Lupus Nephritis: Diagnostic Approach, Management, and Current Treatment

Call for Papers

In the USA, approximately 35% of patients with Systemic Lupus Erythematosus (SLE) have clinical evidence of nephritis at the time of diagnosis. Lupus nephritis (LN) is defined as clinical and laboratory manifestations that meet the American College of Rheumatology (ACR) criteria: persistent proteinuria >0.5 g per day or greater than 3+ by dipstick and/or cellular casts, including red blood cells (RBCs), hemoglobin, granular, tubular, or mixed. A spot urine protein/creatinine ratio of >0.5 can be substituted for the 24-hour protein measurement and an “active urinary sediment” can be substituted for cellular casts. All patients with clinical evidence of active LN, previously untreated, undergo renal biopsy, because it permits the demonstration of immune complex-mediated glomerulonephritis compatible with LN. Treatment of LN should be based in large part on the classification of the type of LN by the International Society of Nephrology/Renal Pathology Society (ISN/RPS). The histological classification of LN considers 6 classes of renal damage. Class I (minimal mesangial disease) and class II (mesangial proliferative LN) generally do not require immunosuppressive treatment. Class III (focal LN) and class IV (diffuse LN) require aggressive therapy with glucocorticoids and immunosuppressive agents. Class V (membranous LN) when combined with class III or IV should be treated in the same manner as class III or IV. Class V alone should be treated with mycophenolate mofetil (MMF) plus prednisone and if the renal function does not improve with intravenously cyclophosphamide plus glucocorticoids. Class VI (advanced sclerosing LN) generally requires preparation for renal replacement. There is evidence that LN may respond to rituximab treatment. However, combinations of rituximab and MMF are being studied and might be considered for those patients who have failed the recommended induction therapies. Belimumab (anti-BlyS/BAFF, a recently approved treatment for SLE) seems to reduce proteinuria. We invite the authors to submit original research and review articles that seek to describe the diagnostic approach, the management, and the current treatment of LN. Potential topics include, but are not limited to:

• Pathophysiology of LN (i.e., proinflammatory molecules, advances in genetics, new antigenic targets of immune responses, etc.)
• Current overview upon pathophysiology of LN
• Histological advances and imaging in LN
• Impact of new current biological drugs targeting the immune system on LN
• Future therapeutic target

Before submission authors should carefully read over the journal’s Author Guidelines, which are located at http://www.hindawi.com/journals/ad/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/ad/lnp/ according to the following timetable:

Lead Guest Editor

• Giuseppe Murdaca, Clinical Immunology Unit, Department of Internal Medicine, University of Genova, Genova, Italy

Guest Editors

• Sudhir Gupta, University of California, Irvine, CA, USA
• Francesco Puppo, Clinical Immunology Unit, Department of Internal Medicine, University of Genova, Genova, Italy