ELECTRON MICROSCOPY IN LUPUS NEPHRITIS (A Case Report).
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ABSTRACT:
SUBMITTER: Sivadas P
PROVIDER: S-EPMC5529764 | biostudies-other | 1994 Jul
REPOSITORIES: biostudies-other
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Project description:IntroductionRefractory lupus nephritis (LN) causes kidney disease progression and increases the risk of loss of renal function. Due to the high specificity and few side effects of biological agents, they are recommended for the treatment of systemic lupus erythematosus. There are few data on telitacicept for the treatment of refractory LN.Case presentationHere, we report the efficacy and safety of telitacicept in the treatment of refractory LN in a 25-year-old female patient. This patient with refractory lupus developed Pneumocystis jirovecii pneumonia while using multitargeted therapy, and the patient's urine protein was rapidly relieved after telitacicept combination with low-dose mycophenolate mofetil (MMF).ConclusionThis result suggests that telitacicept has a positive effect on refractory LN with no significant side effects. Further reports and a registry are necessary to confirm that telitacicept with low-dose MMF should be preferred in refractory LN.
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Project description:We report a rare case of dengue fever triggering systemic lupus erythematosus and lupus nephritis. The patient presented herself during a large outbreak of dengue fever in December 2012 in Maharashtra, India. The diagnosis of dengue fever was confirmed by the presence of NS-1 antigen during the first few days of febrile illness. Eight weeks later, kidney tissue biopsy studies revealed evidence of lupus nephritis on microscopic examination and immunofluorescence. The report interpreted it as focal proliferative glomerulonephritis and segmental sclerosis (Stage IIIC). The case was also found positive for perinuclear antineutrophil cytoplasmic antibodies by indirect immunofluorescence assay. An active and effective management of a case essentially calls for clear perception of differentiating dengue-induced lupus flare, antineutrophil cytoplasmic antibody-related nephropathy, and/or dengue-induced de-novo lupus disease. Dengue viremia may be the trigger for immune complex formation in patients who are predisposed to developing autoimmune diseases. The present case explains the importance of considering the diagnosis of dengue-related lupus nephritis as an atypical occurrence in appropriate situations, as in this case. It would not be improper to regard this escalating disease as an expanded feature of dengue.
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Project description:Isolated or dominant tubulointerstitial lupus nephritis is rare. Here, we reported a 67-year-old man diagnosed with systemic lupus erythematosus (SLE) based on clinical and laboratory criteria, who was showing impaired renal function and non-nephrotic range proteinuria in the past 2 years. Renal biopsy showed almost normal glomeruli, but the tubulointerstitium showed "storiform" pattern with interstitial infiltration of IgG3 predominant plasma cells. Immunofluorescence showed linear and granular staining of IgG and C1q along TBM and interstitium. He started on medium dose of oral steroids and mycophenolate mofetil, which were gradually tapered. As a result, his renal function improved over a few days. Now, he continued on low dose steroids and mycophenolate mofetil with no evidence of relapse.
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Project description:We report a 58-year-old Asian woman who was diagnosed with systemic lupus erythematosus (SLE) and lupus nephritis, together with a mixed pulmonary bacterial and fungal infection including Aspergillus. The infection did not respond well to the routine administration of anti-bacterial and anti-fungal drugs, and the patient's creatinine levels continued to rise and protein remained in her urine. The patient's SLE persisted without going into remission. Finally, surgical resection of the pulmonary aspergilloma brought the SLE back under control.
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Project description:BACKGROUND:Lupus nephritis (LN) is a frequent severe complication of Systemic Lupus Erythematosus (SLE), especially in patients of non-Caucasian ethnicity. Induction treatment for LN consists in the combination of steroids plus a second agent (cyclophosphamide or mycophenolate mofetil) or, as a second-line, calcineurin inhibitors or Rituximab. Induction treatment for LN can be complicated by a series of side effects, the most severe being serious infections. Belimumab is a fully humanized monoclonal antibody that targets soluble B lymphocyte stimulator (BLyS), approved for treatment of serologically active SLE in addition to standard of care. CASE PRESENTATION:A young Hispanic woman was diagnosed with SLE at the age of 15. After several immunosuppressive treatments for arthritic symptoms (high-dose steroids, mycophenolate mofetil, Rituximab, cyclophosphamide) leading to serious complications and scarce clinical improvement, she developed severe LN. Induction treatment with a combination of intravenous high-dose methylprednisolone and cyclophosphamide was started but, after few days, the patient developed cryptococcal meningitis. After institution of appropriate antifungal therapy, treatment with Tacrolimus was attempted but poorly tolerated by the patient and withdrawn. Eventually, Belimumab was initiated off-label as a last resource to treat LN. Belimumab was well tolerated by the patient and resulted in a rapid and marked improvement in clinical symptoms and reduction in proteinuria, serum complement levels and anti-dsDNA titer; of note, the patient developed no infectious complications. CONCLUSIONS:We report the case of a severe LN in a young Hispanic woman who did not respond to conventional and second-line induction therapies, due both to intolerance and to the development of serious infectious complications. Eventually, Belimumab was successfully added to steroids and was well tolerated by the patient, resulting in a marked improvement in clinical and biochemical parameters. We suggest that Belimumab should be considered as a potentially efficacious treatment in patients with LN who cannot tolerate conventional therapies.
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Project description:The complement system is an innate immune surveillance network that provides defense against microorganisms and clearance of immune complexes and cellular debris and bridges innate and adaptive immunity. In the context of autoimmune disease, activation and dysregulation of complement can lead to uncontrolled inflammation and organ damage, especially to the kidney. Systemic lupus erythematosus (SLE) is characterized by loss of tolerance, autoantibody production, and immune complex deposition in tissues including the kidney, with inflammatory consequences. Effective clearance of immune complexes and cellular waste by early complement components protects against the development of lupus nephritis, while uncontrolled activation of complement, especially the alternative pathway, promotes kidney damage in SLE. Therefore, complement plays a dual role in the pathogenesis of lupus nephritis. Improved understanding of the contribution of the various complement pathways to the development of kidney disease in SLE has created an opportunity to target the complement system with novel therapies to improve outcomes in lupus nephritis. In this review, we explore the interactions between complement and the kidney in SLE and their implications for the treatment of lupus nephritis.
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