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What is damaging the kidney in lupus nephritis?

2015; Nature Portfolio; Volume: 12; Issue: 3 Linguagem: Inglês

10.1038/nrrheum.2015.159

1759-4804

Anne Davidson,

Inflammasome and immune disorders

Nephritis remains an important cause of morbidity and mortality in many patients with systemic lupus erythematosus (SLE), but knowledge of the factors contributing to the heterogeneity of kidney disease in these patients has been lacking. This article outlines various pathogenic pathways that contribute to renal damage in SLE and explains how disease phenotyping based on these mechanisms could lead to the novel and individualized therapies for patients with lupus nephritis. Despite marked improvements in the survival of patients with severe lupus nephritis over the past 50 years, the rate of complete clinical remission after immune suppression therapy is <50% and renal impairment still occurs in 40% of affected patients. An appreciation of the factors that lead to the development of chronic kidney disease following acute or subacute renal injury in patients with systemic lupus erythematosus is beginning to emerge. Processes that contribute to end-stage renal injury include continuing inflammation, activation of intrinsic renal cells, cell stress and hypoxia, metabolic abnormalities, aberrant tissue repair and tissue fibrosis. A deeper understanding of these processes is leading to the development of novel or adjunctive therapies that could protect the kidney from the secondary non-immune consequences of acute injury. Approaches based on a molecular–proteomic–lipidomic classification of disease should yield new information about the functional basis of disease heterogeneity so that the most effective and least toxic treatment regimens can be formulated for individual patients.