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)

We studied the effects of symptomatic, antiproteinuric treatment with NSAID's (n = 28) and ACE-inhibitors (n = 14) in patients with proteinuria due to idiopathic membranous glomerulopathy (MGP). These two treatment groups were compared with a group of patients who did not receive antiproteinuric medication (n = 14). Urinary protein loss was effectively lowered by NSAID and ACE inhibitor therapy from 9.5 +/- 1.0 to 4.5 +/- 0.5 g/day (mean +/- SEM) and from 9.8 +/- 1.4 to 3.9 +/- 0.7 g/day respectively, whereas the control group showed a slight fall in proteinuria from 6.9 +/- 0.8 to 5.5 +/- 0.8 g/day. As a result of this treatment hypoalbuminaemia and hypercholesterolaemia improved significantly: serum albumin rose in the NSAID group from 25.4 +/- 1.2 to 29.0 +/- 1.0, and in the ACEi group from 29.9 +/- 1.8 to 32.7 +/- 1.2 g/l (control group from 27.4 +/- 1.6 to 27.8 +/- 1.6 g/l, while cholesterol was lowered in the NSAID group from 8.5 +/- 0.5 to 7.5 +/- 0.4 and in the ACEi group from 8.7 +/- 0.5 to 7.6 +/- 0.4 mmol/l (control group from 9.7 +/- 1.1 to 8.5 +/- 1.0 mmol/l). The antiproteinuric effect of both drugs was well maintained during an 18-month follow-up. Progression towards end-stage renal failure was observed especially in patients with impaired renal function at entry. Remission of proteinuria occurred particularly in patients with lower baseline values of proteinuria, irrespective of the treatment modality.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1992
PMID:Antiproteinuric drugs in patients with idiopathic membranous glomerulopathy. 133 89

Investigations of glomerular anionic charge status in human renal biopsies have previously been restricted, by the techniques and markers used, to staining of sites in pre-embedded tissue. The introduction of a novel marker, cationic colloidal gold, which demonstrates fixed anionic sites in hydrophilic resin (LR Gold)-embedded, ultrathin tissue sections, has now enabled glomerular charge to be evaluated in routine biopsy material. The cationic gold marker detects components which express anionic charge under different pH conditions. The patterns of staining in tissue showing minor glomerular pathology and low proteinuria, together with enzyme-digestion studies indicate that anionic sites are normally associated with heparan sulphate proteoglycans, glycocalyx sialoproteins, hyaluronic acid, and other GBM components which have not yet been characterised. Several charge aberrations involving different pathological mechanisms have been identified using cationic gold. These aberrations may be categorised according to the pathological basis of the charge pattern defect, rather than glomerular disease classification, as a prelude to the precise identification of the anionic sites and their functional importance in relation to the glomerular charge selectivity barrier. The categories which have been defined are: (1) 'Normal', (2) interrupted, (3) neutralised, (4) structurally disorganised, and (5) depleted. As sites are further characterised sub-categorisation is likely. We anticipate that this approach will help to elucidate both the participation of charged components in disease pathogenesis and their role in relation to glomerular proteinuria.
Nephrol Dial Transplant 1991
PMID:Cationic colloidal gold--a novel marker for the demonstration of glomerular polyanion status in routine renal biopsies. 172 90

Although some cases of tubular dysfunction (TD) associated with nephrotic syndrome have been described, the incidence and the characteristics of this complication remain unknown. We investigated the presence of TD (renal glycosuria, aminoaciduria, metabolic acidosis with normal anion gap, hypouricaemia, and throughout hypophosphataemia) in 36 patients with nephrotic syndrome. Ten patients (group 1) showed glycosuria at some time during the course of their illness, ranging from 2.5 to 11.2 g/24 h. In addition, seven of them had metabolic acidosis with normal anion gap, five aminoaciduria, and two hypouricaemia. Membranous glomerulonephritis was the most frequent aetiology in group 1 patients (7 of 10). Proteinuria and serum creatinine (SCr) were significantly higher in group 1 patients than in the 26 remaining patients without TD (group 2): 10.2 +/- 3.7 versus 6.7 +/- 2.9 g/24 h (P less than 0.01) and 3.2 +/- 1.9 versus 1.6 +/- 0.9 mg/dl (P less than 0.05) respectively. The appearance of TD coincided with a clear worsening of renal function in most of group 1 patients. In addition, at the end of follow-up, SCr had increased from 3.2 +/- 1.9 to 5.6 +/- 3.3 mg/dl (P less than 0.05) in this group. In contrast, SCr did not show significant changes in group 2 (1.6 +/- 0.9 versus 2.1 +/- 2.2 mg/dl). In conclusion, a significant proportion (27.7%) of patients with nephrotic syndrome present TD data at some moment of their course; the appearance of this complication appears to be a sign of poor prognosis.
Nephrol Dial Transplant 1991
PMID:Tubular dysfunction in nephrotic syndrome: incidence and prognostic implications. 175 3

