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)

Seven adult patients with idiopathic nephrotic syndrome and with a glomerular histology considered normal but with ultrastructurally provable membranous glomerulonephritis (MNG) were studied. The glomerular lesions were found to represent all ultrastructural evolutionary phases (A,B, and C) of MGN. In patients with serial biopsies, the membranous lesion seemed to have passed through all of its evolutionary phases towards healing (C) without developing spikes or thickening of the glomerular basement membrane (GBM), i.e., the traditional light microscopic characteristics of MGN. This evolution was associated with a benign clinical course. The membranous lesions were associated with a vacuolization visible in obliquely or tangentially cut segments of the GBM in silver-stained paraffin sections. This alteration seemed to be created by irregularities of the argyrophilic lamina densa of the GBM and not by subepithelial deposits, as suggested previously. All seven patients had a remission of the nephrotic syndrome which appeared to be spontaneous and not drug-induced. The amount of proteinuria correlated with the ultrastructural phase of MGN and with the intensity of immunofluorescent staining. In one patient, the latter became negative.
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PMID:Nonprogressive, histologically mild membranous glomerulonephritis appearing in all evolutionary phases as histologically "early" membranous glomerulonephritis. 75 Jun 96

We carried out a retrospective study to investigate the clinical and pathological findings in 31 patients with rheumatoid arthritis (RA). In clinical findings, 17 patients showed nephrotic syndrome, five had isolated proteinuria, two had proteinuria and hematuria and seven had renal failure. In pathological findings, there were 16 patients with membranous nephropathy (MN), two with proliferative glomerulonephritis (DPGN), two with minor glomerular abnormality (MGA), six with amyloidosis, 2 with tubulointerstitial nephritis, and three patients had accompanying lupus nephritis. Eleven of 16 with MGN had been treated with gold, bucillamine or D-penicillamine, so they were diagnosed as drug induced MGN. In the other five patients, we could not decide which drugs induced the nephropathy. The 2 cases of MGA were associated with nephrotic syndrome and acute renal failure, which were caused by non-steroidal antiinflammatory drugs. There were two cases of non-Ig A DPGN, which was regarded as the native nephropathy in RA. The three cases with lupus nephritis were diagnosed as systemic lupus erythematosus by the criteria of the American Rheumatism Association (ARA). In conclusion, the nephropathy in patients with RA was varied and renal biopsy was a useful examination.
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PMID:[Clinicopathological study of nephropathy in patients with rheumatoid arthritis]. 167 90

Whether or not pregnancy adversely affects the natural course of underlying primary renal disease, and whether fetal outcome is influenced by the type of renal disease per se are controversial issues. We retrospectively analyzed the fetal and maternal outcome in 148 women with various, biopsy-proven histological types of primary chronic glomerulonephritis (GN), including IgA GN (52 patients), membranous GN ([MGN] 20 patients), membranoproliferative type 1 GN ([MPGN] 58 patients), focal and segmental glomerulosclerosis ([FSGS] 13 patients), and minimal change nephrotic syndrome ([MCNS] 22 patients), who were pregnant (with a total of 290 pregnancies) after the clinical onset of GN, and in 104 women with reflux nephropathy (with a total of 254 pregnancies). Fetal outcome was poor in the presence of uncontrolled hypertension, nephrotic range proteinuria, and/or impaired renal function at conception or early in gestation, whatever the type of renal disease. An accelerated, more rapid than expected, worsening of maternal renal function was observed in five GN patients of whom four (two IgA, two MPGN) had serum creatinine (Scr) levels greater than 160 mumol/L (1.8 mg/dL) early in gestation, and in five patients with reflux nephropathy whose Scr at conception ranged from 180 to 490 mumol/L (2.0 to 5.5 mg/dL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific controversies concerning the natural history of renal disease in pregnancy. 199 51

