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)

Human hereditary nephritis refers to familial glomerular diseases which may progress to renal failure. Samoyed hereditary glomerulopathy has been shown previously to be a model for hereditary nephritis. Clinical and laboratory studies were performed to follow progression to renal failure in 44 dogs in a family with Samoyed hereditary glomerulopathy. Affected males appeared healthy for their first three months but then became progressively wasted. Proteinuria was detected between two to three months of age; after five months, urine protein electrophoresis showed pre-albumin, albumin and alpha and beta globulin peaks. From three months onward, a reduced glomerular filtration rate was detected. Serum albumin decreased while amylase, urea, creatinine and phosphate increased from four to five months of age. Death from renal failure occurred by 15 months. Carrier females also became thinner and developed proteinuria between two and three months of age, but neither renal failure nor death ensured. Hence, SHG progressed rapidly in affected males but not in carrier females.
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PMID:Samoyed hereditary glomerulopathy: serial, clinical and laboratory (urine, serum biochemistry and hematology) studies. 365 95

During a four-year period, 17 massively obese patients without clinically apparent systemic disease underwent renal biopsy for marked proteinuria. Clinical information and biopsy results were compared with those in 34 normal-body-weight controls matched for age, sex, and similar presentation. Histopathologic changes characteristic of focal glomerulosclerosis were found in nine (53%) of the obese patients and two (6%) of the controls. In addition, five (29%) of the obese patients had occult diabetic nephropathy, while no diabetic changes were seen in controls. Clinically, obese patients resembled controls in most respects. Serum albumin level, however, was higher than in controls (3.5 +/- 0.2 vs 2.5 +/- 0.1 g/dL). Indeed, obese patients with focal glomerulosclerosis had normal serum albumin levels (4.0 +/- 0.1 g/dL). Thus, primary renal disease in massively obese patients with marked proteinuria differed in several important respects from that seen in normal-body-weight patients with a similar degree of proteinuria.
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PMID:Renal disease in patients with massive obesity. 371 96

We studied the efficacy of captopril, an angiotensin-converting enzyme inhibitor in treating persistent moderate or severe proteinuria in children with various glomerular diseases other than minimal-change nephrotic syndrome. Captopril was administered for 3 months to 15 normotensive and nonazotemic or mildly azotemic patients (12 boys, 3 girls) in whom corticosteroid and cytotoxic treatment had failed to induce remission. Urinary protein excretion decreased from 2873.14 +/- 1937.50 (mean +/- s.e.m.) to 1684.71 +/- 1463.13 mg/day (P < 0.05). The reduction in proteinuria was not related to a significant fall in systemic blood pressure or a change in renal function. Serum albumin did not rise and side effects due to captopril were not observed. We concluded that, in the short term, captopril can be used safely and effectively for decreasing the proteinuria of nephrotic children unresponsive to conventional therapy.
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PMID:Efficacy of captopril treatment in children with steroid-resistant nephrotic syndrome. 787 77

We used C3-deficient (C3D) guinea pigs to evaluate the role of C3 in an active model of experimental nephritis. Normal strain 2 (C3N, n = 13) and C3D (n = 6) guinea pigs were immunized with cationized bovine gamma-globulin (CBGG). Fourteen days later (Day 0), daily intravenous injections of CBGG were given for 3 to 7 days and the animals were sacrificed on Day 10 or 21. Immunofluorescence (IF) microscopy of renal tissue revealed two patterns of glomerular IgG deposition: granular loop (11/13 C3N, 3/6 C3D), and predominantly mesangial (2/13 C3N, 3/6 C3D). Codeposited C3 was seen in all C3N and in no C3D animals. Electron microscopy showed subepithelial deposits in all. A significant correlation (P < 0.005) was seen between an animal's IF pattern and its level of serum antibodies to CBGG; those with lower antibody levels exhibited the mesangial pattern. C3D animals had lower mean antibody levels than C3N (P < 0.01), but both IF patterns were represented. Urine protein concentration, which was increased relative to controls, did not differ between C3N and C3D groups, but was significantly greater in those with loop IF. Serum albumin was significantly reduced in animals with loop IF. C3N animals showed a significant reduction in mean serum C3. In this model, immune deposit location and degree of proteinuria are independent of C3 deposition and dependent upon the level of antibody response to CBGG. Induction of antibody to CBGG is impaired in the absence of C3.
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PMID:C3-independent glomerulonephritis in guinea pigs: dependence upon primary humoral response. 799 27

