Journal
NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume -, Issue -, Pages -Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfad154
Keywords
albuminuria; cardiovascular disease; cardiovascular risk; chronic kidney disease; glomerular filtration rate; lupus nephritis; systemic lupus erythematous; treatment
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Chronic kidney disease (CKD) is diagnosed based on glomerular filtration rate (GFR) and urinary albumin:creatinine ratio (UACR). High cardiovascular risk is associated with moderate or severe CKD. The management recommendations for lupus nephritis (LN) and cardiovascular risk in rheumatic and musculoskeletal diseases do not consider albuminuria or CKD. The authors propose a change in the conceptual framework to treat LN as a cause of CKD and apply evidence from large CKD trials.
Chronic kidney disease (CKD) is diagnosed when glomerular filtration rate (GFR) falls below 60 ml/min/1.73 m(2) or urinary albumin:creatinine ratio (UACR) reaches & GE;30 mg/g, as these two thresholds indicate a higher risk of adverse health outcomes, including cardiovascular mortality. CKD is classified as mild, moderate or severe, based on GFR and UACR values, and the latter two classifications convey a high or very high cardiovascular risk, respectively. Additionally, CKD can be diagnosed based on abnormalities detected by histology or imaging. Lupus nephritis (LN) is a cause of CKD. Despite the high cardiovascular mortality of patients with LN, neither albuminuria nor CKD are discussed in the 2019 European League Against Rheumatism (EULAR)/European Renal Association-European Dialysis and Transplant Association recommendations for the management of LN or the more recent 2022 EULAR recommendations for cardiovascular risk management in rheumatic and musculoskeletal diseases. Indeed, the proteinuria target values discussed in the recommendations may be present in patients with severe CKD and a very high cardiovascular risk who may benefit from guidance detailed in the 2021 European Society of Cardiology guidelines on cardiovascular disease prevention in clinical practice. We propose that the recommendations should move from a conceptual framework of LN as an entity separate from CKD to a framework in which LN is considered a cause of CKD and evidence generated from large CKD trials applies unless demonstrated otherwise.
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