Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from 168 patients with various types of chronic glomerulonephritis (GN) were assayed for immune complexes (IC) by two independent methods, a modification of the PEG precipitation test (PEG) and the inhibition of complement-dependent lymphocyte rosette formation (RI). Both assays had different reactivities, the RI being more sensitive than the PEG test. Higher percentages of positivity of these tests were observed in the GN groups than in normal controls. However serial measurements demonstrated that IC were present only intermittently in most instances. The presence of IC correlated with disease activity in patients with focal glomerulosclerosis membranous GN and membranoproliferative GN, while in lupus erythematosus it reflected the effects of different treatment regimens although it had no relationship with clinical symptoms. Nevertheless, our results suggest that these tests are of little help to the clinician to appreciate disease activity and monitor therapy in individual GN patients.
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PMID:Clinical significance of circulating immune complexes detection in chronic glomerulonephritis. 37 Jun 24

Sera from patients with various types of glomerulonephritis (GN) as well as sera from rabbits with acute serum sickness were studied for the presence of circulating immune complexes (IC). The method used is based on the observation that IC inhibit the uptake of IgG aggregates by guinea-pig peritoneal macrophages. Inhibition significantly greater than with normal human sera was found with sera of patients with membranous GN, membranoproliferative GN, focal glomerular sclerosis, minimal change nephrotic syndrome, acute septicaemic glomerular diseases and systemic lupus erythematous. IC were also detected in rabbits with acute serum sickness during the period of immune elimination.
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PMID:Detection of circulating soluble immune complexes in patients with various renal diseases. 124 61

The peripolar cell is a recently described glomerular epithelial cell which is situated within Bowman's capsule at the vascular pole. It contains cytoplasmic granules which contain plasma proteins, although it may also have a secretory function. The relationship between peripolar cells, other granulated glomerular epithelial cells and tubular epithelial cells is unclear. We have studied 242 biopsies from 19 types of renal disease for peripolar cells, other granulated epithelial cells and granulated tubular epithelial cells. Peripolar cells were most numerous in mesangioproliferative glomerulonephritis, IgA nephropathy, focal segmental glomerulosclerosis, membranous glomerulonephritis and lupus nephropathy. Other granulated glomerular epithelial cells were most prominent in diffuse lupus nephropathy, focal glomerulonephritis, acute vascular transplant rejection, crescentic glomerulonephritis and mesangioproliferative glomerulonephritis. Granulation of the tubular epithelium was most prominent in minimal change nephrotic syndrome and amyloidosis. It is likely that the granules in tubular epithelial cells represent lysosomes containing plasma proteins which have been absorbed from the tubular fluid. However, granulation of glomerular cells may represent a more specific response to glomerular damage. In addition, peripolar cells are prominent in only certain diseases, suggesting a specialized function.
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PMID:Peripolar cells and other granulated epithelial cells in renal biopsies. 152 Apr 82

As newer treatment modalities become available for patients with severe lupus nephritis, it becomes increasingly important to identify patients at risk for renal failure. In this study, the records of 90 children presenting with systemic lupus erythematosus over a 13-year period were reviewed. Nineteen were lost to follow-up prior to completion of the study. Of the 71 remaining children, 16 (22%) progressed to chronic renal failure. Persistent hypertension lasting greater than 4 months, anemia, abnormalities of the urinalysis, and elevated serum creatinine level were significantly associated with progression to renal failure. Sex, race, age, abnormalities of creatinine clearance, and 24-hour urine protein collection were not associated with progression to renal failure. Renal biopsies were obtained in 45 children. Biopsies were initially classified according to World Health Organization criteria. Diffuse proliferative glomerulonephritis was significantly associated with progression to renal failure. The 45 biopsies available were reviewed by one of the authors and categorized by activity and chronicity indices. Both the active lesions of fibrinoid necrosis, synechiae, tubular casts, and vasculitic lesions and the chronic lesion of glomerular sclerosis correlated with progression to renal failure. Of the 16 children who progressed to renal failure, 2 had cadaver kidney transplants and are well 5 years posttransplant; 4 had fulminant lupus and died within 1 month of commencing dialysis; 10 began chronic dialysis. Five of the 10 children on chronic dialysis died from sepsis. These data suggest that children with systemic lupus erythematosus who undergo dialysis do poorly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lupus nephritis: prognostic factors in children. 140 32