Dietary supplementation with n-3 polyunsaturated fatty acids (n-3 PUFA) has been shown to reduce proteinuria in experimental models of renal diseases, but their potential role in the treatment of human renal disease is unknown. We administered n-3 PUFA in the form of triglycerides [with eicosapentaenoic (EPA)+docosahexaenoic (DHA) = 3 g/day into 4 patients] and of ethyl esters (EPA+DHA = 7.7 g/day) into 10 patients (one patient twice) with chronic glomerular disease (membranous glomerulonephritis and focal glomerular sclerosis), all diagnosed histologically. Serum albumin was > 2.4 g/dl and serum creatinine < 2.5 mg/dl in all patients. Treatment was given for periods of six weeks, followed by a prolonged follow-up for 27 weeks in 10 cases. Dietary supplementation with n-3 PUFA caused the expected reduction in platelet generation of thromboxane B2 (mean +/- SEM, from 490 +/- 70 ng/ml at baseline, to 342 +/- 147 ng/ml at 6 weeks, P < 0.05) of serum triglycerides (from 236 +/- 60 to 170 +/- 43, P < 0.01), and a prolongation of the bleeding time (from 5.8 +/- 0.4 min to 7.7 +/- 0.4 min, P < 0.01) in patients treated with ethyl esters. A modest but significant reduction in serum total cholesterol was noticed (from 275 +/- 27 to 252 +/- 24 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:n-3 fatty acids reduce proteinuria in patients with chronic glomerular disease. 825 59

The incidence, causes, and consequences of hypoalbuminemia after renal transplantation are not well defined. We examined clinical correlates of serum albumin measured at 3 months, 6 months, 1 year, and annually thereafter in 706 renal transplant recipients who survived at least 6 months with a functioning allograft. Follow-up was 7.0 +/- 4.2 years. Hypoalbuminemia (< or = 3.5 g/dL) was most common at 3 months (31%, n = 692), least common at 1 year (12%, n = 656), and then became increasingly common among survivors, for example, 14% (n = 466) at 4 years, 20% (n = 204) at 8 years, and 29% (n = 77) at 12 years after transplantation. By multiple linear regression, variables that correlated (P < 0.05) with lower serum albumin at 3, 6, 12, and 24 months included age, diabetes, proteinuria, and cytomegalovirus infection. Other independent correlates on at least one of these occasions included renal function and chronic disease (malignancy, liver disease, and cardiovascular disease). Serum albumin, as a time-averaged and time-dependent covariate, was a strong independent risk factor for death using Cox proportional hazards analysis (relative risk for each g/dL increment, 0.26; 95% confidence interval, 0.16 to 0.44 [1.00 = no risk]). The effects of albumin on mortality were independent of age, diabetes, serum lipids, renal function, chronic liver disease, malignancies, and cardiovascular disease. The effects of albumin on mortality were evident even when the analysis was restricted to patients dying several years after albumin was measured. Thus, hypoalbuminemia is common and serum albumin is a strong independent risk factor for all-cause mortality after renal transplantation.
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PMID:Serum albumin and mortality after renal transplantation. 854 25

Human immunodeficiency virus nephropathy (HIVN) continues to challenge nephrologic consultative services at major urban institutions. Although noted in the literature, the decreased incidence of peripheral edema in HIVN has been unexplained to date. In HIV patients, total proteins frequently are found to be elevated due to an elevated globulin fraction. The impact that plasma proteins, specifically globulins, have on the total oncotic pressure has not been reported in HIVN, but may play a role in the paucity of edema noted in this proteinuric population. To evaluate the contributions of serum globulin to the total oncotic pressure and the presence or absence of edema in HIVN, we randomly selected 27 patients with proteinuria greater than 2.5 g/24 hr and serum albumin less than 3.1 g/dL from patients presenting to the nephrology outpatient clinic at the University of Miami/Jackson Memorial Hospital. Seventeen of the patients (63%) had a known diagnosis of HIV infection (group 1). These patients were subdivided into two subgroups: those presenting with clinically evident edema on physical examination (n = 7 [41%]; group 1A) and those who had an absence of edema (n = 10 [59%]; group 1B). Conversely, group 2 comprised 10 patients without known HIV infection, of whom six (60%) had edema (group 2A) and four (40%) did not (group 2B). Blood pressures were noted, and mean arterial pressure was calculated using standard formulas. Serum albumin, serum total proteins, and urine total proteins were measured using standard laboratory methods. Oncotic pressures for albumin (alpha), globulin (beta), and total protein (c) were calculated using the following formula: COPpl = alpha(2.8c + 0.18c2 + 0.012c3) + beta(0.9c + 0.12c2 + 0.004c3). We used Student's t-test to analyze the data. There is no significant difference between the albumin concentrations of HIV patients without edema (group 1B) and non-HIV patients with edema (group 2A), with mean concentrations of 2.3 +/- 0.1 g/dL versus 2.3 +/- 0.15 g/dL, respectively (P = NS). Group 1B, however, has a total oncotic pressure of 17.1 +/- 1.5 mm Hg, whereas both groups with edema (groups 1A and 2A) have statistically significant lower total oncotic pressures (12.1 +/- 2.3 mm Hg and 12.9 +/- 1.1 mm Hg, respectively; P < 0.05). The globulin oncotic pressures may account for some of the differences in total oncotic pressures, being significantly higher for those patients without edema in group 1B compared with group 2A (7.1 +/- 0.9 mm Hg v 3.9 +/- 0.4 mm Hg, respectively; P < 0.05). In patients with HIV, however, the presence or absence of edema is mandated by albumin concentration because both groups have similar globulin concentrations (group 1A 3.1 +/- 0.1 g/dL v group 1B 3.8 +/- 0.3 g/dL; P = NS). Mean arterial pressure does not play a role in edema formation in this study because the HIV patients without edema had the higher blood pressures (group 1B 97.8 +/- 4.7 mm Hg v group 2A 84.7 +/- 5.5 mm Hg; P < 0.05). We conclude that globulins play an important role in maintaining oncotic pressure in low albumin states. HIVN patients with increased serum immune globulin may benefit from higher globulin oncotic pressure, delaying the onset of clinical edema in the setting of proteinuria.
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PMID:Oncotic pressure and edema formation in hypoalbuminemic HIV-infected patients with proteinuria. 939 27

