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)

Subclinical elevation of urinary albumin excretion is a good predictor of later clinical proteinuria. A simple, sensitive and rapid immunoturbidimetric method was developed to quantify urinary albumin excretion (URIN-PAK ImmunoMICRO LAB, Miles Italia Spa). In the presence of polyethylene glycol 6000, immunocomplex between human albumin and its specific antibody are rapidly formed (5-50 min, at room temperature). Absorbance reading are mode U 340 nm (Automatic Analyzer RA 1000, Technicon). The test is specific for albumin failing to cross react with other plasma proteins present in urine, as well as with glibenclamide, chlorpropamide, phenformin, hemoglobin, glucose, urea and thymol. The present method correlates with SCLAVO H-ALBUMIN RIA Kit (r = 0.9917). The test is suitable for clinical use.
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PMID:[Evaluation of a new immunoturbidimetry technique for measuring microalbuminuria]. 193 Sep 2

A prospective study was performed to investigate the outcome and complications of pregnancy in patients with systemic lupus erythematosus. Twenty-nine pregnancies occurred in 22 patients. There were 12 abortions, two spontaneous and 10 induced. Fifteen women had 17 live-born neonates. Neonatal complications included nine premature deliveries, two cases of intrauterine growth retardation, and one of Treacher Collins syndrome. Obstetric complications included threatened abortion (two), placenta previa (two), and preeclampsia (three). Cesarean sections were necessary in five patients. There was no maternal or neonatal mortality. Thirteen episodes of systemic lupus erythematosus relapses were detected by incidents of increasing proteinuria (six), arthritis (four), and vasculitic rash (two). There were no statistical differences in changes in hemoglobin level, erythrocyte sedimentation rate, albumin level, antinuclear antibody titer, or C3 or C4 level between the patients who relapsed and those who did not. Pregnancy could induce a flare of systemic lupus erythematosus in previously normal patients or patients with previously inactive disease. The overall neonatal and maternal survival was good, even in patients who presented during pregnancy. Spontaneous fetal loss was low (2/29 [6.9%]); both cases occurred in mothers with inactive lupus.
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PMID:Outcome of pregnancy in patients with systemic lupus erythematosus. A prospective study. 199 54

We describe the clinical outcome of 13 patients with non-insulin-dependent diabetes mellitus (NIDDM), renal insufficiency, and proteinuria, treated for 12.2 +/- 12.9 months (mean +/- SD) with a low-protein, very-low-phosphorus diet (LPVLP) containing 30 g protein and 11.3 mmol (350 mg) phosphorus. After a control period of 18.2 +/- 20.4 months, LPVLP therapy was initiated and serum urea nitrogen, uric acid, and phosphate, as well as urinary excretion of protein, creatinine, urea nitrogen, uric acid, and phosphate, decreased significantly. There was no change in mean blood pressure, hemoglobin, blood pH, and HCO3-, as well as in serum creatinine, protein, albumin, calcium, magnesium, cholesterol, triglyceride, beta-lipoprotein, and high-density lipoprotein (HDL)-cholesterol. Nitrogen balances were measured over 5 weeks in nine patients. Nitrogen balance increased significantly from a negative balance of -0.795 +/- 1.367 g/d in the first week, to almost neutral in the fourth week, and later, was neutral or positive. Neither uremic symptoms nor signs of malnutrition appeared during the LPVLP period. These results suggest that negative nitrogen balance during the initial few weeks does not predict future nutritional status of patients with diabetic renal failure.
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PMID:Effect of low-protein, very-low-phosphorus diet on diabetic renal insufficiency with proteinuria. 206 52