To suppress the activity of glomerulonephritis, lupus and primary chronic mixed one, 13 children received plasmapheresis synchronously with pulse therapy with cyclophosphamide or prednisolone. Plasmapheresis was carried out daily for 3 days. Six hours after the last session and on days 4 and 5 of the treatment pulse therapy was provided, followed by conventional intake of prednisolone per os in combination with azathioprine or cyclophosphamide. Beneficial therapeutic results were obtained in 10 patients within 3 to 6 weeks. The effect turned out insufficient in a patient with associated systemic lupus erythematosus, and rapid-progressing nephritis and in a child with primary chronic glomerulonephritis of the mesangiocapillary type with fibroplastic transformation and persistent nephrotic syndrome. No therapeutic effect was attained in a patient with focal segmental glomerulosclerosis running its course with long persistent nephrotic syndrome.
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PMID:[Synchronization of plasmapheresis and pulse therapy in the complex treatment of children with highly active glomerulonephritis]. 175 31

MHC class I and II molecules serve as restriction elements for the presentation of antigen-specific T cell reactions and may be implicated in the process of cellular transformation. We have analysed the expression of MHC class I and II antigens including the associated invariant gamma-chain in 100 consecutive renal biopsies by a sensitive immunoperoxidase method using monoclonal antibodies against HLA-ABC, HLA-DR, HLA-DQ, HLA-DP and the invariant gamma-chain (Ii). HLA-ABC was expressed by almost all parenchymal cells except for podocytes. Staining for HLA-DR was found consistently in glomerular and interstitial capillary endothelial cells, in "dendritic" (LCA positive) and most infiltrating interstitial cells but not in mesangial and most extracapillary cells. Similar but weaker positivity was observed for HLA-DQ and -DP. HLA-DR positive infiltrating mononuclear cells in glomeruli were noted in acute glomerulonephritis (GN) and Lupus GN associated with enhanced staining of endothelial cells. In addition, HLA-DR was uniformly or focally expressed by predominantly proximal tubules in 80% of biopsies, especially IgA-GN, focal glomerulosclerosis, acute GN but also in 54% of cases with minimal change nephrosis. HLA-DP and -DQ were only positive in a limited number of HLA-DR positive tubules. The expression of the invariant gamma-chain was comparable with the reactivity for HLA-DR. In addition, all HLA-DR-positive tubules expressed the invariant gamma-chain. Subtyping of T cells in biopsies with DR-positive tubules and interstitial infiltrates (n = 20) showed a predominance of CD 4 positive cells in the majority of cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Expression of class I and class II histocompatibility antigens in inflammatory kidney diseases]. 248 95

The intraglomerular location of coagulation-fibrinolysis factors (CFF) and a platelet membrane antigen (glycoprotein IIb-IIIa; GPIIb-IIIa) was determined in 101 patients with various glomerular diseases. Renal biopsy specimens were examined by immunofluorescence microscopy, using antisera against fibrinogen/fibrin reactive antigen (FRA), cross-linked fibrin degradation products (XL-FDP), fibronectin (FN), factor XIII-subunit a (F-XIIIa), plasminogen (Plg), alpha 2-plasmin inhibitor (alpha 2-PI) and GPIIb-IIIa. Intraglomerular deposits of the CFF were found at high rates in patients with IgA glomerulonephritis (GN), membranous nephropathy (MN) and lupus GN. The coexistence of deposits of these factors was ascertained by the double-staining method. The deposition rates of XL-FDP and GPIIb-IIIa were very low in patients with minimal-change nephrotic syndrome and focal glomerulosclerosis. Some cases of diabetic glomerulosclerosis (DGS) showed CFF deposition. FRA deposits associated with F-XIIIa and FN may indicate the presence of the cross-linked fibrin. Furthermore, the presence of Plg deposits together with alpha 2-PI and XL-FDP suggests the deposition of fibrin followed by fibrinolysis, but not of fibrinogen, and the coexistence of GPIIb-IIIa suggests the involvement of platelets in the reactions. These studies provide evidence that stabilized fibrin deposition with subsequent fibrinolysis and platelet activation take place in glomeruli in a fairly large proportion of patients with IgA GN, MN and lupus GN and in some cases of DGS.
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PMID:Intraglomerular deposition of coagulation-fibrinolysis factors and a platelet membrane antigen in various glomerular diseases. 256 3

