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

The proteinuria of fifteen patients treated with just aminoglycoside or aminoglycoside and either penicillin or cephalosporin was studied. The proteinuria was analysed by means of immunoelectrophoresis, acetate cellulose electrophoresis, thin-layer polyacrylamide gel electrophoresis and sodium dodecylsulphate acrylamide gel electrophoresis. We observed a urinary excretion of free immunoglobulin light chains and an increased urinary excretion of lysozyme in all cases. The increase in urinary excretion of beta-2-microglobulin and retinol-binding-protein appeared only in patients treated with aminoglycoside and cephalosporin. These disturbances disappeared a few days after the treatment was discontinued.
Proc Eur Dial Transplant Assoc 1979
PMID:Low molecular weight proteins as urinary markers of aminoglycoside nephrotoxicity in man. 9 49

Seventeen hypertensive patients were treated with captopril, an orally active inhibitor of converting-enzyme. All patients showed a fall in blood pressure (BP), although in some patients only after the addition of diuretics. In 2 patients a skin rash developed. One patient developed proteinuria. A renal biopsy revealed membranous glomerulopathy. Correlations were found between pretreatment plasma renin activity (PRA) and the decrease in BP, and between pretreatment PRA and the decrease in plasma aldosterone concentration (PAC). Filtration fraction (FF) fell, indicating a decrease in renal vascular resistance. Captopril decreased the sensitivity to exogenous angiotensin I (AI), dependent on the captopril dose used. The sensitivity to exogenous bradykinin increased impressively even on the lowest dose of the drug. These observations suggest extrapulmonary conversion of AI to angiotensin II (AII).
Proc Eur Dial Transplant Assoc 1979
PMID:Treatment of moderate to severe hypertensive patients with an orally active converting-enzyme inhibitor. 23 14

The clinical course of IgA Mesangial Deposits Glomerulonephritis (MDGN) has been investigated in 178 patients for 1 to 32 years (mean 6 years) from the onset of symptoms. Impairment of renal function occurred in 28 patients, 13 of whom required RDT or died in uraemia. Hypertension was observed in 67 patients. The actuarial survival rate at ten years was 91%. A significant correlation was observed between the occurrence of renal failure and the following features: absence of episodes of gross haematuria, early appearance of hypertension, marked proteinuria and sclerosing glomerular lesions. These data suggest that IgA MDGN has generally a very prolonged course, but in a few cases may evolve, sometimes early, to chronic renal failure.
Proc Eur Dial Transplant Assoc 1977
PMID:Long term follow up of IgA mesangial deposits glomerulonephritis. 60 Sep 63

Studies of renal tubular functions were made in two groups of patients with biopsy-proven primary glomerulonephropathies to assess the effects of proteinuria on the tubules. Group I (n = 9) had had minimal proteinuria and Group II (n = 8) had massive proteinuria. At the time the studies were made, all patients were normotensive, free of oedema, and on no dietary or drug therapy; they had normal glomerular filtration rates, serum albumin and total protein concentrations. Patients in Group II had diminished urine concentrating ability, impaired acidifying mechanism, but elevated maximum tubular secretory capacity compared with patients in Group I.
Proc Eur Dial Transplant Assoc 1977
PMID:Massive proteinuria and its effects on renal tubular functions. 60 Sep 66

Molecular weight analyses of urinary proteins in 34 patients following cadaveric kidney transplantation were performed by SDS-PAA-electrophoresis in order to diagnose transplant complications. A micromolecular 'tubular' proteinuria (mw 70-10,000) was found in all post-operative urines. Later on during clinically normal periods the patients exhibited an unphysiological proteinuria of mw 70-40,000. Recurrence of tubular proteinuria was associated with rejection episodes and acute kidney failure. Twelve patients developed a macromolecular glomerular proteinuria (mw greater than 60,000), caused by recurrent glomerulonephritis, glomerular rejection disease or renal vein thrombosis. Steroid treatment reduced the glomerular permeability for macromolecules above mw 65,000.
Proc Eur Dial Transplant Assoc 1975
PMID:Proteinuria as diagnostic marker after human kidney transplantation. 110 54

The risks of treating allograft rejection are primarily related to high-dose steroid therapy. To determine when the possible benefit of anti-rejection therapy might not justify the risks, we analysed 20 severe rejection (SAR) episodes for indices of reversibility. Prior renal function was similar in all patients. Ccr fell to 10 ml/min or less, but degree of renal dysfunction was not predictive of reversibility, nor were time since transplant, oliguro/anuria, proteinuria, or hypertension. The only consistent finding was that function began to improve in reversible rejection 3.8 +/- 1 days after beginning therapy. Our rejection treatment, based on this finding, is to use gram doses of IV prednisolone, up to three times in five to seven days. Among 41 patients with 45 grafts so treated, there was no fatality or gastrointestinal haemorrhage. Other complications (fistulae and/or infections) were related to total dose and frequency, to intensive therapy during severe renal dysfunction or to urinary leaks. Limitation of the period of high-dose steroid therapy was associated with reduced morbidity and mortality in renal allograft recipients.
Proc Eur Dial Transplant Assoc 1975
PMID:Minimising the risks of treating acute allograft rejection. 110 56

