Renal dysfunction and metabolic alterations in patients with intracranial aneurysm rupture: an exploratory multivariable and principal component analysis.

Background and purpose: Intracranial aneurysm rupture causes aneurysmal subarachnoid hemorrhage (aSAH) with substantial morbidity and mortality. We examined whether admission renal and metabolic indices differed according to rupture status at presentation in a treated intracranial aneurysm cohort. We examined associations between admission renal/metabolic indices and rupture status in a treated aneurysm cohort. Materials and methods: We retrospectively reviewed 824 consecutive patients with intracranial aneurysms treated at a single center (January 2018-January 2024), including 344 ruptured aneurysms and 480 treated high-risk unruptured aneurysms. Clinical and laboratory variables were derived from the first admission sample set obtained prior to aneurysm-directed intervention. Univariable and multivariable logistic regression were used to evaluate associations with rupture status at presentation. Principal component analysis (PCA) summarized correlated domains among variables differing between groups. Apparent discrimination in the derivation cohort was assessed using the area under the ROC curve (AUC). Results: Compared with the unruptured group, ruptured patients were younger and had higher admission blood pressure and higher serum creatinine and blood urea nitrogen (BUN), along with more frequent ketonuria and higher urine specific gravity. In multivariable analysis, age (aOR 0.97 per year), systolic blood pressure (aOR 1.02 per mmHg), serum creatinine (aOR 4.91), BUN (aOR 1.06), LDH (aOR 1.01), ketonuria (aOR 3.74), and urine specific gravity (aOR 1.50) remained independently associated with rupture status at presentation, while a history of hypertension (aOR 0.66) and higher potassium, chloride, and calcium were inversely associated. PCA identified three components explaining 50.3% of variance, dominated by renal/hemodynamic indices, urinary abnormalities, and electrolyte indices, respectively. The derivation model demonstrated apparent discrimination within the analyzed cohort (AUC 0.85), without internal or external validation. Conclusion: Renal- and metabolic-related indices measured at admission were associated with rupture status at presentation in this retrospective cohort. Given post-ictus sampling, potential reverse causality, incomplete aneurysm imaging covariates in the full cohort, and limited ascertainment of baseline renal comorbidities (CKD/ADPKD), these findings should be interpreted as hypothesis-generating correlates rather than pre-rupture predictors and warrant prospective validation with standardized sampling timepoints and comprehensive imaging adjustment.