Treatment with total lymphoid irradiation (TLI) and corticosteroids markedly reduced activity of systemic lupus erythematosis in 10 patients with diffuse proliferative lupus nephritis (DPLN) complicated by a nephrotic syndrome. Physiologic and morphometric techniques were used serially before, and 12 and 36 mo post-TLI to characterize the course of glomerular injury. Judged by a progressive reduction in the density of glomerular cells and immune deposits, glomerular inflammation subsided. A sustained reduction in the fractional clearance of albumin, IgG and uncharged dextrans of radius greater than 50 A, pointed to a parallel improvement in glomerular barrier size-selectivity. Corresponding changes in GFR were modest, however. A trend towards higher GFR at 12 mo was associated with a marked increase in the fraction of glomerular tuft area occupied by patent capillary loops as inflammatory changes receded. A late trend toward declining GFR beyond 12 mo was associated with progressive glomerulosclerosis, which affected 57% of all glomeruli globally by 36 mo post-TLI. Judged by a parallel increase in volume by 59%, remaining, patent glomeruli had undergone a process of adaptive enlargement. We propose that an increasing fraction of glomeruli continues to undergo progressive sclerosis after DPLN has become quiescent, and that the prevailing GFR depends on the extent to which hypertrophied remnant glomeruli can compensate for the ensuing loss of filtration surface area.
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PMID:Outcome of the acute glomerular injury in proliferative lupus nephritis. 276 Feb 19

Monoclonal antibodies (mAbs) (4F2 and 7E12) were prepared against heparan sulfate proteoglycan (HSPG) isolated from bovine glomeruli. Enzyme linked immunosorbent assays (ELISA) and immunoblotting demonstrated that the mABs reacted with HSPG. Indirect immunofluorescence (IF) showed that the mAbs stained renal basement membranes (BMs) and BMs in other organs of normal bovine and human tissues in patterns typical of HSPG. Immunoinhibition studies, and immunoblotting of heparan lyase digested HSPG, indicated that the mAbs recognize HSPG core protein. In kidney biopsies from patients with acute poststreptococcal GN, intact linear glomerular BM (GBM) staining for HSPG was noted despite markedly widened capillary loops. In membranous and in diffuse proliferative lupus GN, loss of HSPG staining was demonstrated at sites of immunodeposition of IgG or C3, while increased staining for HSPG was noted in areas of newly formed GBM. Extensive loss of HSPG was seen in areas of glomerular sclerosis and necrosis. In biopsies from patients with minimal change glomerulonephritis (GN) and mesangioproliferative lupus GN, a normal linear GBM distribution of HSPG was noted. The findings are discussed in the context of current knowledge regarding the pathogenesis of glomerular injury. MAbs to BM HSPG should prove useful for future immunochemical studies, and for the study of diseases of the basement membrane.
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PMID:Monoclonal antibodies to heparan sulfate proteoglycan: development and application to the study of normal tissue and pathologic human kidney biopsies. 297 30

A number of clinical laboratory and biopsy-derived parameters were assessed for their prognostic significance in the short (24 months), intermediate (60 months) and long terms in 45 patients (43 female, 2 male) with diffuse proliferative lupus glomerulonephritis (DPGN). The factors evaluated were serum creatinine (SCr) and urinary protein at time of biopsy, initial dose of prednisone and immunosuppressive after biopsy, activity index (AI), chronicity index (CI), their individual components, extent of extraglomerular (tubulo-interstitial) immune deposits (EGD) and mean number of intraglomerular monocytes per glomerulus (NSE index). Using proportional hazards analysis to evaluate the parameters, SCr (P = 0.003), AI (P = 0.005) and NSE index (P = 0.038) were shown to be significant predictors of outcome when all variables except the components of AI and CI were considered. When AI and CI were omitted but their components included, SCr (P = 0.0005), NSE index (P = 0.024), extent of karyorrhexis (P = 0.035) and glomerulosclerosis (P = 0.033) were then demonstrated to be significant prognostic factors of DPGN. The results suggest that intraglomerular monocyte infiltration has a protective effect and confirm that AI index is a relatively powerful predictor of outcome. Histologic and nonhistologic biopsy factors contribute significant additional prognostic information to that provided by SCr.
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PMID:Prognostic factors in diffuse proliferative lupus glomerulonephritis. 319 70


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