Silent nephritis in systemic lupus erythematosus

Zabaleta-Lanz, Mercedes; Vargas-Arenas, R E; Tapanes, F J; Daboín, Iraida; Pinto, Josuel Alfredo Vilela; Bianco, N. E.

doi:10.1191/0961203303lu259oa

Cited by 70 publications

(51 citation statements)

References 24 publications

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“…Several reports describe that the vast majority of SLE patients have glomerular deposits of both IgG and C1q even in the absence of clinically overt renal disease (32)(33)(34). This glomerular C1q could potentially serve as a target for anti-C1q autoantibody.…”

Section: Discussionmentioning

confidence: 99%

Anti-C1q autoantibodies deposit in glomeruli but are only pathogenic in combination with glomerular C1q-containing immune complexes

Trouw¹,

Groeneveld²,

Seelen³

et al. 2004

J. Clin. Invest.

208

134

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Anti-C1q autoantibodies are present in sera of patients with several autoimmune diseases, including systemic lupus erythematosus (SLE). Strikingly, in SLE the presence of anti-C1q is associated with the occurrence of nephritis. We have generated mouse anti-mouse C1q mAb's and used murine models to investigate whether anti-C1q autoantibodies actually contribute to renal pathology in glomerular immune complex disease. Administration of anti-C1q mAb JL-1, which recognizes the collagen-like region of C1q, resulted in glomerular deposition of C1q and anti-C1q autoantibodies and mild granulocyte influx, but no overt renal damage. However, combination of JL-1 with a subnephritogenic dose of C1q-fixing anti-glomerular basement membrane (anti-GBM) antibodies enhanced renal damage characterized by persistently increased levels of infiltrating granulocytes, major histological changes, and increased albuminuria. This was not observed when a non-C1q-fixing anti-GBM preparation was used. Experiments with different knockout mice showed that renal damage was dependent not only on glomerular C1q and complement activation but also on Fcγ receptors. In conclusion, anti-C1q autoantibodies deposit in glomeruli together with C1q but induce overt renal disease only in the context of glomerular immune complex disease. This provides an explanation why anti-C1q antibodies are especially pathogenic in patients with SLE.

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Section: Discussionmentioning

confidence: 99%

Anti-C1q autoantibodies deposit in glomeruli but are only pathogenic in combination with glomerular C1q-containing immune complexes

Trouw¹,

Groeneveld²,

Seelen³

et al. 2004

J. Clin. Invest.

208

134

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“…In biopsy studies, because of the high frequency of subclinical evidence of LN (immune complex deposition with minimal mesangial proliferation), over 90% of patients have been diagnosed with LN. 35 Furthermore, the disease duration in these patients was less than 1 year, which would not allow for proper classification of renal status. Finally, this study did not examine association with renal insufficiency, which was the outcome that fully accounted for our positive findings.…”

Section: Ras Gene Polymorphisms and Lupus Nephritismentioning

confidence: 95%

Renin–angiotensin system gene polymorphisms predict the progression to renal insufficiency among Asians with lupus nephritis

et al. 2005

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The renin-angiotensin system (RAS) is a strong candidate as a mediator for the development and progression of lupus nephritis (LN). We performed an ethnically stratified analysis of 642 systemic lupus erythematosus (SLE) patients to determine whether various functional RAS gene polymorphisms are associated with SLE renal outcomes. Patients were genotyped for two angiotensin-converting enzyme (ACE) gene polymorphisms: Alu insertion/deletion (I/D) and 23 949 (CT) 2/3 , and for two angiotensinogen (Atg) gene polymorphisms: M235T and C-532T. Multivariate analyses demonstrated associations between the ACE I/D, ACE (CT) 2/3 and Atg C-532T functional polymorphisms and LN among Asians. In stratified analyses among LN cases according to high vs low glomerular filtration rate (GFR), associations remained significant for the ACE D (odds ratio (OR) 5.9, P ¼ 0.001) and (CT) 2 (OR 6.2, P ¼ 0.001) alleles among Asian subjects with low GFR. Lastly, we found allelic dosedependent associations between the ACE I/D (P ¼ 0.003), ACE (CT) 2/3 (P ¼ 0.005) and Atg M235T (P ¼ 0.04) polymorphisms, and GFR analyzed as a continuous variable among Asians. These findings suggest a significant role for ACE and Atg gene sequence variation and severity of LN among Asians with SLE.

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“…4 Silent nephritis, now recognized as a serious pathologic abnormality of the kidney, presents in some patients with SLE, in the absence of abnormal urinalysis findings or other clinical features such as elevated serum creatinine and hypertension. 5 Biopsy of the kidney is thus considered to be of prime importance in some patients with SLE, as accurate diagnosis of biopsy-proven lupus nephritis (BPLN) allows for the instigation of an appropriate treatment strategy that can improve the survival rates of patients with SLE. 6,7 However, the prognosis of LN still varies greatly from region to region, and is likely to be affected by genetic, racial, and other epidemiologic factors.…”

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confidence: 99%

A Systematic Review and Meta-analysis of Prevalence of Biopsy-Proven Lupus Nephritis

et al. 2018

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Objectives: This study aims to conduct a meta-analysis to clarify the epidemiologic characteristics of biopsy-proven lupus nephritis (BPLN), including those relating to its prevalence and prognosis. Patients and methods: A literature search for relevant studies was conducted in the electronic databases of PubMed, Google Scholar, Embase, and Cochrane trial register. The following search terms were used for original articles published between January 1982 and April 2016: "lupus nephritis" or systemic lupus erythematosus ('SLE') or 'systemic lupus erythematous' and "pathology" or 'epidemiology' or prevalence or incidence. Pooled estimates with 95% confidence intervals were calculated. Results: Nineteen studies were included (mean age of SLE patients at renal biopsy: ~30 years). Of total BPLN patients, 85% were females. BPLN developed in 29% of SLE patients, and accounted for 60% of secondary glomerular diseases in renal biopsy databases. BPLN prevalence among SLE patients was higher in Saudi Arabia compared with pooled Europe/USA data (43% vs 26%, p<0.05). Pooled BPLN prevalence among secondary glomerular diseases patients was higher in Asian/Latin American countries than in Europe (63% vs 34%, p<0.05). Overall five-, 10-and 20-year survival rates of BPLN patients were 94%, 86%, and 71%, respectively, which were higher than those before 1995 (84%, 72%, and 52%, respectively) and lower than those after 1995 (96%, 89%, and 80%, respectively) (all p<0.05). Class IV nephritis, present in 40% of BPLN patients, was a risk factor for renal failure that contributed to poor prognosis. Conclusion: Lupus nephritis is a common complication of young female patients with SLE, and the most prevalent etiology of secondary glomerular diseases. Attention should be paid to class IV nephritis due to its high frequency and association with poor prognosis.

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Silent nephritis in systemic lupus erythematosus

Cited by 70 publications

References 24 publications

Anti-C1q autoantibodies deposit in glomeruli but are only pathogenic in combination with glomerular C1q-containing immune complexes

Anti-C1q autoantibodies deposit in glomeruli but are only pathogenic in combination with glomerular C1q-containing immune complexes

Renin–angiotensin system gene polymorphisms predict the progression to renal insufficiency among Asians with lupus nephritis

A Systematic Review and Meta-analysis of Prevalence of Biopsy-Proven Lupus Nephritis

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