Shrunken Pore Syndrome: A New and More Powerful Phenotype of Renal Dysfunction Than Chronic Kidney Disease for Predicting Contrast‐Associated Acute Kidney Injury

BACKGROUND: Shrunken pore syndrome (SPS) as a novel phenotype of renal dysfunction is characterized by a difference in renal filtration between cystatin C and creatinine. The manifestation of SPS was defined as a cystatin C–based estimated glomerular filtration rate (eGFR) <60% of the creatinine‐based eGFR. SPS has been shown to be associated with the progression and adverse prognosis of various cardiovascular and renal diseases. However, the predictive value of SPS for contrast‐associated acute kidney injury (CA‐AKI) and long‐term outcomes in patients undergoing percutaneous coronary intervention remains unclear. METHODS AND RESULTS: We retrospectively observed 5050 consenting patients from January 2012 to December 2018. Serum cystatin C and creatinine were measured and applied to corresponding 2012 and 2021 Chronic Kidney Disease Epidemiology Collaboration equations, respectively, to calculate the eGFR. Chronic kidney disease (CKD) was defined as a creatinine‐based eGFR <60 mL/min per 1.73 m(2) without dialysis. CA‐AKI was defined as an increase in serum creatinine ≥50% or 0.3 mg/dL within 48 hours after contrast medium exposure. Overall, 649 (12.85%) patients had SPS, and 324 (6.42%) patients developed CA‐AKI. Multivariate logistic regression analysis indicated that SPS was significantly associated with CA‐AKI after adjusting for potential confounding factors (odds ratio [OR], 4.17 [95% CI, 3.17–5.46]; P<0.001). Receiver operating characteristic analysis indicated that the cystatin C–based eGFR:creatinine‐based eGFR ratio had a better performance and stronger predictive power for CA‐AKI than creatinine‐based eGFR (area under the curve: 0.707 versus 0.562; P<0.001). Multivariate logistic analysis revealed that compared with those without CKD and SPS simultaneously, patients with CKD and non‐SPS (OR, 1.70 [95% CI, 1.11–2.55]; P=0.012), non‐CKD and SPS (OR, 4.02 [95% CI, 2.98–5.39]; P<0.001), and CKD and SPS (OR, 8.62 [95% CI, 4.67–15.7]; P<0.001) had an increased risk of CA‐AKI. Patients with both SPS and CKD presented the highest risk of long‐term mortality compared with those without both (hazard ratio, 2.30 [95% CI, 1.38–3.86]; P=0.002). CONCLUSIONS: SPS is a new and more powerful phenotype of renal dysfunction for predicting CA‐AKI than CKD and will bring new insights for an accurate clinical assessment of the risk of CA‐AKI.