Lupus Nephropathy Without Clinical Renal Involvement

Mahajan, S K; Ordóñez, Nelson G.; Feitelson, P J; Lim, Victoria S.; Spargo, Benjamin H.; Katz, A I

doi:10.1097/00005792-197711000-00004

Cited by 95 publications

(34 citation statements)

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“…A dissociation between clinical and pathological disease measures in lupus nephritis can occur in humans (33). The pathological measures of glomerular disease used in this study do seem to be valid measurements, as BUN levels and pathological variables were strongly correlated ( p Ͻ 0.001 in all cases).…”

Section: Discussionmentioning

confidence: 51%

Transgenic Expression of a Soluble Complement Inhibitor Protects Against Renal Disease and Promotes Survival in MRL/lprMice

Bao

Haas

Boackle

et al. 2002

The Journal of Immunology

105

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To investigate the role of complement in lupus nephritis, we used MRL/lpr mice and a transgene overexpressing a soluble complement regulator, soluble CR1-related gene/protein y (sCrry), both systemically and in kidney. Production of sCrry in sera led to significant complement inhibition in Crry-transgenic mice relative to littermate transgene negative controls. This complement inhibition with sCrry conferred a survival advantage to MRL/lpr mice. In a total of 154 animals, 42.5% transgene-negative animals had impaired renal function (blood urea nitrogen > 50 mg/dl) compared with 16.4% mice with the sCrry-producing transgene (p < 0.001). In those animals that died spontaneously, MRL/lpr mice with the sCrry-producing transgene did not die of renal failure, while those without the transgene did (blood urea nitrogen values of 46.6 ± 9 and 122 ± 29 mg/dl in transgene-positive and transgene-negative animals, respectively; p < 0.001). Albuminuria was reduced in those transgenic animals in which sCrry expression was maximally stimulated (urinary albumin/creatinine = 12.4 ± 4.3 and 36.9 ± 7.7 in transgene-positive and transgene-negative animals, respectively; p < 0.001). As expected in the setting of chronic complement inhibition, there was less C3 deposition in glomeruli of sCrry-producing transgenic mice compared with transgene-negative animals. In contrast, there was no effect on glomerular IgG deposition, levels of anti-dsDNA Ab and rheumatoid factor, or spleen weights between the two groups. Thus, long-term complement inhibition reduces renal disease in MRL/lpr mice, which translates into improved survival. MRL/lpr mice in which complement is inhibited still have spontaneous mortality, yet this is not from renal disease.

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Section: Discussionmentioning

confidence: 51%

Transgenic Expression of a Soluble Complement Inhibitor Protects Against Renal Disease and Promotes Survival in MRL/lprMice

Bao

Haas

Boackle

et al. 2002

The Journal of Immunology

105

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“…Renal inflammation and changes of diffuse proliferative glomerulonephritis are seen in patients with no abnormalities of the urinary sediment (115,116). Important covariates.…”

Section: Resultsmentioning

confidence: 99%

The American college of rheumatology response criteria for proliferative and membranous renal disease in systemic lupus erythematosus clinical trials

Liang

Schur

Fortin

et al. 2006

Arthritis & Rheumatism

229

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“…Histological changes on renal biopsies are detected in almost all patients with systemic lupus erythematosus (SLE), even in cases involving no clinical evidence of renal disease (8,9), and the term 'silent lupus nephritis (LN)' is generally recognized to reflect a histopathological diagnosis of LN without clinical renal abnormalities (10,11). The prevalence of silent LN type V is relatively low.…”

Section: Discussionmentioning

confidence: 99%

Membranous Nephropathy that First Presented in Pregnancy

et al. 2013

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A 37-year-old woman at 17 weeks of gestation who was first noted to have proteinuria and microscopic hematuria at 13 weeks of gestation was admitted to our hospital with proteinuria that progressed to nephrotic syndrome (NS). Despite the treatment with prednisolone, including methylprednisolone pulse therapy, the NS worsened. The patient underwent an elective abortion at 21 weeks of gestation, and the NS then went into partial remission. A renal biopsy revealed membranous nephropathy (MN). There was no evidence of secondary MN. This is the first reported case of subclinical idiopathic MN that first developed in pregnancy.

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Lupus Nephropathy Without Clinical Renal Involvement

Cited by 95 publications

References 0 publications

Transgenic Expression of a Soluble Complement Inhibitor Protects Against Renal Disease and Promotes Survival in MRL/lprMice

Transgenic Expression of a Soluble Complement Inhibitor Protects Against Renal Disease and Promotes Survival in MRL/lprMice

The American college of rheumatology response criteria for proliferative and membranous renal disease in systemic lupus erythematosus clinical trials

Membranous Nephropathy that First Presented in Pregnancy

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