This analysis of IMG has focused on the long-term natural history and current approaches to therapy of this disorder. It seems clear that IMG is intrinsically a relatively benign disease, particularly in certain populations. Risk factors for an unfavorable course can often be identified at the discovery of disease. For example older age at onset, male sex, very heavy proteinuria (greater than 10 g/d), sustained hypertension, impaired renal function, and significant chronic tubulointerstitial lesions in the initial renal biopsy all portend an unfavorable outcome. Contrariwise, patients lacking these prognostic features usually do quite well with a high likelihood of spontaneous complete or partial remissions and stable renal function. Once a complete remission has occurred, whether spontaneous or therapy induced, the long-term evolution of the disorder is quite favorable. Some patients may present with what appears to be "idiopathic" MGN, only to later demonstrate underlying disease, such as neoplasia, chronic viral infection, or systemic lupus erythematosus. Glucocorticoids alone, particularly when administered orally, do not seem to have significant beneficial effects over the long term; however, high-dose intravenous methylprednisolone may at times reverse declining renal function in patients with severe nephrotic syndrome. A small subset of patients may display a remitting and relapsing course following treatment with oral glucocorticoids, resembling to some extent patients with minimal change disease. Combination of alkylating agents, either cyclophosphamide or chlorambucil with glucocorticoids is very likely beneficial for the group of patients having an intrinsically unfavorable prognosis or for patients who demonstrate progressive renal insufficiency. At the present time it is not known whether regimens that involve long-term therapy with oral cyclophosphamide combined with glucocorticoids are superior to, equivalent to, or inferior to regimens that involve the cyclical use of intravenous methyl-prednisolone oral prednisone, and oral chlorambucil. Very long-term use of cyclophosphamide, in excess of 12 months, is probably associated with unacceptable long-term risks, particularly the emergence of neoplasia. Long-term follow-up, more than 10 years, will be required to establish the magnitude of the oncogenic potential of existing shorter term regimens of cyclophosphamide-glucocorticoid combinations and for cyclical regimens using chlorambucil. Further data is required to establish the role of cyclosporine, nonsteroidal antiinflammatory agents and intravenous immunoglobulins in the treatment of patients with IMG. ACE inhibitors, sometimes combined with nonsteroidal antiinflammatory agents, may have some usefulness in patients with heavy proteinuria and declining but not advanced renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The therapy of idiopathic membranous glomerulonephritis. 203 23

Total serum IgE was measured in 119 cases of primary glomerular diseases and 33 normal healthy persons. Statistically significant higher levels were noted in minimal change disease (MCD; median: 630 U/ml), IgM nephropathy (IgMN; 618 U/ml), focal glomerulosclerosis (FGS; 373 U/ml) and membranous glomerulonephritis (MGN; 144 U/ml). A higher level of serum IgE was noted in association with more frequent relapse or steroid resistance in MCD and IgMN and in FGS with nephrotic syndrome. A small group of IgA nephropathy with nephrotic range proteinuria was also noted to have extraordinarily high serum IgE. These findings suggest that IgE may play an important role in the pathogenesis of MCD, IgMN, and FGS and may serve as a prognostic indicator in terms of steroid responsiveness in MCD and IgMN.
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PMID:Serum IgE in primary glomerular diseases and its clinical significance. 338 Feb 16

A case of HB virus associated MPGN type III was described for the first time in a 10 year old Japanese girl. She was followed for a period of 7 years with serial serological work-up and renal biopsy. When she was found seropositive for HBe antigen was stained predominantly in capillary walls, but HBs antigen was also detected in capillary walls and mesangium. The results suggest that both HBe- and HBs antigen antibody immune complexes may play a significant role in the development of HB virus associated nephropathy; HBe antigen for MGN and HBe- and HBs antigens for MPGN type III. Although HB virus associated nephropathy is believed to be a rather benign disorder, the present case warrants a close follow-up because of chronicity of massive proteinuria and renal pathology.
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PMID:A case of membranous proliferative glomerulonephritis type III (Burkholder) with the deposition of both HBeAg and HBsAg. 636 17

Protectin (CD59) is a low molecular weight glycophosphoinositol-anchored inhibitor of the membrane attack complex of complement (MAC) that is present, for example, on the membranes of endothelial cells and on epithelial cells of glomeruli and distal tubuli. To examine for the possibility that CD59 becomes detached from cell surfaces following cell injury, this study evaluated renal excretion of CD59 in patients with idiopathic membranous glomerulonephritis (MGN; N = 21), diabetic nephropathy (DNP; N = 15) and in healthy control subjects (N = 13). CD59 in human urine was quantitated by a competitive solid-phase radioimmunoassay having approximately 13 kDa soluble urinary CD59 as a standard. Immunofluorescence microscopy demonstrated a decreased expression of CD59 in the glomeruli of MGN patients. Using a Triton X-114 phase separation method 91 to 97% of urinary CD59 was found to be in a soluble form without anchor-associated phospholipid. The mean (+/- SEM) level of urinary CD59 was 5.6 +/- 0.2 micrograms/ml in MGN patients, 3.7 +/- 0.4 micrograms/ml in healthy controls (P < 0.001) and 2.6 +/- 0.1 in DNP patients (P < 0.001). When related to urinary creatinine (UCr) the corresponding values were 11.9 +/- 5.6, 4.8 +/- 0.3 (P = 0.021) and 4.4 +/- 0.2 (P < 0.002), respectively. The amount of CD59 in urine correlated with the urinary excretion of soluble terminal complement complexes, SC5b-9 (r = 0.594, P < 0.006) in MGN patients. The excretion of CD59 also correlated with the excretion of the inflammatory mediator IL-1 beta (r = 0.671, P = 0.001) but not with TNF-alpha (r = 0.314, P = 0.178). No correlation of CD59 excretion was observed with duration of the disease level of proteinuria, serum albumin concentration or serum creatinine level. Based on these findings we speculate that the increased excretion of CD59 into urine in MGN patients is due to complement activation and inflammation induced shedding of CD59 from glomerular cells.
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PMID:Urinary excretion of protectin (CD59), complement SC5b-9 and cytokines in membranous glomerulonephritis. 754 24