Epidemiologic data on the incidence of gross proteinuria in people with diabetes are important in medical counseling, in projecting estimates of needs and costs of health care, and for developing approaches to prevent renal complications. We performed a population-based incidence study in southern Wisconsin of insulin-taking diabetic persons diagnosed before 30 years of age. The presence of gross proteinuria (greater than or equal to 0.30 g/L) was determined by means of a reagent strip. The incidence of proteinuria in a 4-year interval was 14.4% (95% confidence interval, 11.7% to 17.0%). The relative risk of developing proteinuria after 4 years for those with glycosylated hemoglobin levels in the highest quartile compared with those in the lowest quartile was 3.0 (95% confidence interval, 1.6 to 5.3). The incidence of proteinuria was also associated with higher diastolic blood pressure, being male, taking more insulin, and having more severe retinopathy at the baseline examination. The relationship between glycosylated hemoglobin level and the incidence of proteinuria was significant even after controlling for these other risk variables. These data suggest that hyperglycemia, as measured by glycosylated hemoglobin level, is a significant risk factor for the development of gross proteinuria.
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PMID:The incidence of gross proteinuria in people with insulin-dependent diabetes mellitus. 206 75

Genetically diabetic mice (db/db) were given 50 mg/kg body weight/day substance L, a nontoxic basic amino acid and compared to control diabetic mice without treatment. The oral administration of the compound was started at the age of 3 months and the animals were sacrificed at the age of 7 months. No adverse effects were observed in animals given the substance L. Total food consumption, drinking water intake and body weight were comparable between the groups. Nonenzymatic glycosylation of serum proteins and hemoglobin was not significantly different in the groups. Renal pathological lesions in the control diabetic mice showed glomerular mesangial expansion and on electron microscopy thickened glomerular basement membranes with a mean thickness of 3,204 +/- 186 A. Treated animals showed significantly less mesangial crescents and thinner glomerular basement membrane thickness of 2,520 +/- 252 A (p less than 0.01). The experimental animals showed in addition a lower mean kidney weight. Glomerular but not tubular proteinuria was reduced in the treated group. Basement membrane collagen type IV isolated from kidneys of experimental animals was more soluble in acidity and showed a lower degree of cross-linking as evaluated by SDS-polyacrylamide gel electrophoresis. We conclude that substance L is beneficial to diabetic renal changes. We suggest that this positive effect could be due to the inhibition of glucose-mediated abnormal cross-linking of collagenous structures by the interaction of substance L with reactive carbonyl residues of glycosylation adducts of collagen. Other possible mechanisms are discussed.
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PMID:The effect of substance L on glucose-mediated cross-links of collagen in the diabetic db/db mouse. 207 11

In a retrospective study, we analyzed the prevalence of diabetes-associated late complications in 549 type 1 (insulin-dependent) diabetic patients who have been treated at the University Hospital of Ulm between 1980 and 1987. Retinopathy, proteinuria and neuropathy depended on the duration of the disease, whereas age was the major determinant of large vessel disease. After 20 years of diabetes, 85% of the patients showed retinopathy, half of them proliferative retinopathy, 52% had persistent proteinuria (greater than 500 mg/day), 20% of them were under dialysis. 74% of the patients showed signs of peripheral and/or autonomic neuropathy, 19% had manifestations of large vessel disease. There was no consistent correlation between the levels of glycosylated hemoglobin and the occurrence of diabetic late complications. However, hypertension was closely associated with both small and large vessel disease.
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PMID:[Prevalence of secondary complications in patients with type I diabetes mellitus. Results of a retrospective analysis of 549 type I diabetic patients of the Ulm University clinic]. 208 8

Thrombotic thrombocytopenic purpura (TTP) is a syndrome that occurs mainly in adults with multiorgan microvascular thrombosis consisting of thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, renal involvement, and fever. The female to male ratio is 3:2, and peak incidence occurs in the 3rd decade of life. Clinical signs are the consequence of hyaline thrombosis and occlusion of capillaries and arterioles. Renal ailment manifests itself in hematuria and proteinuria with azotemia and even overt renal failure. In severe disease, azotemia is typical of hemolytic uremic syndrome (HUS). TTP was first described in 1925 by Moschcowitz. The clinical picture of TTP consists of a prodromal phase, a viruslike disease occurring in up to 40% of patients. 60% have neurologic disturbances, 90% have purpura initially, and fever occurs in all. Anemia is often severe with hemoglobin values of 7-9 gm/dl, renal involvement in 90%, and renal failure in 40-80% of patients. Clinical variants include the acute and fulminant variety mortality, the chronic form, and the relapsing form. Predisposing factors and triggering agents are autosomal recessive inherited traits in acute idiopathic TTP, systemic diseases, tumor antigens, pregnancy and puerperium, viruses (endotoxins for HUS), and possibly oral contraceptives and hypertension. Therapy includes corticosteroids (prednisone 100-400 mg/day); heparin for postpartum HUS; and antiplatelet agents (Dextran 70, aspirin, and dipyridamole in high doses). The infusion of PGI2 is controversial; splenectomy is also questionable; and vincristine, azathioprine, and cyclophosphamide have unproven efficacy. Fresh-frozen plasma exchange is the method of choice as it produces survival in 90%. Others are iv immunoglobulins, vitamin E, and dialysis and renal transplant. Platelet transfusions are contraindicated because of sudden death and decreased survival.
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PMID:Thrombotic thrombocytopenic purpura and related disorders. 210 74

