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Updated: Oct 2, 2026
Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Development and internal validation of a clinical nomogram for identifying lupus nephritis in patients with systemic
1Department of Rheumatology and Clinical Immunology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Henan University People's Hospital, Zhengzhou, Henan, China.
Objective:
Lupus nephritis (LN) is one of the most severe manifestations of systemic lupus erythematosus (SLE). This study aimed to develop and internally validate a clinical nomogram based on routinely available clinical and laboratory variables for identifying LN in patients with SLE.
Methods:
This retrospective study included 132 patients with SLE after exclusion of one patient with missing LN status from an initial cohort of 133 patients. The C3/C4 ratio was calculated as serum C3 divided by serum C4, and the albumin-creatinine index (ACI) was calculated as serum albumin divided by serum creatinine. The primary multivariable logistic regression model included age, sex, C3/C4 ratio, ACI, and log-transformed anti-dsDNA antibody. Total SLEDAI score was excluded from the primary model because its renal and serological descriptors overlap with the outcome and candidate predictors. The complete-case analysis included 131 patients. Model performance was assessed using receiver operating characteristic analysis, calibration analysis, the Hosmer-Lemeshow test, Brier score, bootstrap internal validation, decision curve analysis (DCA), and clinical impact curve analysis.
Results:
Among the 132 eligible patients, 80 (60.6%) had LN and 52 (39.4%) did not. Compared with patients without LN, those with LN had lower C3, C4, albumin, ACI, hemoglobin, and platelet count and higher creatinine, triglyceride, anti-dsDNA antibody, and SLEDAI scores. In the primary multivariable model, a higher ACI was independently associated with lower odds of LN (adjusted OR per 0.1-unit increase = 0.429, 95% CI 0.315-0.586, p < 0.001). The C3/C4 ratio (p = 0.789) and log-transformed anti-dsDNA antibody (p = 0.201) were not independent predictors. The model showed good discrimination (AUC = 0.888, 95% CI 0.830-0.940), acceptable calibration (Hosmer-Lemeshow χ2 = 7.451, p = 0.489), and a Brier score of 0.132. The bootstrap-corrected AUC was 0.868.
Conclusion:
A clinical nomogram based on routinely available variables showed good discrimination after internal validation for identifying LN among patients with SLE. ACI was the only independent predictor in the primary model. The C3/C4 ratio was not independently associated with LN and should be interpreted as an exploratory complement indicator rather than an established predictor. External validation is required before clinical implementation.
