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)

In this work 42 patients with active Schistosoma mansoni infection and renal involvement were examined. Of these, 16 had asymptomatic proteinuria (group I) and 26 had the nephrotic syndrome (group II). Fifteen nonschistosomal patients with idiopathic nephrotic syndrome were included as control cases (group III). Renal biopsy specimens were obtained from all patients and controls. These were examined by light microscopy (LM), by direct immunofluorescence microscopy using antisera against human IgG, IgM, IgA, C3, C4, C1q, and fibrinogen, and by indirect immunofluorescence microscopy using monoclonal antibodies directed against the circulating schistosome antigens, circulating anodic antigen (CCA) and circulating cathodic antigen (CCA). Schistosomal-specific deposits were seen in the renal glomeruli in 24 of the 42 schistosomal patients but in none of the 15 control patients. Although schistosomal-specific deposits were seen in seven of the 16 patients presenting with asymptomatic proteinuria, no morphological changes could be seen by LM. On the other hand, schistosomal-specific deposits could be seen in the kidneys of 17 of the 26 patients presenting with the nephrotic syndrome. All but one specimen showed morphological changes when examined by LM. These were consistent with mesangioproliferative glomerulonephritis in seven, focal segmental glomerulosclerosis in five, mesangiocapillary glomerulonephritis in two, membranous glomerulonephritis in one, and focal segmental hyalinosis in one patient. The present study clearly suggests that (a) schistosomal-specific nephropathy does exist in human settings, (b) it is an immune complex disease, and (c) CAA and CCA are major responsible antigens.
Nephrol Dial Transplant 1988
PMID:Characterisation of kidney lesions in early schistosomal-specific nephropathy. 314 Jan 23

Using an original technique permitting repeated plasma exchange in the rat, we have tested this therapeutic approach in animals actively immunised with horseradish peroxidase, and in rats with HgCl2-induced autoimmune glomerulonephritis. Plasma exchange effectively removes circulating IgG anti-horseradish peroxidase antibodies from the sera of immunised rats. When applied to the model of HgCl2-induced antiglomerular basement membrane glomerulonephritis in Brown-Norway rats, this technique is also remarkably effective. In these rats, proteinuria is abolished during the plasma exchange treatment period and no circulating antiglomerular basement membrane antibodies can be detected. These antibodies are, however, found in the ultrafiltrates of exchanged rats. Serum IgE, characteristically elevated in HgCl2-treated rats, is also markedly diminished in exchanged rats. Control rats treated with infusions of fresh frozen plasma or with heparin alone did not show any improvement in disease severity. These results suggest that plasma exchange alone can attenuate antiglomerular basement membrane nephritis in HgCl2-treated rats. This observation may be of relevance for the treatment of human antiglomerular-basement membrane-mediated glomerulonephritis.
Nephrol Dial Transplant 1988
PMID:Plasma exchange in a rat model of autoimmune glomerulonephritis. 314 Jan 25

Hepatic fibrosis in the pathogenesis of schistosomal glomerulopathy cannot be explained by any positive influence of hepatocellular injury. In order to examine the potential role of impairment of hepatic macrophage function, the t1/2 plasma clearance of 99mTc-sulphur colloid was studied in 30 patients with schistosomal glomerulopathy, ten normal volunteers, ten cases of uncomplicated intestinal schistosomiasis, ten non-schistosomal cirrhotic patients and ten non-schistosomal nephrotic patients. Liver and renal biopsies were obtained from appropriate groups and examined by light microscopy and glomerular immunofluorescence. There was a significant correlation between t1/2 of sulphur colloid clearance and proteinuria, mesangial hypercellularity, and predominance of IgA glomerular deposits. These data indicate that hepatic macrophage dysfunction is an important factor in the pathogenesis of schistosomal glomerulopathy, and that IgA plays a major role in advanced glomerular lesions. The degree of impairment of hepatic macrophage function may influence the pattern and severity of glomerular lesions depending upon the affection of IgA clearance mechanisms.
Nephrol Dial Transplant 1988
PMID:Hepatic macrophage function in schistosomal glomerulopathy. 314 17