The kidney is involved in virtually all individuals who inherit the sickle cell form of hemoglobin. Though asymptomatic and relatively common, proteinuria in patients with sickle cell anemia (SS) over 40 years old is associated with reduced creatinine clearance. The subclinical increase in urinary albumin is termed microalbuminuria and is a marker of preclinical glomerular damage. The aim of the present study was to determine the presence of microalbuminuria measured by radioimmunoassay in patients with sickle cell disease. The study included 41 patients with SS, 11 patients with hemoglobin SC disease, 4 subjects with S beta-thalassemia and 10 normal controls. All subjects were teenagers or adults. Sixteen SS patients (40%) and 1 SC (9%) and 1 S beta (25%) patient presented mean urinary albumin excretion (UAE) above normal values (30 mg/l. No correlation was observed between UAE and age, creatinine clearance, hemoglobin level or %HbF. These parameters, as well as the presence of leg ulcers, were not significantly different between SS patients with and without UAE above 30 mg/dl. The high prevalence of microalbuminuria in patients with sickle cell anemia indicates that glomerular damage is common. The connection between microalbuminuria and clinical nephropathy has been demonstrated in diabetes and may indicate a sign of early disease rather than a marker for susceptibility. Thus, microalbuminuria may be an early indicator of glomerular damage for patients with sickle cell disease.
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PMID:Microalbuminuria in sickle cell disease. 213 17

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

Thrombomodulin is an endothelial cell membrane protein acting as a cofactor for the activation of plasma protein C. Recently, it was found that soluble forms of thrombomodulin exist in plasma. Although the physiological significance of circulating thrombomodulin is presently obscure, it may reflect injury of the endothelial cell. In the present study, we examined plasma thrombomodulin concentrations in 106 Type 2 (non-insulin-dependent) diabetic patients. Plasma thrombomodulin was determined by a sandwich ELISA employing monoclonal anti-thrombomodulin antibodies. The patients with proteinuria had higher plasma thrombomodulin concentrations (61.0 +/- 36.0 ng/ml) compared to the patients without proteinuria (33.6 +/- 9.5 ng/ml, P less than 0.001) and control subjects (32.8 +/- 6.5 ng/ml, P less than 0.001). Plasma thrombomodulin concentrations were positively correlated with the level of serum creatine, blood urea nitrogen, urinary albumin and urinary beta 2-microglobulin (P less than 0.001 for each), but not with fasting plasma glucose, hemoglobin A1c or fructosamine. Elevated plasma thrombomodulin was also observed in the patients with pre-proliferative (63.4 +/- 28.9 ng/ml) or proliferative retinopathy (57.4 +/- 34.7 ng/ml), but not in the patients with non-proliferative retinopathy (33.5 +/- 12.9 ng/ml) or those without retinopathy (32.4 +/- 8.9 ng/ml). Even in the 81 diabetic subjects without proteinuria as determined by a dip and read method, and whose serum creatinine was lower than 1.0 mg/dl, the plasma thrombomodulin concentration was significantly higher in the patients with pre-proliferative (41.5 +/- 4.4 ng/ml) and proliferative retinopathy (41.0 +/- 12.8 ng/ml) compared to the patients without retinopathy (32.2 +/- 8.8 ng/ml) and those with non-proliferative retinopathy (31.9 +/- 7.8 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma thrombomodulin concentration in diabetes mellitus. 217 97


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