Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

16 patients with membranoproliferative glomerulonephritis had a mean serum chloride level significantly higher than that in normal subjects or in comparable groups of patients with nephrotic syndrome secondary to either systemic lupus erythematosus or to other primary nephrotic glomerular diseases. Differences in the severity of histologic alterations of the renal interstitium did not correlate with the different levels of serum chloride seen in these groups. The increased chloride concentration may be partially explained as a compensating reaction for a decrease in protein anions. However, a renal tubular acidifying defect demonstrated in one of our patients may also contribute to the hyperchloremia in some cases.
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PMID:Hyperchloremia associated with membranoproliferative glomerulonephritis. 87 38

A 56-yr-old black woman with absence of the eighth component of complement and a disease compatible with systemic lupus erythematosus is described. Her disease is characterized by the presence of photosensitive "malar" rash, alopecia, polyarthritis, and nephrotic syndrome. Hemolytic and immunochemical assays of the serum complement components were normal, except for C8 which was undetectable. Hemolytic activity could be restored to normal by the addition of functionally pure C8. In vitro tests to investigate the functional integrity of the classical and alternative pathways indicated that the functions mediated by activation of C3 and C5 were intact whereas heatlabile bactericidal activity was totally absent. Addition of C8 restored this function to normal levels. One of two brothers of the proband was shown to have serum C8 levels approaching 50% of normal indicating the hereditary nature of the defect. HLA typing studies showed that the normal brother had identical haplotypes to the proband while the proposed heterozygous brother only shared one haplotype with the patient, suggesting that the gene controlling the C8 defect was not closely linked to the major histocompatibility complex. If the association of a connective tissue disease and absence of a terminal component of complement is not coincidental, these results suggest that C8 deficiency may be associated with a subtle defect in the defense mechanisms to viral infection leading to viral persistance and perhaps to diseases such as systemic lupus erythematosus where chronic viral infections have been implicated.
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PMID:Absence of the eighth component of complement in association with systemic lupus erythematosus-like disease. 89 74

Glomerular changes, and cellular and tissue responses of antibody-forming organs in 37 cases (20 cases with nephrotic syndrome and 17 cases without the syndrome) of systemic lupus erythematosus (SLE) were described. The glomerular changes were classified into 3 types, i.e., proliferative glomerulitis, membranous transformation, and wire-loop lesion from the standpoint of glomerular functional structure and its alterations. As to the responses of antibody-forming organs, hypoplasia of myeloid tissue, atrophy of lymph follicles of spleen and lymph nodes, atrophy and decrease in numbers of lymphocytes of thymus, proliferation and infiltration of plasma cells and plasmocytoid basophilic mononuclears, and proliferation of basophilic reticulum cells at the cost of differentiated antibody-forming organ tissues of bone marrow, spleen, lymph nodes, etc. were noted. Immunological bases of glomerular changes were considered and discussed in the light of pathological findings of SLE presented here and suggestions from experimental pathological studies in this field. Pathogenic roles of antigen-antibody complexes as well as anti-glomerular basement membrane (anti-GBM) antibody were considered in relation to the histologic manifestations of glomeruli in SLE or lupus nephritis.
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PMID:Pathology of lupus nephritis with special reference to the immunological bases of glomerular changes. 91 71

During a period of 4 years urine samples from 54 patients with systemic lupus erythematosus (SLE) were repeatedly analysed for the activities of lactate dehydrogenase (LDH), leucine aminopeptidase (LAP) and alanine aminopeptidase (AAP). Increased urinary enzyme levels were consistently found in 8 patients with severe lupus nephritis and the nephrotic syndrome, as well as in 9 patients with chronic lupus nephritis resistant to therapy. A further group of 9 patients with lupus nephritis responded favourably to immunosuppressive therapy with arrest of kidney-damaging processes; a concomitant normalization of urinary enzyme levels was observed, giving an accurate reflection of the progression of the disease. Another 14 SLE patients showed raised enzyme levels preceding the development of clinical signs of nephropathy. The last 14 SLE patients displayed neither nephropathy nor altered enzyme activities. The determination of urinary enzyme activities is, therefore, considered to be a useful supplement to the routine biochemical analyses performed on the urine in cases of SLE.
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PMID:[The value of urinary enzyme determinations in systemic lupus erythematosus (author's transl)]. 96 Jul 3

We report here four cases of systemic lupus erythematosus associated with the nephrotic syndrome and renal vein thrombosis and review six familiar cases previously noted in the literature. Renal biopsy in each of our cases showed changes consistent with the membranous type of lupus nephropathy. We discuss the exclusive appearance of this pattern in relation to renal vein thrombosis in other forms of renal disease. The occurance of renal vein thrombosis in patients with systemic lupus erythematosus and the nephrotic syndrome supports the evidence that the thrombosis is a complication rather than a cause of the nephrotic syndrome. The presence of pleuritic pain in a patient with systemic lupus erythematosus and the nephrotic syndrome should alert the clinician to the possibility of renal vein thrombosis and pulmonary emboli. With appropriate diagnosis and anticoagulation therapy, our patients had a benign course during 7 to 48 months of follow-up.
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PMID:Renal vein thrombosis, nephrotic syndrome, and systemic lupus erythematosus: an association in four cases. 96 21

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

A study of renal biopsy specimens obtained in Senegal from 24 children and six adults with nephrotic syndrome showed two unusual varieties of nephropathy--namely, an extramembranous glomerulonephritis associated with hypocomplementaemia (four cases), a combination previously described only in systemic lupus erythematosus, and a "tropical nephropathy" (16 cases). The latter, though lacking the diffuse glomerular deposits of immunoglobulin described in quartan malarial nephropathy (Q.M.N.), showed a curious progressive and segmental glomerulosclerosis, characterized by a "flaking" or fibrillary splitting of the glomerular capillary wall, seen in Q.M.N. Serological evidence of malaria was lacking in a third of the childhood cases.
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PMID:"Topical nephropathy" and "tropical extramembranous glomerulonephritis" of unknown aetiology in Senegal. 109 12

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.
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PMID:Membranous nephropathy: an overview. 120 87

Extramembranous glomerulonephritis is an uncommon but distinct pathologic lesion in children. The diagnosis is established by the characteristic light, immunofluorescent, and ultrastructural abnormalities in renal biopsy specimens. This report describes seven of the ten children with this lesion studied in the past 11 years. Emphasis is given to the comparison of four children with idiopathic membranous glomerulonephritis with three others who presented with a nephrotic syndrome but subsequently developed evidence of systemic lupus erythematosus. Two of the latter three children, and three others with SLE and MGN not described in detail, demonstrated deposition of IgA by immunofluorescence along glomerular capillaries. Five of six children with SLE and MGN had microtubular structures in glomerular endothelial cells demonstrable by electron microscopy. These observations suggest that children with MGN require careful and continuing study for evidence of SLE.
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PMID:Extramembranous glomerulonephritis in childhood: relationship to systemic lupus erythematosus. 124 50

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


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