The effect of blood pressure reduction on the progression rate of chronic renal failure (CRF) was studied in 28 patients with CRF of diverse aetiology entering a prospective study (observation time 7-24 months, mean 16 months). Endogenous creatinine clearance was 12-66 ml/min (mean 30 +/- 3 ml/min). We aimed to keep the blood pressure below 160/90 mmHg. Dietary protein was not restricted. The progression rate of CRF was assessed from the regression coefficients of the regressions of creatinine clearance and the inverse of s-creatinine, respectively, on time. Progression rate and the means of all recordings of mean arterial blood pressure (MAP) and urinary protein excretion, respectively, in each patient during the prospective phase were compared with retrospective data from the proceeding period (observation time 4-25 months, mean 19 months). The patients received various combinations of antihypertensive drugs including diuretics, beta-blockers and vasodilatory drugs. In 19 patients MAP decreased from 109 +/- 2 to 102 +/- 2 mmHg (group I), whereas MAP increased from 105 +/- 2 to 108 +/- 2 mmHg in nine patients (group II). In group I proteinuria was significantly lower (P less than 0.05) and the progression of CRF was approximately 50% slower (P less than 0.01) in the prospective phase than in the retrospective phase; no changes were observed in group II. Calculated for all patients, significant correlations were observed between the change in MAP and the change in progression rate and protein excretion, respectively. These results indicate that lowering of blood pressure results in decreased proteinuria and retardation of the progression of CRF irrespective of the aetiology.
Nephrol Dial Transplant 1988
PMID:Reduction of blood pressure retards the progression of chronic renal failure in man. 314 19

The immunosuppressive effectiveness and nephrotoxic side-effects of either high-dose cyclosporin (CsA) (16 mg/kg per day) or low-dose (9 mg/kg per day) in combination with azathioprine (Aza) (1 mg/kg per day) were studied in 80 renal transplant patients who also received low-dose corticosteroids. At 3 months, patients who received high-dose CsA were randomly assigned to either continuation of CsA or conversion to Aza, whereas in the triple-therapy group either CsA or Aza was discontinued. No differences in patient (97.5%) or graft survival (90%-92.5%) were found at 1 year. There were no differences in the incidence of primary non-functioning kidneys. The incidence of acute rejection episodes was 45% in the high-dose CsA group and 55% in the group treated with low CsA doses together with Aza (not significant). At 3 months the mean creatinine clearance was 60 +/- 4 ml/min (mean +/- SEM) in the high-dose group (mean cumulative CsA dose 0.96 g/kg) compared with 55 +/- 3 ml/min in the low-dose group (mean cumulative CsA dose 0.60 g/kg). At 1 year no differences in the degree of proteinuria or the incidence of hypertension was found between the different groups. The best mean creatinine clearance at 1 year (77 +/- 5 ml/min) was found in patients who received high doses of CsA for 3 months followed by conversion.
Nephrol Dial Transplant 1988
PMID:High- and low-dose regimens of cyclosporin in renal transplantation: immunosuppressive efficacy and side-effects. 314 26

