic patients with or without tobacco consumption. Initiation of dialysis treatment or death of the patient were the end points of the study. 36 patients with type 2 diabetes complicated with diabetic nephropathy were included in the study, 16 smoked and 20 did not. The main outcome measures were proteinuria, arterial blood pressure, HbAlc, serum-creatinine and creatinine clearance, which were controlled at least every six months. In the smoking diabetic patients the mean (SD) creatinine-clearance decreased from 82 +/- 10 to 10 +/- 6 ml/min/1.73 m2 over a period of 62 +/- 21 months. The rate of decline of the creatinine-clearance was 1.24 +/- 0.34 ml/min/month. In the non-smoking patients the creatinine-clearance decreased from 79 +/- 8 to 9 +/- 3 ml/min/1.73 m2 within 79 +/- 27 months. The rate of decline in the creatinine-clearance was 0.99 +/- 0.35 ml/min/month (p < 0.025). HbAlc, systolic and diastolic blood pressure as well as serum cholesterol and triglycerides were not significantly different in both patient groups. Therefore, we conclude that cigarette smoking promotes the progression of diabetic nephropathy in patients with type 2 diabetes, just as it is known in type 1 diabetic patients.
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PMID:Influence of cigarette-smoking on the progression of clinical diabetic nephropathy in type 2 diabetic patients. 934 85

Urinary excretion rate and total clearances of albumin, IgG, IgA and alpha 1-microglobulin, together with selectivity index and proteinuria, were determined by computerized nephelometry in 187 IDDM and NIDDM diabetic out-patients and in 39 healthy subjects in order to perform a prompt clinical assessment of diabetic nephropathy. Significant correlations between nephelometric and RIA procedures were demonstrated for the urinary excretion of albumin (p < 0.001) and total IgG (p < 0.001) in diabetic patients and healthy subjects. Nephelometry allowed us to classify diabetic patients in different stages of nephropathy: non nephropathic, normoalbuminuric with hyperfiltration, with incipient (microalbuminuric) and overt nephropathy (macroalbuminuric). Thirty consecutive subjects were analyzed within 1 h from the beginning of the procedure. A normal tubular function was demonstrated in non nephropathic, hyperfiltering and in 34% of microalbuminuric diabetic patients. On the contrary, in 66% of microalbuminuric and in 93% of macroalbuminuric patients alpha 1-microglobulin urinary levels were found above the upper normal limit. Urinary excretion of IgA was significantly increased only in macroalbuminuric diabetic patients (p < 0.001); this marker might therefore characterise the stage of overt nephropathy. Computerized nephelometry can be considered as a prompt, reproducible and high sensitive approach in the clinical evaluation of proteinuria and tubular function in diabetic renal disease.
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PMID:Nephelometry in the clinical assessment of glomerular proteinuria and tubular function in diabetic nephropathy. 934 86

We measured erythrocyte Na+/Li+ and Na+/H+ countertransport (CT) activity (millimoles per liter per cell per hour) in 10 healthy control subjects (age, 38 +/- 4 years; body mass index, 25 +/- 1 kg/m2) and in 25 hypertensive patients with non-insulin-dependent diabetes mellitus ([NIDDM] age, 49 +/- 3 years; body mass index, 29 +/- 1 kg/m2; fasting plasma glucose, 157 +/- 12 mg/dL) 4 weeks after discontinuation of previous antihypertensive treatment. Na+/Li+ CT was significantly increased in hypertensive NIDDM patients compared with controls (0.56 +/- 0.04 v 0.30 +/- 0.03, P < .01), whereas Na+/H+ CT was similar to control levels (21 +/- 1 v 20 +/- 2). A positive correlation was found between Na+/Li+ CT and the severity of insulin resistance (r = .69, P < .01), mean arterial pressure ([MAP] r = .64, P < .01), plasma triglyceride concentration (r = .46, P < .05), and plasma total cholesterol (r = .41, P < .05). An inverse correlation was found between Na+/Li+ CT activity and plasma insulin concentration (r = -.47, P < .05). No relationship was observed between Na+/Li+ CT activity and either creatinine clearance or proteinuria. Stepwise multiple regression analysis for all metabolic variables and blood pressure showed that only the severity of insulin resistance was positively correlated with increased Na+/Li+ CT activity. Na+/H+ and Na+/Li+ CT activity were not altered by 3 hours of euglycemic physiologic hyperinsulinemia (84 +/- 3 microU/mL). Hypertensive NIDDM subjects were treated for 3 months with captopril, nifedipine, or doxazosin. After captopril, a reduction of Na+/H+ CT was observed (22 +/- 4 v 13 +/- 2, P < .05); Na+/Li+ CT decreased after doxazosin (0.56 +/- 0.06 v 0.45 +/- 0.05, P < .05) and nifedipine (0.52 +/- 0.06 v 0.42 +/- 0.05, P < .05). In conclusion, in hypertensive NIDDM subjects, (1) Na+/Li+ CT is increased and is correlated with the level of insulin resistance and the MAP; (2) acute physiologic hyperinsulinemia does not affect Na+/Li+ or Na+/H+ CT activity; and (3) Na+/H+ CT activity is reduced by captopril, and Na+/Li+ CT is decreased by doxazosin and nifedipine.
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PMID:Na+/Li+ and Na+/H+ countertransport activity in hypertensive non-insulin-dependent diabetic patients: role of insulin resistance and antihypertensive treatment. 936 92

To study the relationship of the concentration of serum lipoprotein (a) [Lp(a)] with diabetic complications in non-insulin dependent diabetes mellitus (NIDDM), 100 non-diabetics with 150 patients with NIDDM were compared. There was no difference in Lp(a) concentration (P > 0.5) between the two groups. Lp(a) concentration was not significantly correlated with the levels of total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, apolipoprotein A-I, apolipoprotein B in both groups. In NIDDM group, patients with hypertension, macro- and microangiopathy had higher levels of Lp(a) than those without these complications (P < 0.001 and P = 0.002 respectively). Lp(a) level was positively related to presence of macroangiopathy (r = 0.185, P = 0.024) and proteinuria (r = 0.316, P < 0.001) in NIDDM.
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PMID:[Lipoprotein (a) and non-insulin dependent diabetes mellitus]. 938 40


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