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)

Renal tissues from 37 patients with glomerulopathies involving glomerular crescents were investigated using an immunofluorescence technique. Immunohistologic findings revealed two kinds of crescents, those with fibrinogen deposits (active), and those without (inactive). The degree of IgG deposition in glomeruli with active crescents was much higher than in glomeruli with inactive crescents in acute glomerulonephritis (AGN) and chronic glomerulonephritis (CGN). Active crescents were observed only in biopsy specimens taken within three months after the onset of acute glomerulonephritis or the acute exacerbation of chronic glomerulonephritis. These findings suggest that in AGN and CGN active crescents occur in an earlier stage of glomerular lesions and a more active stage in the immunological process than inactive crescents. The significance of active crescents in SLE, diabetic nephropathy and nephropathy associated with rheumatic arthritis was not evaluated due to the small number of patients.
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PMID:Immunohistologic findings in the glomerular crescents in various renal diseases. 37 95

With the aim of determining the relative prevalence of the diseases underlying chronic renal failure (CRF) in a large homogeneous black tropical population, the autopsy records of the Obafemi Awolowo University Teaching Hospital over a four year period were studied. Out of a total of 702 cases coming to autopsy during this period, 66 (9.4%) died as a result of CRF. The highest number of cases of CRF fell within the 31-40 year age group with a male/female ratio of 1.28:1. Chronic glomerulonephritis was responsible for 40.9% of cases, malignant nephrosclerosis 16.6%, benign nephrosclerosis 7.6% while endstage renal disease (ESRD) was responsible for 15.4%. A miscellaneous group of diseases was responsible for 19.7%, about half of which was due to chronic pyelonephritis. Rarer causes of CRF were diabetic nephropathy, multiple myeloma, systemic lupus erythematosus and analgesic nephropathy.
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PMID:The pathological basis of chronic renal failure in Nigerians. An autopsy study. 149 21

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

We have conducted an immunocytochemical analysis to investigate the presence of the recently described vascular cell adhesion molecule-1 (VCAM-1) in human kidney, using the anti-VCAM-1 monoclonal antibody 1.4C3. In normal control tissue VCAM-1 was present on some (but not all) parietal epithelial cells lining Bowman's capsule. Forty-nine of fifty clinical biopsy specimens were characterised by the additional presence of VCAM-1 on proximal tubular cells. This was most marked in biopsies of patients with interstitial nephritis or systemic vasculitis with crescentic nephritis, but was also observed in biopsies with minimal change, IgA or lupus nephropathy, or from patients with diabetic nephropathy, amyloid, or gout. Proximal tubule VCAM-1 correlated significantly with the number of transferrin-receptor-positive leukocytes (r = 0.607, p less than 0.0001) in the interstitium, but not with expression of HLA-DR by tubular cells. Surprisingly, VCAM-1 was not observed on vascular endothelial cells in these biopsies, even in the presence of a marked infiltrate; this contrasts with other tissues (e.g. skin and synovium). The presence of VCAM-1 on tubular cells in the inflamed kidney indicates the potential for these cells to interact with mononuclear cells, either as accessory cells or as cytotoxic targets. The unexpected absence of VCAM-1 in renal vascular endothelial cells suggests local differences in the endothelial cells of this organ.
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PMID:Expression of VCAM-1 in the normal and diseased kidney. 172 89

The role of angiotensin-converting-enzyme inhibitors (ACEIs) in the treatment of progressive renal disease is described. Researchers have evaluated the use of ACEIs in patients with two types of progressive kidney disease: diabetic nephropathy and renal insufficiency associated with connective-tissue disease. When introduced early in the course of diabetic nephropathy, ACEIs appear to produce greater reductions in urinary protein concentrations than do other antihypertensive agents, even when systemic blood pressure does not decrease. They also slow the rate of decline of renal plasma flow and glomerular filtration rate. Results are less impressive when ACEIs are initiated at a later stage of disease. Captopril has been shown to be associated with a decline in serum creatinine level in patients with systemic scleroderma, and with reductions in blood pressure and increases in the glomerular filtration rate in patients with systemic lupus erythematosus. Because these patients were receiving other agents that might have influenced study outcome, specific conclusions about the efficacy of ACEIs in connective-tissue disease cannot yet be drawn. They may, however, be recommended as adjunctive agents in treatment of this condition. The relative safety of the ACEIs, combined with their ability to arrest or slow the progression of renal failure, makes them primary options in the management of selected renal diseases.
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PMID:Use of angiotensin-converting-enzyme inhibitors in the management of renal disease. 199 85

