Why the study?
Diabetic kidney disease and metabolic dysfunction-associated steatotic liver disease frequently coexist in T2DM, but real-world evidence regarding the associations of atorvastatin with both renal and hepatic surrogate markers remains limited.
Population
612 patients with T2DM
Comparison
Atorvastatin 10–20 mg/day vs atorvastatin 40 mg/day vs no statin
Design
Retrospective observational study
Follow-up
six months
Answers are grounded in this paper and cite their sources.
May support dose-dependent renal benefit with atorvastatin in T2D; hypothesis-generating and requires RCT confirmation before practice change.
Background/Objectives: Diabetic kidney disease (DKD) and metabolic dysfunction-associated steatotic liver disease (MASLD) frequently coexist in patients with type 2 diabetes mellitus (T2DM) and share common pathophysiological mechanisms. Although atorvastatin has been investigated for potential renal and hepatic effects, real-world evidence regarding its associations with both renal and hepatic surrogate markers remains limited. This study investigated the association between atorvastatin therapy and longitudinal changes in urinary albumin-to-creatinine ratio (UACR) and liver stiffness measured by vibration-controlled transient elastography (VCTE) in patients with T2DM. Methods: This retrospective observational study included 612 patients with T2DM who were categorized into three groups according to atorvastatin treatment: no statin (n = 198), atorvastatin 10–20 mg/day (n = 205), and atorvastatin 40 mg/day (n = 209). UACR and liver stiffness were assessed at baseline and after six months. Between-group comparisons and multivariable linear regression analyses were performed to evaluate the independent association of atorvastatin therapy with changes in renal and hepatic surrogate markers. Results: Baseline UACR and liver stiffness were comparable among the three groups. During six months of follow-up, UACR increased in the no-statin group (+8.64 mg/g) but decreased significantly in the atorvastatin 10–20 mg (−27.68 mg/g) and 40 mg (−44.64 mg/g) groups (overall p < 0.001). Similarly, liver stiffness remained unchanged in the no-statin group (−0.02 kPa) but decreased by 0.42 kPa and 0.93 kPa in the atorvastatin 10–20 mg and 40 mg groups, respectively (overall p < 0.001). In multivariable models adjusted for baseline outcome values and relevant clinical covariates, both atorvastatin treatment groups remained significantly associated with lower six-month UACR and liver stiffness compared with the no-statin group (all p < 0.001). Conclusions: Atorvastatin treatment intensity was associated with differences in six-month UACR and liver stiffness in patients with T2DM, with numerically greater reductions observed in the 40 mg/day group. These observational findings are hypothesis-generating and require confirmation in prospective studies before causal or long-term clinical benefits can be established.
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Öztürk et al. (2026) studied this question.
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