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)

Diabetic renal disease is a clinical syndrome in which proteinuria is followed by the development of renal failure, and is commonly associated with the concomitant development of hypertension. In insulin-dependent diabetic (IDDM) patients, hypertension often first appears in the microalbuminuric phase of diabetic nephropathy whereas in non-insulin-dependent diabetic (NIDDM) patients, hypertension often antecedes nephropathy and may precede the diagnosis of diabetes. Antihypertensive regimens including diuretics, vasodilators such as hydralazine, beta-blockers and ACE inhibitors reduce proteinuria and delay the decline in renal function in IDDM patients with established nephropathy. No such data are as yet available for calcium antagonists. In microalbuminuric diabetic patients with hypertension, conventional antihypertensive agents, ACE inhibitors and calcium antagonists have been shown to decrease urinary albumin excretion. In the diabetic patient with normal blood pressure and microalbuminuria, there is much less information. It appears likely that ACE inhibitors reduce or retard the rate of increase in albuminuria in these patients. The effect on ultimately delaying or preventing renal failure remains unknown although the preliminary evidence is encouraging. Data on calcium antagonists remain inconclusive with some reports suggesting an increase in proteinuria with the dihydropyridine calcium antagonists. However, a recent longer term study suggested that nifedipine may prevent the rise in albuminuria which is generally observed in the untreated normotensive microalbuminuric subject.
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PMID:The management of diabetic proteinuria. Which antihypertensive agent? 150 44

Urinary albumin excretion rate (AER) was measured in non-diabetic controls (n = 143) and newly diagnosed impaired glucose tolerant (IGT, n = 64) and non-insulin-dependent (type 2) diabetic patients (n = 146). AER progressively increased from non-diabetic [3.7 (1.1-51.3) micrograms/min, median (5-95th centile)] to IGT [4.8 (1.3-53.7)] and diabetic [7.3 (1.4-91.6)] groups. Eight percent of non-diabetic, 19% of IGT and 23% of type 2 diabetic patients showed 'microalbuminuria' (AER, 20-200 micrograms/min) (non-diabetic vs diabetic P less than 0.01, non-diabetic vs IGT NS, IGT vs diabetic NS). AER was directly related to waist-hip ratio (P less than 0.001) and HbA1 (P less than 0.01) in diabetic patients; 80% of diabetic patients with microalbuminuria were men (P less than 0.06 compared to 'normoalbuminuric' diabetic patients). Association of AER with waist-hip ratio was present in men as well as women. Thus, in the newly diagnosed type 2 Indian diabetic patients AER is associated with central obesity in addition to its well known association with hyperglycaemia. Our findings offer a possible explanation for the increased risk of proteinuria in diabetic men than in women because men are centrally more obese. It could also explain previous reports of higher AER in migrant Asian diabetic patients in the U.K. compared to native white Caucasian diabetic patients because Asians are known to be more centrally obese.
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PMID:Urinary albumin excretion rate (AER) in newly-diagnosed type 2 Indian diabetic patients is associated with central obesity and hyperglycaemia. 151 62

A cohort of 63 Type 1 insulin-dependent diabetic patients were first characterized for overnight urinary albumin excretion rate (AER) in 1967. In 1981, seven out of eight (87%) patients with initial AER greater than or equal to 30 less than or equal to 140 micrograms/min (microalbuminuria) developed clinical proteinuria compared to only 2 out of 55 (4%) patients with initial AER less than 30 micrograms/min. The same cohort of patients was reassessed in 1990 after a total follow-up period of 23 years. The aim was to investigate the role of microalbuminuria in the prediction of total/cardiovascular mortality and the development of renal failure, in addition to clinical proteinuria. The initially microalbuminuric patients had a significantly higher risk of developing not only clinical proteinuria (relative risk 9.3, 95% C.I. 1.36 to 3.10, P less than 0.05), but also of dying from a cardiovascular cause (relative risk 2.94, 95% C.I. 1.18 to 7.34, P less than 0.05). The rate of progression to renal failure was higher but not significantly so in the microalbuminuric (2 of 8) compared to the normoalbuminuric (4 of 53) group (relative risk 3.31, 95% C.I. 0.72 to 15.24, NS). In insulin-dependent diabetic patients microalbuminuria is a powerful predictor of clinically overt diabetic renal disease as well as cardiovascular mortality.
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PMID:Prognostic significance of microalbuminuria in insulin-dependent diabetes mellitus: a twenty-three year follow-up study. 151 6

