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)

A patient with systemic lupus erythematosus (SLE), followed up over a six-month period, exhibited numerous immunologic abnormalities and varied renal pathologic features. Initial findings included minimal glomerular lesions, serum antibodies directed solely against nuclear RNA protein, and lupus band test showing pure IgM deposition. These findings suggested a good prognosis. Subsequently, the patient developed acute renal failure secondary to an interstitial lupus nephritis, without progression of the glomerular abnormality. Serum antibodies to the nuclear non-nucleic acid macromolecule and single stranded and native DNA were demonstrated concurrently. New skin deposits of IgG and IgA in addition to IgM also were observed. This patient demonstrates the potential progression of lupus renal disease despite the initial favorable prognostic indicators.
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PMID:Acute renal failure secondary to interstitial lupus nephritis. 30 20

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.
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PMID:Drug-induced renal disease. 38 1

Current studies indicate that a thrombotic microangiopathy (TMA) identifies patients with systemic lupus erythematosus (SLE) who are at high risk of progressing to end-stage renal disease. We have observed two patients with SLE and one patient with a primary antiphospholipid syndrome (APS) who developed acute renal insufficiency with thrombocytopenia. Renal biopsies showed a TMA characterized by thrombi or by cellular and mucoid intimal hyperplasia of small arteries and arterioles. No arterial or arteriolar immune-complex deposits were detected by immunofluorescent or electron microscopy. Biopsies from one SLE patient and the APS patient showed no immune-complex glomerular disease. Both had serum antiphospholipid antibodies (aPL). aPL were not detected in the serum of the other SLE patient who had an active lupus nephritis. Acute renal failure and thrombocytopenia resolved in each case following treatment by plasmapheresis or prednisone and heparin. None of the patients were initially treated with cytotoxic drugs. As more knowledge is gained, the accurate identification of renal vascular lesions in SLE or related diseases could influence renal prognosis and choice of therapy. The cases reported here provide further evidence that a TMA can cause acute renal failure independent of lupus nephritis. TMA should be distinguished from other forms of renal vascular disease, particularly a noninflammatory lupus microangiopathy, which is probably mediated by subendothelial immune-complex deposits. The absence of immunoglobulin deposits in vessels involved by a TMA indicates that microvascular thrombosis is promoted by mechanisms other than those usually attributed to immune-complex disease. Phospholipid reactive antibodies may be pathogenetic in some cases.
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PMID:Renal thrombotic microangiopathy in patients with systemic lupus erythematosus and the antiphospholipid syndrome. 149 68

The patient was a 74 years-old male who had suffered arthralgia since April 1986. Gold therapy was performed from June 1986 based on a diagnosis of rheumatoid arthritis (RA). This treatment was ineffective and administration of D-penicillamine (D-Pc) was started from March 1987, which alleviated the arthralgia. However, proteinuria appeared, and the nephrotic syndrome (NS) and acute renal failure (ARF) gradually developed. Four items, not including the renal symptoms, fulfilled the diagnostic criteria for systemic lupus erythematosus (SLE). Thereafter, D-Pc was withdrawn, and the symptoms were improved by hemodialysis and steroid therapy. This case was considered to be NS and ARF caused by treatment of RA with rather small doses of D-Pc (18.3 g in total), but the involvement of other factors could not be ruled out. Since the four items conforming to the SLE diagnostic criteria were alleviated by steroid therapy, the case was considered to be drug-related lupus-like syndrome. In recent years, D-Pc has frequently been used in the treatment of RA and its effects have been confirmed. However, side effects often appear, and considerable caution is required in the presence of drug-related SLE as well as proteinuria. When drug-related SLE is suspected, withdrawal of the drug concerned and steroid therapy appear to be useful.
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PMID:[A case report of rheumatoid arthritis which showed acute renal failure, nephrotic syndrome and drug-related lupus-like syndrome caused by D-penicillamine]. 208 56

Patients with lupus nephritis and severe renal failure progress to end-stage renal disease despite aggressive therapy to suppress immunologic function. Within this group is a small subset presenting with rapid progression of renal failure and requiring dialytic support. We reviewed the clinicopathologic data of four such patients who were able to terminate dialysis after acute renal failure due to lupus nephritis. Three of these patients have remained independent of dialysis up to 4 years, and one patient returned to dialysis 1 month following discontinuation. Although glomerular pathology was variable in the four patients, a lesion common to all at presentation was acute tubular necrosis. It is suggested that tubular necrosis may cause reversible renal failure when part of the nephropathy of disseminated lupus treated with corticosteroids.
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PMID:Histopathologic evaluation of lupus patients with transient renal failure. 381 70

