These findings were similar to those of our previous study

These findings were similar to those of our previous study.24 This suggests that patients with LN and renal damage were more prone to hypocomplementemia, indicating that lower serum complement levels were associated with more severe pathological lesions. Anti-dsDNA antibodies are unique to patients with SLE and thus represent an SLE-specific antibody. with those without renal damage. Anti-dsDNA and anti-Sm antibody positivity rates and 24-hour proteinuria were significantly increased, while hemoglobin, serum albumin, C3 and C4 levels, and estimated glomerular filtration HPGDS inhibitor 2 rate were significantly decreased in HPGDS inhibitor 2 patients with severe LN compared with patients with moderate LN. Conclusions LN can display various clinical manifestations, laboratory indexes, levels of disease activity, and pathological types in adult patients. Keywords: Systemic lupus erythematosus, clinical analysis, lupus nephritis, pathogenesis, disease activity, renal damage Introduction Systemic lupus erythematosus (SLE) is usually a diffuse autoimmune-mediated connective tissue disease mainly manifested by immune inflammation, involving multiple systems and organs.1 Previous studies showed that approximately 50% of patients with SLE experience renal damage, and histopathological studies confirmed that 100% of patients with SLE had varying degrees of renal pathological changes.2 Lupus nephritis (LN) is the most severe form of organ damage in patients with SLE and one of the most common secondary glomerular diseases, accounting for approximately 70% of secondary glomerular diseases based on histopathological examination.3 Importantly, LN frequently remains unrecognized until it has developed into full-blown nephritic and/or nephrotic syndrome with renal failure.4 Changes in several indicators, including the presence or increase of protein in the urine, positive autoantibodies, and decreased hemoglobin and complement levels, may reflect SLE disease activity and renal damage. However, the sensitivity and specificity of these indicators and their associations with clinical PPARgamma manifestations remain controversial. The associations between these indicators and disease activity, renal damage, and pathological lesions, and their clinical relevance thus remain unclear. In this retrospective study, we analyzed the clinical and laboratory data for 156 patients with LN and analyzed the associations among disease characteristics, including disease activity, degree of renal damage, and severity of pathological type. Patients and methods Subjects Adult patients initially diagnosed with LN at the Affiliated Hospital of Youjiang Medical University for Nationalities between July 2013 and November 2017 were included in this study. All patients fulfilled the Systemic Lupus International Collaborating Clinics 2012 classification criteria for SLE.5 Patients were excluded if they had rheumatoid arthritis, skin inflammation, systemic sclerosis, nodular polyarteritis, epilepsy, organic brain disease, psychosis, idiopathic thrombocytopenic purpura, or HPGDS inhibitor 2 a primary glomerular disease. The study protocol was approved by the ethics committee of Affiliated Hospital of Youjiang HPGDS inhibitor 2 Medical University for Nationalities. Written informed consent was obtained from each patient. The study was conducted in accordance with the principles of the Declaration of Helsinki. Diagnostic criteria Disease activity was evaluated according to the SLE disease activity index 2000 (SLEDAI-2K).6 Patients fulfilling any of the following criteria were diagnosed with LN: 24-hour urine protein level >0.5?g or +++; tubules (erythrocyte tubules, granulotubules, or mixed tubules) and/or renal dysfunction (according to the pathological classification standard established by International Society of Nephrology/Renal Pathology Society in 2003 and the National Institutes of Health pathological index of lupus nephritis); and abnormal renal biopsy. The pathological classification standard established by the International Society of Nephrology/Renal Pathology Society in 2003 was used for pathological classification of LN. The following features were considered as clinical manifestations of LN: simple hematuria (gross or microscopic hematuria without proteinuria); simple proteinuria (proteinuria without hematuria); hematuria and proteinuria (main manifestations of hematuria and proteinuria); nephrotic syndrome (heavy proteinuria 3.5?g/24 hour, hypoproteinemia 30?g/L, hyperlipemia, and edema); and renal dysfunction (significantly increased blood urea nitrogen and creatinine, accompanied by anemia, hypertension, and edema). Groups All patients HPGDS inhibitor 2 with LN were divided into the following subgroups: active LN (SLEDAI-2K score >10) and inactive LN (score 10); LN with renal damage (estimated glomerular filtration rate [eGFR] ?