Serum lipoprotein(a) and risk of contrast-induced nephropathy in patients with type 2 diabetes mellitus.
To assess the predictive value of serum lipoprotein(a) [Lp(a)] for contrast-induced nephropathy in patients with type 2 diabetes mellitus (T2DM).
Consecutive T2DM patients who underwent coronary angiography (CAG) or percutaneous coronary intervention (PCI) between January 2019 and December 2021 were enrolled. Baseline Lp(a) was measured before the operation. CIN was defined as an increase in serum creatinine of more than 25% or 44 μmol within 72 h of contrast administration. The relationship between Lp(a) and CIN risk was analyzed.
A total of 928 T2DM patients were included. CIN developed in 11.1% (103/928) of patients. The Lp(a) level was significantly higher in patients with CIN than in non-CIN patients (311.12 ± 278.66 vs. 254.19 ± 274.56 mg/L, P = 0.048). Patients were divided into three groups based on Lp(a) levels: <150 mg/L (n = 428), 150 mg/L-300 mg/L (n = 266), and ≥300 mg/L (n = 234). Each group stratified by increasing Lp(a) concentrations had incrementally greater risks of CIN (7.2% vs. 12% vs. 17.1%, P < 0.001). Multivariate logistic regression analysis showed that patients with Lp(a) ≥300 mg/L had a 2.41-fold higher risk of CIN than those with Lp(a)< 150 mg/L (OR = 2.41, 95% CI: 1.38-4.21, P = 0.002). Additionally, for each increase of 1 logarithmic unit in Lp(a), the risk of CIN increased by 1.27 times (OR = 1.27, 95% CI: 1.01-1.64, P = 0.045).
A higher serum Lp(a) level indicates an increased risk of CIN in T2DM patients undergoing CAG or PCI and can serve as an independent predictor of CIN in this population. This study's findings will aid in the clinical prevention and treatment of contrast agent-induced kidney disease.
Consecutive T2DM patients who underwent coronary angiography (CAG) or percutaneous coronary intervention (PCI) between January 2019 and December 2021 were enrolled. Baseline Lp(a) was measured before the operation. CIN was defined as an increase in serum creatinine of more than 25% or 44 μmol within 72 h of contrast administration. The relationship between Lp(a) and CIN risk was analyzed.
A total of 928 T2DM patients were included. CIN developed in 11.1% (103/928) of patients. The Lp(a) level was significantly higher in patients with CIN than in non-CIN patients (311.12 ± 278.66 vs. 254.19 ± 274.56 mg/L, P = 0.048). Patients were divided into three groups based on Lp(a) levels: <150 mg/L (n = 428), 150 mg/L-300 mg/L (n = 266), and ≥300 mg/L (n = 234). Each group stratified by increasing Lp(a) concentrations had incrementally greater risks of CIN (7.2% vs. 12% vs. 17.1%, P < 0.001). Multivariate logistic regression analysis showed that patients with Lp(a) ≥300 mg/L had a 2.41-fold higher risk of CIN than those with Lp(a)< 150 mg/L (OR = 2.41, 95% CI: 1.38-4.21, P = 0.002). Additionally, for each increase of 1 logarithmic unit in Lp(a), the risk of CIN increased by 1.27 times (OR = 1.27, 95% CI: 1.01-1.64, P = 0.045).
A higher serum Lp(a) level indicates an increased risk of CIN in T2DM patients undergoing CAG or PCI and can serve as an independent predictor of CIN in this population. This study's findings will aid in the clinical prevention and treatment of contrast agent-induced kidney disease.