The effect of cyclosporin on proteinuria was studied in 11 patients with steroid-responsive nephrotic syndrome (10 minimal change nephropathy, one IgM nephropathy) and in four patients with steroid-resistant nephrotic syndrome from focal segmental glomerulosclerosis. Cyclosporin (mean initial dose 7.7 mg/kg per day) produced a complete remission of proteinuria in 15 nephrotic episodes in the ten patients with minimal-change nephropathy after a mean 14.3 days (range 7-23 days) of therapy. All patients remained in remission while receiving cyclosporin (mean duration of follow-up 147 days; range 40-230 days). However, when cyclosporin was discontinued on nine occasions in five patients, all relapsed after a mean 47.8 days (range 7-180 days). Four of the five patients were subsequently rechallenged with cyclosporin and all responded. Maintenance cyclosporin therapy to prevent relapse was not associated with any adverse effects, and there was no significant difference between the creatinine clearance before and after 30 days of therapy (86.9 +/- 19.3 and 81.7 +/- 23.5 ml/min respectively, P greater than 0.1). The patient with steroid-responsive IgM nephrotic syndrome did not respond to cyclosporin, and there was no significant effect of cyclosporin on proteinuria in the four patients with FSGS. Cyclosporin is an effective agent for the treatment of patients with frequently relapsing minimal-change nephropathy who became steroid dependent when cyclophosphamide is contraindicated. However, unlike cyclophosphamide, long-term remissions which persist after treatment is withdrawn are not obtained, and patients may be said to be cyclosporin dependent.
Nephrol Dial Transplant 1988
PMID:Cyclosporin in the treatment of steroid-responsive and steroid-resistant nephrotic syndrome in adults. 314 13

Seven patients with minimal-change nephrotic syndrome confirmed by renal biopsy were treated with cyclosporin (CsA). Four patients had frequent relapses and three others had primary steroid resistant nephrotic syndrome. Corticosteroids were discontinued as soon as CsA whole blood trough values of 200-500 ng/ml (RIA method) were reached. A full remission, defined as complete disappearance of proteinuria, was achieved in five patients under this treatment. In the two other patients proteinuria was reduced. Two patients experienced an acute episode of dose-dependent nephrotoxicity; however, overall renal function, as determined by the creatinine clearance, was stable. Control biopsies in five patients after a mean treatment period of 10 months showed no significant vascular or interstitial toxicity.
Nephrol Dial Transplant 1988
PMID:Long-term treatment of minimal-change nephrotic syndrome with cyclosporin: a control biopsy study. 314 14

Twenty-one patients with schistosomal-specific nephropathy (18 nephrotics and three with non-nephrotic proteinuria) were given anti-schistosomal treatment (oxamniquine and praziquantel). The schistosomal specificity of the kidney lesions was assessed by the detection of schistosomal-specific antigens (CAA and CCA) and antibodies deposited in the renal glomeruli of these patients. After anti-schistosomal treatment, the patients were followed for clinical and laboratory changes occurring within 12 months. In addition, 15 patients had a second kidney biopsy and the histopathological and the immunopathological findings were compared with those observed in the first biopsy. Based on clinical, laboratory and histopathological evaluations, none of the patients subjected to the study showed regression of the kidney lesion following antischistosomal treatment; in fact three patients showed progression in their lesions, one of them reaching end-stage renal failure. The histopathology of these three cases was focal segmental glomerulosclerosis. Our data suggest that anti-schistosomal treatment in an established disease state, will not produce remission.
Nephrol Dial Transplant 1988
PMID:Effect of anti-schistosomal treatment on schistosomal-specific nephropathy. 314 16

Interstitial foam cells are occasionally seen in patients with the nephrotic syndrome. In a group of patients with the nephrotic syndrome we were able to demonstrate that these cells express markers characteristic of the monocyte/macrophage lineage. Their presence was related to the previous duration of proteinuria, but they had no apparent influence on the subsequent evolution of renal function. The mechanisms leading to their presence are unknown.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Interstitial foam cells in the nephrotic syndrome belong to the monocyte/macrophage lineage. 385 73

Diabetic donors are still reluctantly accepted as potential organ donors because of supposed poor graft function caused by diabetic lesions. The results of transplantation of six kidneys from three donors with insulin dependent diabetes mellitus are reported. All three donors had a normal creatinine clearance and absence of proteinuria. Renal biopsies were taken. Five grafts are still functioning, six months to two years after transplantation with a mean creatinine clearance of 69ml/min (range 51-95). Three of five biopsies taken six months after transplantation showed marked decrease of the diabetic lesions. On the basis of these findings it seems justified to accept kidneys from diabetic donors for transplantation.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Results of transplantation of kidneys from diabetic donors. 388 78


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