In a retrospective study the incidence and consequences of acute renal failure were evaluated in 324 renal transplantations performed in our centre. The overall incidence of acute renal failure was 31.2%. In recipients with acute renal failure, patient and graft survival were significantly worse than in those without acute renal failure (P less than 0.02 and P less than 0.0001 respectively). Acute renal failure also increased the morbidity during the first 3 months after transplantation. Three months after transplantation renal function as determined by serum creatinine and proteinuria, was less satisfactory. Factors influencing the incidence of acute renal failure appeared to be: match grade on the AB locus, percentage of antibodies, duration of dialysis, number of blood transfusions prior to transplantation, anastomosis time and total ischaemia time. Recipients transplanted for the first time were less likely to develop acute renal failure, but also for this group total ischaemia time was a prognostic factor for the development of acute renal failure. When recipients were allocated to different classes of total ischaemia time it appeared that the incidence of acute renal failure differed, especially between groups with total ischaemia time 32-36 h (27%) and 36-40 h (38%). The difference in acute renal failure between these groups was also reflected in a difference in graft survival for total ischaemia time less than 36 h and greater than 36 h. Thus, it appears that acute renal failure has a detrimental effect on graft survival and postoperative morbidity in renal transplantation. Total ischaemia time is one of the prognostic factors for the development of acute renal failure. To improve renal transplantation results it is worth attempting to shorten total ischaemia time.
Nephrol Dial Transplant 1991
PMID:Detrimental effect of acute renal failure on the survival of renal allografts: influence of total ischaemia time and anastomosis time. 177 54

Five patients (median age 63 years) with severe crescentic glomerulonephritis had acute renal failure (median plasma creatinine 930, range 690-1390). Following induction of immunosuppressive treatment all patients achieved recovery of adequate renal function (median creatinine 440, range 290-570 mumol/l). After 3-6 months of continuous remission, all patients, despite stable renal function developed increasing proteinuria (median 4.4 g/24 h, range 3.2-6.1), and enalapril (5-20 mg per day) was substituted or introduced as antihypertensive therapy. Immunosuppression was not altered. After 1 year, renal function remained stable in four patients and plasma creatinine increased initially in one patient before becoming stable: proteinuria was reduced substantially in all patients to a median of 0.8 g/24 h, range 0.2-1.3). Patients with severe crescentic glomerulonephritis may develop persistent or increasing proteinuria despite successful treatment of acute disease. We have used enalapril to reduce proteinuria and maintain function in such patients.
Nephrol Dial Transplant 1991
PMID:Effect of enalapril on proteinuria and renal function in patients with healed severe crescentic glomerulonephritis. 179 92

Sixty patients with primary glomerulonephritis and nephrotic range proteinuria (most resistant to corticosteroid therapy) were given killed BCG inoculations as a major part of combined therapy with levamisole, 3 of every 7 days, and corticosteroids in 53 patients. Following treatment 80% of patients showed complete or partial remission of proteinuria with significant improvement in urinary protein excretion, serum albumin, blood urea, and serum creatinine. Thirteen of 15 patients followed up for 1-2 years and more had complete remission at the latest review, as did five of six patients followed for less than 1 year. The longer the course of the combined immunostimulant treatment, the lower the recurrence rate. The beneficial effects of retreatment in recurrent cases were much more rapid in onset than on initial treatment. The phagocytic function of monocytes was examined in a separate group of 24 patients with primary glomerulonephritis. Function was found to be significantly depressed but could be returned to normal following BCG inoculation. Associated with the improved monocyte phagocytic function there was a significant decrease in urinary protein excretion.
Nephrol Dial Transplant 1991
PMID:Clinical studies in the use of BCG and levamisole in the treatment of glomerulonephritis. 195 53

