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)

14 cases of idiopathic rapidly progressive glomerulonephritis (I. R. P. G. N.) treated by heparin between 1968 and 1974 were collected by the authors. Extra-capillary crescents (E. C. C.) occurred in 75 to 100% of glomeruli in ten patients and in 50 to 75% in four. Gross proteinuria, hematuria and renal failure were always present. 9 patients were admitted with primary oligo-anuric renal failure. 11 patients were treated by repeated hemodialysis before and during anticoagulant treatment. Heparin was given by intra-venous injection every 3 hours for one to two months with Howell times range from 150 to 200% of control. Heparin was the only treatment in 6 cases, and was given with dipyridamole in 4, with prednisone in 3 and with azathioprine in one case. 5 severe or fatal hemorragic complications were observed. The clinical course was usually unfavorable with 5 early deaths, 3 provisional steady-states with 2 late deaths. Six patients were treated by periodic hemodialysis. Repeat kidney biopsies were obtained in 8 patients. The findings suggest that heparin affects mainly the E. C. C. and fibrinoid deposits but not glomerular sclerosis. The inefficiency of all current treatments of primary oligo-anuric IRPGN is stressed. In patients with better initial renal function choice between anticoagulant and/or immuno-depressive drugs must be scrutinized in individual cases bearing in mind potential iatrogenic complications. In equivocal cases, patients should be referred to the chronic hemodialysis and/or transplantation program.
 ...
PMID:The use of heparin in the treatment of idiopathic rapidly progressive glomerulonephritis. 124 88

Glomerular permselectivity and dynamics were evaluated serially in 14 nephrotic patients with membranous glomerulopathy (MG). Analysis of transglomerular dextran sieving, before and again after proteinuria remitted, revealed persistent depression by 60-80% of glomerular pore density and the two-kidney ultrafiltration coefficient, Kf. The glomerular filtration rate was lowered by half on each occasion. Morphometric examination of glomeruli in a second group of 16 nephrotic patients with MG revealed a low prevalence of glomerulosclerosis (5 +/- 3%) and a twofold increase in filtration surface due to marked glomerular hypertrophy. Presumably, widening by threefold of the basement membrane and/or epithelial podocytes accounted for the computed reduction in ultrafiltration capacity. There was no correlation between glomerular structure and the subsequent course of MG over the ensuing 24-96 mo. Rather, a twofold expansion of the interstitial compartment predicted those who went on to exhibit progressive renal insufficiency. We conclude that increasing resistance to water flow by walls of patent and perfused glomerular capillaries is the proximate cause of progressive renal insufficiency in MG.
 ...
PMID:Extent and course of glomerular injury in human membranous glomerulopathy. 128 82

The effect of AST-120 was examined in the rat model of CRF induced by adriamycin (ADM), which is known to induce focal glomerular sclerosis (GS). ADM (2mg/kg) was injected intravenously twice at a 3-wk interval. After 14 wks, rats were paired with control (C) and AST-120 (A) groups according to levels of BUN and proteinuria. Then, the rats were fed regular rat chow with (A, n = 10) or without (C, n = 10) AST-120. After 28 wks, there were more GS in C. Averaged sclerosis index (SI, 0-4 scale) in C was 1.97 (0.94-3.22), while 1.61 (0.60-2.97) in A. When GS was advanced in C (SI > 2.0), largely ameliorated SI was noted in A (2.61 vs. 1.97, C vs. A, p < 0.05 by paired W-test, n = 5 each). Also, in these rats, BUN, serum creatinine and Ht were all improved in A (p < 0.05). Thus, AST-120 was effective in CRF rats induced by ADM when uremia was advanced. The data also indicates that a reduction of uremic toxins could improve glomerular histology and renal function in CRF.
 ...
PMID:[Effect of oral adsorbent (AST-120) in the rat model of chronic renal failure induced by adriamycin]. 128 5

Reflux nephropathy (RN), the main complication of the vesico-ureteral reflux (VUR), relatively frequent in adults, is often the consequence of recurrent urinary infections in the child, hood or during pregnancy. Unilateral RN has generally a benign course but the bilateral one, with important nephron destruction, leads to focal and segmental glomerulosclerosis, manifested by high levels of proteinuria. A certain degree of cicatrization and renal failure are followed by progressive impairment of the remaining renal function, even if VUR is cured. An early diagnosis, treatment of the acute bacterial infection, adequate ingestion of liquids, regulation of the intestinal transit and complete bladder voiding by miction, associated with hypotensive and antiinfectious drug therapy lead to VUR disappearance in 80% of the cases, avoiding renal failure. Surgery is indicated only in the patients with severe reflux and with congenital or obstructive anomalies, as well as in the case of recurrent infection resistant to antibiotherapy.
 ...
PMID:Reflux nephropathy in adults. 129 13

