Patients with chronic kidney disease frequently have worse outcomes following percutaneous coronary intervention (PCI) compared to patients with normal renal function. Furthermore, they more commonly have elevated serum markers of inflammation, which may be either directly or indirectly associated with a state of accelerated atherosclerosis. We sought to assess the relationship among glomerular filtration rate (GFR), systemic inflammation, and long-term death after PCI.

In patients undergoing PCI, the intensity of vascular inflammation was measured using baseline ultrasensitive C-reactive protein (us-CRP), and GFR was calculated using the Modification of Diet in Renal Disease formula. Their association with long-term death was compared using multivariate Cox regression analysis including an interaction element for us-CRP and GFR, baseline clinical, biochemical, and angiographic variables.

In 4522 patients (mean age 65 ± 11 years) having undergone PCI, 332 (7.3%) deaths occurred over the median duration of follow-up of 20.1 months (interquartile range 8.5-31.3 months). The mean GFR was 77 ± 33 mL/min per 1.73 m² with a median us-CRP of 3.75 mg/L (interquartile range 1.5-10.1 mg/L). Both increasing levels of CRP (log rank P < .001) and decreasing levels of GFR were univariate predictors of long-term death (P < .001). In a multivariate model, both GFR and us-CRP retained independent predictive value for long-term death.

Although baseline us-CRP and GFR are both independent predictors of long-term death after PCI, in concert, they impart a markedly exaggerated hazard of mortality.