Cyclophosphamide was administered orally, in a dose just sufficient to depress the white-cell count to 3000-4000 per mm3 (mean 1.5 mg/kg/day), to 27 patients with proliferative glomerulonephritis for 12 months; 26 patients acted as controls. Cyclophosphamide conferred no benefit as judged by mortality, morbidity, renal function (serum creatinine and creatinine clearance) or proteinuria. The side effects of cyclophosphamide included permanent amenorrhoea in five of seven menstruating women. Since no controlled trial has yet shown that any immuno-suppressive drug benefits proliferative glomerulonephritis we question whether such drugs should be administered in this disease except in the course of planned prospective trials.
Proc Eur Dial Transplant Assoc 1975
PMID:A controlled trial of cyclophosphamide in the treatment of proliferative glomerulonephritis. 110 60

Renal biopsy and clinical data from 60 patients with crescent formation were correlated. Nephropathy was related to infection (15 cases), malignancy (four) and trichlorethylene exposure (two). Four cases had extrarenal signs. Isolated proteinuria was found 0.5-20 yr before biopsy in 16. Only 17 patients had rapidly progressive glomerulonephritis on clinical criteria. Nineteen patients (35%) are alive with functioning kidneys. Outcome was significantly related to percentage crescentic involvement (p less than 0.02) and oliguria (p less than 0.05) and renal function (p less than 0.01) at presentation. Preceding infection was a favourable sign. Extracapilly glomerulonephritis is not a single entity.
Proc Eur Dial Transplant Assoc 1975
PMID:The significance of extracapillary proliferation. 119 75

The influence of pregnancy on the progression of diabetic nephropathy in diabetic women with pre-existing moderate renal insufficiency is a subject of considerable controversy in the literature. In four of five female patients with type I diabetes mellitus with pre-existing impaired renal function (creatinine clearance less than 80 ml/min), significant proteinuria (greater than 2 g/24 h urine) and hypertension we have found a further decline in renal function during pregnancy, with an increased deterioration rate of creatinine clearance in comparison to the time before and after pregnancy. The mean decline of the glomerular filtration rate was 1.8 ml/min per month during pregnancy and 1.4 ml/min per month postpartum until the start of dialysis treatment. The difference in the progression of diabetic nephropathy during and after pregnancy can be explained by increased hypertension during pregnancy, especially in the third trimester, despite an intensified antihypertensive therapy. The long-term effect of pregnancy on renal function in our patients was therefore an earlier requirement for renal replacement therapy than would have been expected without pregnancy.
Nephrol Dial Transplant 1992
PMID:Influence of pregnancy on progression of diabetic nephropathy and subsequent requirement of renal replacement therapy in female type I diabetic patients with impaired renal function. 131 67

Several authors described a high incidence of proteinuria with frequent progression to nephrotic syndrome and/or renal failure in patients with HIV infection. Though renal histological changes were rather non-specific, the existence of a specific, HIV-associated glomerulopathy was postulated. We repeatedly investigated proteinuria and serum creatinine in 203 HIV-infected patients. One hundred and twenty-two patients (group 1) had early stages of the disease without opportunistic infections, 81 suffered from acute opportunistic infections (group 2). In patients with a positive qualitative test (Combistix), quantitative measurement (Biuret) for proteinuria was carried out; when proteinuria was greater than 0.5 g/24 h, SDS gel electrophoresis was performed. None of the patients of group 1 had a proteinuria greater than 0.5 g/24 h or an elevated serum creatinine. Eleven of 81 patients from group 2 had a proteinuria between 0.5 and 3 g/24 h; one further patient of group 2 developed a transient proteinuria of 7.7 g/24 h. Only three of the proteinuric patients showed a glomerular pattern in SDS gel electrophoresis, all three during acute CMV or EBV infections. Fourteen of 81 group 2 patients showed a transient elevation of serum creatinine (x +/- SD of the maximum serum creatinines: 225.3 +/- 163 mumol/l), most during pentamidine therapy for Pneumocystis carinii infection; one patient treated with high-dose acyclovir had to be temporarily dialysed. In the investigated 203 HIV patients no nephrotic syndrome and no sustained elevation of serum creatinine greater than 200 mumol/l was observed. All cases of proteinuria and elevation of serum creatinine were associated with severe opportunistic infections and the administration of potentially nephrotoxic antibiotics.
Nephrol Dial Transplant 1992
PMID:Lack of clinical evidence for a specific HIV-associated glomerulopathy in 203 patients with HIV infection. 131 85


1 2 3 4 5 6 7 8 9 10 Next >>