Eicosapentaenoic acid (EPA) can induce a shift in prostaglandin and leukotriene synthesis. The effects of EPA supplementation of the diet on the progression of chronic renal failure (CRF) were evaluated in a model of 5/6 renal mass ablation in rats. After 30 or 60 days of CRF, elevation in single-nephron glomerular filtration rate due to an increase in glomerular plasma flow and hydraulic pressure was observed. These hemodynamic alterations were followed by a rise in proteinuria and glomerular sclerosis. EPA treatment for 30 or 60 days did not substantially modify the hemodynamic or morphological profiles induced by renal mass ablation. In the present non-immune model of CRF, preglomerular vasodilation with glomerular hyperperfusion and hypertension were responsible, at least in part, for the presence of proteinuria and glomerular sclerosis. No additional vasodilation was observed in the present model of CRF, and, thus, hemodynamic effects induced by EPA did not modify renal damage, in contrast to the EPA effects observed in immune-mediated models of CRF.
 ...
PMID:Effect of eicosapentaenoic acid on the progression of chronic renal failure in rats. 130 Apr 41

Patients with end-stage renal failure secondary to idiopathic nephrotic syndrome are at risk of initial disease recurrence after kidney transplantation (30%). Selective proteinuria can appear immediately after transplantation and focal glomerular sclerosis with graft loss can occur in 10% of patients with recurrence. Current immunosuppressive protocols do not seem to influence the recurrence rate in adult patients and the efficacy of therapeutic plasma exchanges remains controversial. We have previously demonstrated that plasma exchanges, proposed early before glomerular sclerosis, were able to significantly reduce proteinuria without affecting albuminemia or glomerular filtration. We report here on three patients who suffered immediate recurrence after transplantation and were treated with plasma immunoadsorption onto protein A column (Excorim, Lund); these patients had prior histories of steroid-resistant focal glomerular sclerosis. This procedure is more specific than plasma exchange in that it cleared the serum of immunoglobulins, significantly decreased proteinuria in only two cases (from 14 to 5 g/d and 2.5 to 0.8 g/d) and eliminated it in the third case (from 3 to 0.1 g/d). The modifications of proteinuria levels appeared as early as the second immunoadsorption sequence and returned to pre-immunoadsorption values within 2 to 8 weeks. These observations argue for the protein A binding of plasmatic factor(s) involved in idiopathic, nephrotic syndrome and allow us to progress to the characterization of this(ese) factor(s).
 ...
PMID:Effects of plasma-protein A immunoadsorption on idiopathic nephrotic syndrome recurring after renal transplantation. 130 Aug 88

Increasing evidence supports a role of glomerular cell proliferation in the development of focal or diffuse glomerulosclerosis. This study investigates the chronology and sequence of cellular events that precede glomerulosclerosis in 5/6 nephrectomized rats. Within three days of renal ablation, a phenotypic switch occurred in which some mesangial cells expressed alpha-smooth muscle actin. This was followed by proliferation of mesangial cells, and to a lesser degree endothelial cells from day 5 to week 4 as detected by immunostaining for the proliferating cell nuclear antigen (PCNA). Glomerular cell proliferation was accompanied by increased immunohistochemical expression of PDGF B-chain. In situ hybridization showed no glomerular PDGF B-chain mRNA expression at the induction of proliferation (day 5), and a marked increase between week 1 and 4 in operated rats. In parallel, increased expression of PDGF receptor beta-subunit protein and mRNA was demonstrated by immunohistochemistry and Northern analysis of total glomerular RNA. The onset of glomerular cell proliferation was also associated with mild glomerular platelet accumulation (as defined by 111In-labelled platelet studies) as well as with fibrinogen deposition. Proteinuria, glomerular sclerotic changes, and leukocyte infiltration all followed cell proliferation. The glomerular leukocyte infiltrate consisted of monocytes/macrophages and increased markedly at week 10 in rats with renal ablation. Thus, our results suggest that in the remnant kidney model: 1) proliferation of intrinsic glomerular cells precedes glomerulosclerosis; 2) proliferation may be initiated by degranulating platelets and sustained by PDGF released from intrinsic glomerular cells; and 3) glomerular monocyte/macrophage infiltration occurs after the proliferation, and may possibly contribute to the development of glomerular sclerotic changes.
 ...
PMID:Glomerular cell proliferation and PDGF expression precede glomerulosclerosis in the remnant kidney model. 131 22