The prevalence of raised Na+/Li+ countertransport (CT) activity (greater than 0.41 mmol/liter RBC/hr) was assessed in 185 consecutive insulin-dependent diabetic patients attending an outpatient diabetic clinic. Normoalbuminuria was defined as an overnight albumin excretion rate (AER) of less than 20 micrograms/min (N = 121), microalbuminuria as AER between 20 and 150 micrograms/min (N = 35) and macroalbuminuria as AER greater than or equal to 150 micrograms/min (N = 29). The prevalence of elevated Na+/Li+CT (greater than 0.41 mmol/liter RBC/hr) was 21.5, 42.8 and 51.7% (P = 0.0005), in patients with normo-, micro- and macroalbuminuria, respectively. In the whole group, Na+/Li+CT was significantly related to mean blood pressure (MBP; rs = 0.37, P less than 0.001) and AER (rs = 0.38, P less than 0.001). In a multiple regression analysis the significant correlates of AER, as a continuous variable, or of proteinuria (micro + macroalbuminuria), as a categorical variable, were Na+/Li+CT, MBP, duration of diabetes and glycosylated hemoglobin (HbA1). The frequency of normoalbuminuric patients with high Na+/Li+CT activity fell with duration of diabetes. The risk of proteinuria was significantly greater in patients with raised Na+/Li+CT compared to those with Na+/Li+CT within the normal range (odds ratio 3.8, 95% CI, 1.9 and 7.8). A relative excess of patients with proteinuria (micro + macroalbuminuria) was found in the group with elevated Na+/Li+CT and HbA1 above the median value (8.05%) of the whole population (chi 2 = 9.7, P less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of raised sodium-lithium countertransport activity in type 1 diabetic patients. 151 10

24-hour ambulatory blood-pressure measurements were obtained according to criteria of the German Hypertension League in 61 non-insulin-dependent diabetic patients after admission to hospital under clinical routine conditions. 30 patients had no signs of nephropathy; 15 patients showed signs of proteinuria of more than 0.5 g/d and/or renal insufficiency, and 16 patients were on chronic hemodialysis renal replacement therapy. Despite antihypertensive therapy, the majority of NIDDM patients with nephropathy and/or dialysis therapy were hypertensive. Hypertension of non-nephropathic patients showed a better response to therapy. About 50% of all patients with nephropathy had a higher mean arterial blood pressure at night than during the daytime. In about 25% of all diabetics with nephropathy, we found, during night time, an especially pronounced increase of both systolic and diastolic blood pressure of more than 5% above the daytime values. Diabetic patients without nephropathy already show a reduced night/daytime variation of blood pressure, however, inverse circadian rhythm as a sign of prognostically non-favorable autonomic neuropathy was found almost exclusively in the nephropathic diabetic patients.
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PMID:[24-hour blood pressure measurement in type-2 diabetic patients with and without nephropathy]. 151 18

A matched case-control study was performed to assess the prevalence of pathological proteinuria (greater than 50 mg/l) 18-34 years after onset of insulin-dependent diabetes mellitus (IDDM), in relation to intensive insulin therapy. Three groups of patients were studied greater than or equal to 18 years after onset of IDDM. In patients of group A and group B, intervention took place greater than or equal to 8 years after onset of IDDM: group A changed from traditional insulin therapy to continuous subcutaneous insulin infusion (CSII), and patients of group B changed from traditional insulin treatment (less than 3 injections/day) to multiple daily insulin injection therapy. Patients of group C continued traditional insulin therapy without intervention. The prevalence of pathological proteinuria was 3/21, 5/21, and 15/21 in group A, B, and C, respectively; 22.0 (95% confidence interval: 19.5 to 24.5) years, 22.1 (19.9 to 24.3) years, and 22.6 (20.2 to 25.0) years after onset of IDDM in group A, B, and C. The prevalence of pathological proteinuria differed significantly between group A and B vs. group C (x2 = 16.2, p less than 0.001; odds ratio 15 (3.2 to 70.3)). Glycosylated haemoglobin was 7.5 (6.9 to 8.1)% in group A, 7.6 (6.3 to 8.3)% in group B, and 8.9 (8.2 to 9.6)% in group C. In group A and B, 4/21 patients had hypertension, compared to 11/21 patients in group C. In group B, 1/21 patients had serum-creatinine greater than 130 mumol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathological proteinuria in patients with insulin-dependent diabetes mellitus: relation to intensive insulin therapy. 152 68