A controlled trial of cyclosporine in patients diagnosed with progressive membranous nephropathy (MGN) was carried out to determine whether cyclosporine (D) would be more effective than placebo (P) in reducing the rate of deterioration in renal function. Patients (N = 64) with MGN were placed on a restricted protein diet (< or = 0.9 g/kg) and followed closely for 12 months (Part 1). Patients at high risk of progression based on an absolute loss in creatinine clearance (CCr) of > or = 8 ml/min and persistent nephrotic range proteinuria (Pr) were selected and randomly assigned to either (D) (N = 9) or (P) (N = 8) for 12 months (Part 2). No differences in the two groups were noted at entry. After 12 months, the improvement in CCr slope in ml/min/month was significantly greater in the D patients (D + 2.1 vs. P + 0.5, mean difference 1.6; 95% CI 0.3 to 3.0, P < 0.02). This improvement was maintained in six of eight D (75%) over a mean follow-up period of 21 months. Daily Pr also improved with D (by month 3, D - 4.5 g/day vs. P + 0.7 g/day, P = 0.02) and was sustained in six of eight (75%) D patients. When Pr was expressed as a function of their concurrent CCr, the D versus P patients' time to halving was faster (P = 0.02) and absolute number higher (4/9 D vs 0/8 P). In the D group a trend towards worse hypertension and an increase in the number of transient rises in serum creatinine were noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A controlled trial of cyclosporine in patients with progressive membranous nephropathy. Canadian Glomerulonephritis Study Group. 778 10

Independently of tumor mass or metastases, up to 80% of patients with a variety of neoplastic diseases are exposed to continuous antigenemia (eg, tumor-associated antigens, reexpressed fetal antigens, viral antigens, or autologous antigens of autoimmunity). These antigens stimulate antibody production and form circulating immune complexes and antiideotypic cryoimmunoglobulins. In many instances these immune reactants are deposited or formed in situ in the glomerular mesangium and capillary walls. Multifactorial microhematuria is common among cancer patients; proteinuria without overt NS is found more often in patients with malignancy than in controls and indicates a worse prognosis. Under the proper conditions of host susceptibility and immune deposit nephritogenicity, a few adult cancer patients (< 1%) may develop glomerular injury and overt paraneoplastic renal disease. The glomulopathy, most often MGN, usually is manifested by NS, active urine sediment, and/or diminished glomerular filtration. Significant renal impairment, usually associated with ECGN, is uncommon. In many instances successful treatment of the neoplasm has induced a partial or complete remission of the associated glomerulopathy. The occurrence of overt renal disease in the presence of a malignancy generally augurs a poor prognosis. Whether all patients over the age of 50 with NS caused by MGN should be subjected to especially rigorous cancer surveillance is still an open question, however, prudence, if not cost-consciousness, would seem to favor the affirmative.
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PMID:Paraneoplastic glomerulopathies. 832 26

We studied direct and indirect methods of measuring membrane charge by detecting fixed anionic sites with polyethylenimine (PEI) on the glomerular basement membrane (GBM) and Alcian blue on red blood cell (RBC) membrane (ABRBC), respectively, in 40 children with nephrotic syndrome (NS). Size selectivity of the GBM was measured indirectly by fine analysis of urinary proteins with sodium dodecyl sulfate-polyacrylamide gel electrophoresis in 22 of these children. Correlation between ABRBC and PEI was strongest (r = 0.79; p = 0.0037) in 11 children with steroid-responsive NS (SRNS), moderate (r = 0.31) in 10 children with focal glomerulosclerosis (FGS), and absent in 14 children with hepatitis B antigen membranous nephropathy (MGN) and 5 with mesangioproliferative glomerulonephritis (MPGN). ABRBC and PEI were reduced in the group as a whole as compared with their controls (ABRBC: 44.53 +/- 9.81 vs 71.54 +/- 12.14, p < 0.05; PEI: 16.31 +/- 4.34 vs 33.3 +/- 1.09, p < 0.005). This reduction was greater in SRNS (26.35 +/- 7.15 p = 0.004) but was also detected in the remainder of the group taken together (52.31 +/- 26.07, p < 0.001). Excretion of glomerular proteins was restricted by size (< or = 80 kd) in SRNS but unrestricted (< or = 80 kd plus > 80 kd) in FGS, MGN, and MPGN. The main cause of proteinuria is likely to be depletion of negative charge on the GBM in SRNS, and distortion of capillary pore size in MGN and MPGN, with probable overlap of these mechanisms in each disease, especially in FGS. Basement membrane injury appears widespread in SRNS but confined to the kidney in MGN and MPGN.
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PMID:Direct and indirect tests of pore size and charge selectivity in nephrotic syndrome. 863 48


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