Sera from 305 consecutive patients in a renal biopsy series were analyzed for the presence of anti-entactin antibodies by ELISA. Of these patients, 59% had primary glomerulonephritis, 21% had secondary glomerulonephritis, while 20% had other nephropathies (noninflammatory conditions like amyloidosis, diabetic nephropathy, nephrosclerosis, etc.). Forty-one of these patients (13.4%) were positive for IgG/IgM antibodies against entactin: 60% of them had primary glomerulonephritis, 35% had secondary glomerulonephritis, while the remaining 3 patients had other nephropathies. Fifteen (70%) of the 23 patients with primary glomerulonephritis had proliferative glomerulonephritis (PGN), whereas 13 (87%) of the 15 patients with secondary glomerulonephritis were due to systemic connective tissue diseases (SCTD): 7 due to SLE, 4 due to SLE like SCTD and two due to other SCTD. There was a peak of incidence corresponding to the group aged 18 to 30 years. A majority of these patients (12 of the total 17) had primary glomerulonephritis and were associated with nephrotic or subnephrotic grade proteinuria, poorly or nonresponsive to immunosuppressive treatment and associated, in several cases, with progressive deterioration of renal function. In addition, there was a tendency to another peak in the age group 51 to 60 years. Most of these patients (6 of the total 8) had glomerulonephritis secondary, mainly, to SLE or SLE like SCTD with milder degree of proteinuria and better preserved renal functions. Anti-entactin antibodies were not found in certain glomerulonephritides like IgA nephropathy and those secondary to systemic vasculitides and in control subjects (healthy subjects, and patients with a variety of non-renal disorders including inflammatory diseases).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating anti-entactin antibodies in patients with glomerulonephritis. 206 16

The number of hospitalized renal patients and the number of days they stayed in hospitals were studied in Finland 1969-1982. In 1969 3.3% and in 1982 1.7% of all bed-days available were occupied by renal patients. The number of hospitalized renal patients first decreased and after 1976 no notable changes were observed. A rising trend in the number of patients as well as in the corresponding bed-days was seen in diabetic nephropathy, lupus nephropathy, renal amyloidosis and polycystic kidney disease. A declining trend, in contrast, was observed in renal infections and nephritis. The proportion of patients over 70 years increased during the study period. An approximation of the outcome of renal diseases was made using the ratio of the number of deaths against the number of hospitalized renal patients. The outcome of patients under 50 years has improved. A slight improvement was observed in most renal diseases, partially due to the increased capacity of dialysis treatment and renal transplantations.
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PMID:Hospitalization for renal diseases in Finland 1969-1982. 318 39

The complement receptor for C3b of the epithelial cells of human glomeruli is structurally and functionally very similar or identical to CR1, the complement receptor for C3b and C4b present on the membrane of red cells and leukocytes. Four monoclonal antibodies directed against separate epitopes of CR1 react with an antigen in the glomeruli, which appears to be present on the epithelial podocytes. Moreover, the monoclonal antibodies very effectively inhibit the binding of C3b-bearing red cells to the glomeruli. The pattern of immunofluorescence of the receptor was normal or slightly altered in patients with minimal change disease, mesangial proliferative glomerulonephritis (GN), or idiopathic membranous GN. Glomeruli with endocapillary proliferation showed some attenuation of staining. Glomeruli in which the capillary tuft architecture was altered, or of patients with systemic lupus erythematosus, or of patients with diffuse diabetic nephropathy tended to have few foci or no staining for the receptor. No correlation was found between the intensities of staining of the C3b receptor and of C3 antigen deposited in the glomeruli.
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PMID:Monoclonal antibodies to human complement receptor (CR1) detect defects in glomerular diseases. 622 55

Renal diseases other than diabetic nephropathy were found in 10 of 122 diabetic patients who underwent renal biopsy between 1960 and 1982. These diseases included lupus glomerulonephritis, acute post-streptococcal glomerulonephritis, membranoproliferative glomerulonephritis (type I), focal glomerulosclerosis, idiopathic membranous nephropathy, and nonspecific immune complex glomerulonephritides. Because some of these disorders can alter the management and prognosis of renal disease in diabetic patients, the appearance of urinary abnormalities or deterioration in renal function inconsistent with the natural history of diabetic nephropathy raises the possibility of a nondiabetic renal disease and should lead to a more detailed evaluation.
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PMID:Nondiabetic renal disease in patients with diabetes mellitus. 622

Simultaneous studies of serum and urinary proteins in 294 adult proteinuric patients are presented. Our data showed that these studies can provide valuable guides for clinical diagnosis. In the group of idiopathic nephrotic syndrome, hypoalbuminemia, hypogammaglobulinemia and hyper-alpha 2 globulinemia were most marked. Urinary protein electrophoresis (PEP) showed a well-selective pattern with albumin and beta globulin as the main constituents. In the other groups of proteinuric patients the hypoalbuminemia and hyper-alpha 2 globulinemia were milder and urinary PEP generally showed non-selective pattern. In the groups of acute glomerulonephritis and lupus nephropathy, C3 was generally decreased; polyclonal gammopathy was frequently encountered and alpha 1 acid glycoprotein was markedly increased. In the cases of chronic glomerulonephritis and diabetic nephropathy and the levels of gamma globulin, C3 and alpha 2 acid glycoprotein were usually within normal limits. Urinary protein selectivity index in this series of adult patients was not a useful diagnostic parameter.
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PMID:Simultaneous studies of serum and urinary proteins for evaluation and diagnosis of glomerular damages in proteinuric patients. 722 87


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