Admission C-reactive protein-to-albumin ratio and serum creatinine in relation to in-hospital mortality in non-HIV tuberculous meningitis: a retrospective cohort study.

Abstract

Background: The independent and joint associations of admission C-reactive protein-to-albumin ratio (CAR) and serum creatinine with mortality in tuberculous meningitis (TBM) remain uncertain.

Methods: We analyzed a single-center retrospective cohort of non-HIV patients hospitalized with TBM from October 2013 to January 2024. Exposure measurements were the first tests within 24 h of admission, before acute interventions. Multivariable logistic regression modeled both exposures continuously, adjusted for age nonlinearly and prespecified covariates, and tested exposure nonlinearity and interaction. Covariate-only multiple imputation generated 20 datasets. Cohort-specific upper-quartile groups were descriptive. An adult sensitivity analysis used estimated glomerular filtration rate (eGFR) calculated with the 2021 CKD-EPI equation.

Results: Among 1,574 eligible patients, 187 died in hospital. The primary analysis included 1,563 patients and all 187 deaths; 11 survivors lacked CAR (n = 3) or creatinine (n = 8), without overlap. Creatinine showed evidence of nonlinearity (P = 0.022), whereas CAR did not (P = 0.105). The linear CAR estimate was near the null (adjusted odds ratio [OR] per doubling, 1.02; 95% confidence interval [CI] 0.88-1.18); the interaction P value was 0.065. Relative to serum creatinine of 48 µmol/L, adjusted ORs for death were 1.31 (95% CI: 1.11-1.55) at 65 µmol/L, 1.49 (1.15-1.92) at 80 µmol/L, and 1.62 (1.17-2.24) at 100 µmol/L. Descriptive group mortality ranged from 9.02% when both markers were below their 75th percentiles to 19.38% when both were at or above them. Among 1,372 adults, the OR per 10 mL/min/1.73 m² lower eGFR was 1.045 (0.984-1.109; P = 0.150).

Conclusions: Admission creatinine had a nonlinear adjusted association with in-hospital mortality in non-HIV TBM. CAR yielded a near-null linear estimate, and the interaction analysis did not establish effect modification. Unmeasured neurological severity limits interpretation; these results do not define kidney dysfunction, a clinical cutoff, or a clinically useful prediction model.