Crescentic lupus glomerulonephritis (greater than or equal to 50% crescents) occurred in 16% of systemic lupus erythematosus (SLE) patients biopsied over a 32-month period. All had underlying WHO class IV lupus nephritis. These patients more frequently manifested with acute renal failure usually of the non-oliguric type, had heavier proteinuria and lower serum albumin, but were otherwise indistinguishable from non-crescentic WHO class IV lupus nephritis in their other renal and extrarenal manifestations or in their serological findings. Crescentic lupus glomerulonephritis may occur in patients at first presentation with SLE, or develop in patients after prolonged follow-up initially for lupus nephritis of WHO class IV or other classes. Combined methylprednisolone pulse therapy, immunosuppressives, antiplatelet agents with or without anticoagulant produced good initial responses. Prognosis was unfavorable for inadequately treated patients or for patients with persistent nephrotic syndrome and crescents.
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PMID:Crescentic lupus glomerulonephritis. 673 93

Acute interstitial pneumonitis is a well-recognized, although rare, complication of systemic lupus erythematosus (SLE) that has been associated with a poor prognosis. Fulminant lupus pneumonitis, acute renal failure, and RBC hypoplasia occurred in a 14-year-old girl. The patient's condition was managed with large-volume plasmapharesis, dialysis, and immunosuppressive therapy. Her respiratory, renal, and hematologic changes all resolved, and response was maintained with cyclophosphamide and prednisolone therapy. Although serologic evidence of SLE persisted, clinically, the patient was well four years after the initial appearance of SLE. There are several acute pulmonary manifestations of SLE, and plasmapheresis may be useful in the management of some of these conditions.
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PMID:Fulminant lupus pneumonitis with acute renal failure and RBC aplasia. Successful management with plasmapheresis and immunosuppression. 724 96

We report here, a patient of systemic lupus erythematosus (SLE) with severe fibrinoid necrosis in the afferent arteriole of the glomerulus, in whom antiphospholipid antibody might have contributed to the pathogenesis. A 24-year-old female who was suffering from severe anemia with fragmented red blood cells, acute renal failure and thrombocytopenia, was admitted to our hospital. Further examinations revealed findings compatible with active lupus nephritis. Moreover, she was found to be positive for antiphospholipid antibody, and anticardiolipin antibody, as well as for lupus anticoagulant and syphilis test. Intensive treatment by methylprednisolone pulse therapy, hemodialysis, and double filtration plasmapheresis were performed. However, 13 days after admission she died suddenly because of intracranial hemorrhage. Pathological investigation of renal tissue revealed severe fibrinoid necrosis of the arterioles mainly in the glomerular afferent arteriole associated with diffuse proliferative lupus nephritis. In this case, hemolytic uremic syndrome (HUS) was associated with SLE. Antiphospholipid antibody was considered to be not only an accelerator in the arterial lesions of HUS, but also an initiator of HUS itself.
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PMID:[A case of systemic lupus erythematosus associated with severe fibrinoid necrosis located mainly in the glomerular afferent arteriole]. 769 57

We report a case of a child who was first seen for acute renal failure and periarteritis nodosa. Angiography findings confirmed this diagnosis. Ultrasound scan revealed large tricuspid valve vegetation, as well as minute vegetation on the right ventricular wall. All vegetation disappeared after 12 months of immunosuppressive therapy. Serology findings for lupus were negative. All clinical and laboratory findings strongly support the hypothesis that this previously undescribed heart involvement is caused by PAN.
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PMID:Tricuspid valve vegetation in a child with periarteritis nodosa. 809 45

A 45-year-old woman who had been diagnosed as having systemic lupus erythematosus (SLE) at the age of 28 years and who had been in remission developed severe urinary frequency, watery diarrhea, vomiting and weight loss. She also developed acute renal failure and her serological examination was consistent with active SLE. She had a markedly decreased urinary bladder capacity of 20 ml with hydroureteronephrosis. Histopathological study of her urinary bladder biopsy specimen showed mucosal edema, infiltration by lymphocytes and granulocytes, and deposition of IgA in the epithelium and submucosal region. We diagnosed this as a case of lupus cystitis. The patient's symptoms were alleviated by bilateral nephrostomy and corticosteroid therapy. In the present episode the patient showed none of the usual symptoms of SLE. This case and others reported in the literature show that lupus cystitis presents with specific signs and symptoms and therefore, this syndrome may represent a specific clinical manifestation of SLE.
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PMID:Systemic lupus erythematosus relapse with lupus cystitis. 857 46


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