Seven diabetic patients with membranous nephropathy were immunohistologically studied in order to clarify the role of extrinsic insulin in membranous nephropathy. In three cases (group A), granular deposits of insulin were detected along the glomerular capillary wall with indirect immunoperoxidase technique using anti-porcine insulin antibody, where IgG and C3 were deposited in the identical pattern. The other four cases (group B), 8 of idiopathic membranous nephropathy, and 5 of diabetic glomerulosclerosis showed no insulin deposit in the glomerulus. Clinically, proteinuria was heavier in group A (mean +/- SE; 32.0 +/- 5.4 g/day) than in group B (5.5 +/- 0.5). Nephrotic syndrome developed after the beginning of the therapy with porcine insulin, and in two of them, proteinuria was ameliorated after porcine insulin was replaced by human insulin. Since porcine insulin is a heterologous peptide for human beings and has antigenicity when injected into patients, immune complex composed of insulin and anti-insulin antibody may cause membranous nephropathy in some diabetic patients treated with this animal insulin.
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PMID:Insulin deposits in membranous nephropathy associated with diabetes mellitus. 155 Dec 52

Diabetic nephropathy typically presents more than a decade after diagnosis of diabetes and correlates with the duration of poorly controlled disease. Diabetic nephropathy begins as glomerular hypertension and hyperfiltration, followed by microalbuminuria and the development of hypertension, overt proteinuria, nephrotic syndrome, and a progressive decline in the glomerular filtration rate. Increasing expansion of the glomerular mesangium correlates with loss of function, resulting in uremia. This process eventually leads to the need for dialysis or renal transplantation in 30 percent of patients with insulin-dependent diabetes. By lowering intraglomerular pressure through enhanced glycemic control, inhibition of angiotensin and limitation of protein intake, severe nephropathy may be prevented, delayed or even partially reversed. Treatment must stress control of hypertension.
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PMID:Diabetic nephropathy: early detection, prevention and management. 155 42

In an investigation into the effect of prostaglandin E1 on proteinuria in nephrotic diabetic nephropathy, five patients were treated with 40 micrograms prostaglandin E1 administered intravenously over 2 h twice daily for 4 weeks. The following parameters were compared before and after treatment: protein excretion in urine; total serum protein concentration; serum albumin concentration; creatinine clearance; blood urea nitrogen; and serum creatinine content. A further five patients with nephropathy resulting from non-insulin-dependent diabetes mellitus were selected as controls. Analysis of the results using Student's t-test showed no significant change in any of the parameters before and after treatment.
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PMID:Influence of prostaglandin E1 on slight proteinuria in non-azotaemic diabetics. 156 24

Percutaneous renal biopsies were performed in 30 diabetic patients who presented with proteinuria. Tissues were studied for evidence of an immune lesion using immunofluorescence techniques. No consistent pattern of binding of FITC labelled polyvalent, monospecific IgG, IgA, IgM and labelled bovine insulin antisera in various diabetic renal lesions could be demonstrated. The binding of labelled insulin was observed even in biopsies of patients who had never received exogenous insulin therapy. It was therefore concluded that there is no evidence to support an immune pathogenesis in the morphogenesis of the diabetic renal lesions, nor do these lesions occur as a result of insulin therapy.
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PMID:An immunofluorescence study of renal lesions in diabetes mellitus. 157 64


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