Some degrees of protein deficiency, suggestive of abnormal protein metabolism, are a well-known feature of chronic renal failure (CRF). Serum albumin concentration, an index of malnutrition and deranged protein metabolism, is frequently decreased relatively early in CRF, even in absence of heavy proteinuria: a more subtle but characteristic abnormality is found in the plasma profile of amino acids. In addition, there is an accumulation in the plasma and tissues of many products of protein metabolism; some of these have been considered as uremic toxins, while others are largely undefined. The origin of abnormalities in protein metabolism are multifactorial. The defect are caused at least partly by dietary deficiency, as well as by the inability of the failing kidney to excrete normal end products of nitrogen and protein metabolism and by the effect of altered uremic milieu on overall metabolism.
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PMID:[Protein and amino acid metabolism in chronic renal failure]. 955

Fifteen patients of idiopathic nephrotic syndrome who failed to respond to 8 weeks of corticosteroid therapy formed the material for this study. There were 10 males and 5 females, age ranging from 4 to 56 years. Three patients had hypertension. Histological lesions were focal and segmental glomerulosclerosis (FSGS) in 8; membranous glomerulonephritis in 3; mesangial proliferative glomerulonephritis in 2 and membranoproliferative glomerulonephritis in 2 patients. Proteinuria ranged from 3.64 to 8.66 g/1.73 m2/day. Serum albumin ranged between 2.2 to 3.3 g/dl. Serum creatinine was elevated > 1.5 mg/dl in 3 cases. After discontinuing steroids, enalapril was started in a dose of 2.5 mg/day and increased by 2.5 mg/day every 3-4 days till the maximum tolerated dose but not exceeding 20 mg/day. Proteinuria, serum albumin and serum creatinine estimations were done every 4 weeks for six months and every three months thereafter. Patients were followed up for 6 to 30 months. Proteinuria decreased to < 1.5 g/1.73 m2/day in 12 patients (80%) and to < 0.5 g/1.73 m2/day in 10 patients (66.7%) by 8 weeks. There was no significant decrease in proteinuria in 3 (20%) patients; two of these were cases of FSGS and one of membranoproliferative glomerulonephritis. Oedema, hypoalbuminaemia and hypercholesterolaemia returned to normal in all patients who had a decrease in the proteinuria. There was no correlation between the histological lesion and response to enalapril. There was no rise in the serum creatinine level above the baseline in any of the patients. Except for cough in one patient, no other significant side effects were observed. We conclude that enalapril is effective in reducing proteinuria and thereby the morbidity in steroid resistant nephrotic syndrome irrespective of the underlying pathology.
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PMID:Efficacy of enalapril in the treatment of steroid resistant idiopathic nephrotic syndrome. 1099 84

Primary membranoproliferative glomerulonephritis (MPGN) has a poor long-term prognosis, with 40 per cent of patients reaching end-stage renal failure after 10 years of observation. Approximately 35 per cent of patients die due to complications of the nephrotic syndrome. This study investigates the effect of acetylsalicylic acid (ASA) combined with dipyridamole on proteinuria and renal function in nephrotic MPGN patients with normal/moderately reduced glomerular filtration rate (GFR). Fourteen patients with biopsy-proven type I MPGN received ASA (1000 mg/day) and dipyridamole (300 mg/day) for 24 months. Proteinuria was reduced from 6.8 +/- 2.4 g/day to 1.1 +/- 0.6 g/day (p < 0.001). Serum albumin levels increased from 2.2 +/- 0.5 g/dL to 3.7 +/- 0.4 g/dL (p < 0.001) during the study period after 24 months compared to baseline. Serum creatinine and GFR did not significantly change in patients treated with acetylsaliclylic acid and dipyridamole during the observation period (p < 0.05). Our study suggests that ASA combined with dipyridamole significantly reduces proteinuria without impairing renal function in patients with MPGN.
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PMID:Effect of acetylsalicylic acid and dipyridamole in primary membranoproliferative glomerulonephritis type I. 1223 Feb 99


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