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
Nephrol Dial Transplant 1991
PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

Six cases of chronic renal failure related to granulomatous renal sarcoidosis are reported and compared with data in the literature. The particular features of sarcoidosis granulomatous interstitial nephritis should be emphasised because presentation may be misleading. Renal failure usually presents with a rapidly progressive course, either isolated or associated with mild proteinuria and sterile leukocyturia, while extrarenal localisations may be absent. Diagnosis should be suspected on the basis of elevated or paradoxically normal serum calcium concentrations, due to increased plasma concentrations of calcitriol, while immunoreactive circulating parathormone concentrations are depressed. Calcitriol as well as angiotensin-converting enzyme could represent unregulated secretion products from granulomatous tissue and their plasma concentrations may roughly reflect activity of the disease. Early corticosteroid treatment dramatically improves renal function but long-term renal prognosis may be oblitered due to progressive chronic renal failure related to fibrosis scarring.
Nephrol Dial Transplant 1990
PMID:Renal granulomatous sarcoidosis: report of six cases. 210 82

Treatment of patients with membranous glomerulonephritis with prednisone on alternate days results in a decreased proteinuria on non-prednisone days. We have studied this phenomenon in more detail in 14 patients (11 M, 3 F) with membranous glomerulonephritis. Mean age +/- SD of the patients was 47 +/- 14 years, mean endogenous creatinine clearance 94 +/- 35 ml/min, and median proteinuria 8.8 g/24 h (range 5.0-30.0 g/24 h). Glomerular filtration rate (GFR, inulin clearance), effective renal plasma flow ERPF, PAH clearance), and proteinuria were measured on a control day (C), and six days after the start of alternate-day prednisone treatment, on the third non-prednisone day (NP3, 24-28 h after the last dose of prednisone). Proteinuria decreased from 6.1 mg/min (3.2-9.8 mg/min) (C) to 2.5 mg/min (1.0-7.7 mg/min) at NP3 (median, interquartile range; P less than 0.01), the percentage decrease averaged 45 +/- 8%. The decrease of proteinuria was correlated with baseline GFR (r = 0.75; P less than 0.01). GFR and ERPF did not change significantly, but filtration fraction decreased significantly from 14.5 +/- 0.8% (C) to 13.5 +/- 0.9% (NP3; P less than 0.05). Fractional excretion of albumin, IgG, and transferrin decreased significantly, by -40 +/- 8%, -52 +/- 6%, and -52 +/- 7% respectively. Fractional excretion of beta 2-microglobulin decreased significantly less by -12 +/- 10%. We conclude that proteinuria is decreased on non-prednisone days in patients with membranous glomerulonephritis treated with alternate-day steroids. The observed decrease of filtration fraction suggests that a reduction of glomerular pressure is involved. In addition, the magnitude of the decrease of proteinuria might indicate a change in glomerular permselectivity characteristics.
Nephrol Dial Transplant 1990
PMID:Decreases of proteinuria during alternate-day prednisone therapy in nephrotic syndrome. 212 25

Proteinuria and renal xanthine metabolising enzymes, xanthine oxidase and xanthine dehydrogenase, were evaluated in Adriamycin-treated rats fed standard (21% casein) and low-protein (6% casein) diets. In rats fed a standard diet Adriamycin was associated with increased activities in the kidney of xanthine oxidase and xanthine dehydrogenase and induced massive proteinuria. The pharmacological block of both enzymes by allopurinol and tungsten block of both enzymes by allopurinol and tungsten reduced proteinuria to one-third of the original levels. Rats fed a low-protein diet presented decreased levels of renal xanthine oxidase and xanthine dehydrogenase and were only slightly proteinuric. Finally, rats shifted from a low-protein diet to a normal one developed massive proteinuria in spite of normal or slightly decreased levels of renal xanthine oxidase and xanthine dehydrogenase. We conclude that a low-protein diet is effective in decreasing the levels of xanthine metabolising enzymes that are in part responsible for the renal damage due to Adriamycin. This is not however the unique mechanism by which the low-protein diet protects against the development of proteinuria in Adriamycin nephrosis; other factors must also be hypothesised.
Nephrol Dial Transplant 1990
PMID:Low-protein diet and xanthine-metabolising enzymes in adriamycin nephrosis. 212 63


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