1. To elucidate the mechanisms by which cyclosporin A diminishes proteinuria, we studied 20 patients with severe nephrotic syndrome. Biopsy-established pathologies included minimal change disease (n = 5), membranous glomerulopathy (n = 6), membranoproliferative glomerulonephritis (n = 5) and focal segmental glomerulosclerosis (n = 4). Before, at the end of a 90 day course of cyclosporin A, and finally 1 month after stopping cyclosporin A we determined 24 h protein excretion. Measurements of glomerular filtration rate, effective renal plasma flow, fractional clearance rates of albumin and immunoglobulins with different charges and the transglomerular sieving of uncharged dextrans of broad size distribution were used to study the effects of cyclosporin A on renal perfusion and the glomerular filtration barrier. The findings were analysed with a theoretical model of solute transport. 2. Among the different forms of glomerulopathy the response to low-dose cyclosporin A (trough levels 32.0-36.9 ng/ml) varied markedly. In minimal change disease, proteinuria decreased from 9.5 +/- 3.1 to 1.3 +/- 0.2 g/24 h (mean +/- SEM, P less than 0.01). This response was due to restoration of the charge selectivity of the glomerular barrier. The depressed value of the glomerular permeability coefficient also returned to normal. Glomerular filtration rate, effective renal plasma flow and renal vascular resistance did not change. Proteinuria returned after stopping cyclosporin A, although it did not reach pretreatment levels. In membranous glomerulopathy, proteinuria fell from 9.9 +/- 1.5 to 1.8 +/- 0.3 g/24 h (P less than 0.01). Changes in protein excretion and dextran sieving were compatible with an increase in glomerular permselectivity and a decrease in filtrate flow through the 'shunt' pathway. Glomerular filtration rate was maintained, although effective renal plasma flow fell significantly. Proteinuria relapsed after stopping cyclosporin A. In membranoproliferative glomerulonephritis and focal segmental glomerulosclerosis proteinuria did not respond to cyclosporin A, although cyclosporin A exerted important haemodynamic effects. 3. In minimal change disease and membranous glomerulopathy cyclosporin A exerts its beneficial effects on proteinuria through changes in the properties of the glomerular barrier, resulting in increased charge and size selectivity, respectively.
 ...
PMID:Effects of cyclosporin A on glomerular barrier function in the nephrotic syndrome. 132 May 44

The effects of a calcium antagonist, manidipine, on the outcome of the remnant kidney model of chronic renal failure in rats were studied. After 5/6 nephrectomy (5/6 Nx), rats were assigned to one of the following groups, and fed: Nx without manidipine, group 1; diet with 0.01% manidipine, group 2. A sham 5/6 Nx group was also included as the control. Each diet contained the same calories (3.44 kcal/g) and protein (25% casein). Increased systolic blood pressure seen after 8 weeks postablation was less with manidipine in group 2. Group 2 also had significantly less proteinuria. By 12 weeks postablation, group 1 showed severe parenchymal damage, characteristic of end-stage renal pathology. These changes were prevented by manidipine. The percentage of glomeruli with severe structural damage including sclerosis and/or hyalinosis, arbitrarily defined as glomerular sclerosis index (GSI) was significantly less in group 2 (41 +/- 11%) compared with group 1 (58 +/- 10%). Tubulointerstitial injury (TII) was also less in group 2 (29.1 +/- 9.1%) compared with group 1 (45.1 +/- 10.3%). Sham-Nx control group without manidipine showed normal renal morphology (GSI, 0.2 +/- 0.6, TII, 3.8 +/- 1.0). These results indicate that manidipine attenuates the development of end-stage renal pathology in the remnant kidney model of chronic renal failure in rats. The mechanism(s) remains to be elucidated.
 ...
PMID:Manidipine attenuates a progressive renal injury in remnant kidneys of rats. 134 96

It is widely known that the severity of glomerular sclerosis is proportional to the degree and chronicity of proteinuria and that the degenerative changes of glomerular epithelial cells that are associated with overflow albuminuria can be experimentally induced by the injection of large quantities of heterologous albumin. Such evidence suggests that autologous albuminuria per se may have a harmful effect on the kidneys. To examine the cause and effect relationship between renal lesions and albuminuria, we produced Adriamycin-induced experimental focal glomerular sclerosis in Nagase analbuminemic (NA) rats and control Sprague-Dawley (SD) rats and observed both the renal functional and histologic changes for 20 weeks. At week 4 after injection of Adriamycin glomerular epithelial lesions including foot process fusion were similarly revealed by an electron microscopic study in both groups in spite of the presence of a large difference in the amount of proteinuria (SD rats: 491 +/- 84 mg/day, NA rats: 43 +/- 30 mg/day) and albuminuria (SD rats: 383 +/- 73 mg/day, NA rats: 2 +/- 1 mg/day). At week 20, a light microscopic study showed the same degree of glomerular sclerosis and hyalinosis and tubulointerstitial changes associated with a decrease in inulin clearance in both groups. The increased glomerular accumulation of immunoglobulin M or complement 3 and glomerular trapping of aggregated human immunoglobulin G were also similar between the SD and NA groups. In summary, renal destruction of Adriamycin-nephropathy was not dependent on the degree of albuminuria. These results suggest that albuminuria is not an aggravating factor in focal glomerulosclerosis.
 ...
PMID:Albuminuria is not an aggravating factor in experimental focal glomerulosclerosis and hyalinosis. 137


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