High-sensitivity C-reactive protein and the risk of chronic kidney disease progression or acute kidney injury in post–myocardial infarction patients

• Published in: The American heart journal Vol. 216; pp. 20 - 29
• Main Authors: Fu, Edouard L., Franko, Mikael Andersson, Obergfell, Achim, Dekker, Friedo W., Gabrielsen, Anders, Jernberg, Tomas, Carrero, Juan Jesús
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.10.2019; Elsevier Limited
• Subjects: Acute Kidney Injury - blood; Acute Kidney Injury - epidemiology; Acute Kidney Injury - etiology; Aged; Aged, 80 and over; Antibiotics; Arteriosclerosis; Atherosclerosis; Biomarkers - blood; Biomarkers - metabolism; C-reactive protein; C-Reactive Protein - analysis; C-Reactive Protein - metabolism; Cardiovascular diseases; Creatinine; Creatinine - blood; Disease Progression; Emergency medical care; Emergency medical services; Epidermal growth factor receptors; Female; Follow-Up Studies; Glomerular filtration rate; Glomerular Filtration Rate - physiology; Health care; Health risks; Health services utilization; Heart attacks; Hemodialysis; Hemoglobin; Humans; Immunosuppression; Infections; Inflammation; Inflammation - blood; Inflammation - diagnosis; Kidney diseases; Kidneys; Laboratories; Male; Medicin och hälsovetenskap; Myocardial infarction; Myocardial Infarction - blood; Myocardial Infarction - complications; Patients; Plasma; Progressions; Proteins; Regression Analysis; Renal Insufficiency, Chronic - blood; Renal Insufficiency, Chronic - physiopathology; Renal Insufficiency, Chronic - therapy; Renal Replacement Therapy; Risk; Sensitivity; Subgroups; Sweden; Time Factors; Transplants & implants; Sweden
• ISSN: 0002-8703; 1097-6744; 1097-6744
• DOI: 10.1016/j.ahj.2019.06.019

Persistent, low-grade inflammation likely participates in the pathophysiology of both atherosclerosis and kidney disease. Although high-sensitivity C-reactive protein (hsCRP) predicts future cardiovascular risk in patients with chronic kidney disease (CKD), it is unknown whether hsCRP levels predict adverse renal outcomes in patients with cardiovascular disease. We studied all myocardial infarction (MI) survivors undergoing hsCRP testing >30 days after their MI during routine health care in Stockholm, Sweden (2006-2011), with available information on estimated glomerular filtration rate (eGFR). HsCRP tests measured during hospitalization/emergency room visits, followed by antibiotics or indicative of acute illness, were excluded, together with patients with ongoing/recent cancer, chronic infections, or immunosuppression. Inflammation was defined over a 3-month baseline window. Study outcomes were CKD progression (composite of doubling plasma creatinine, renal replacement therapy, or renal death) and acute kidney injury (AKI, acute creatinine peaks according to Kidney Disease: Improving Global Outcomes criteria). Multivariable Cox regression was used to adjust for age, sex, eGFR, hemoglobin, time since MI, comorbidities, undertaken procedures, and medications. A total of 12,905 patients (62% men, mean age 73 years and 3 years since MI) were included, of whom 35% had an eGFR<60 mL/min/1.73 m2. The mean (SD) hsCRP was 3.0 (4.4) mg/L. Baseline hsCRP levels were increasingly higher across lower eGFR categories. During a median follow-up of 3.2 years, 1,019 CKD progressions and 1,481 AKI events were recorded. Patients with hsCRP ≥2 mg/L were at higher risk of both CKD progression (adjusted hazard ratio 1.42; 95% CI 1.21-1.66) and AKI (1.29; 1.13-1.47) compared to those with hsCRP <2 mg/L. This association persisted across single CKD severity stages and after further hsCRP categorization into 4 groups (≤1, 1-3, 3-10, >10 mg/L). Results were robust across subgroups of patients and after exclusion of events occurring during the first 6-12 months. In post-MI patients undergoing routine health care, elevated hsCRP was associated with subsequent risk of AKI and progression of CKD, irrespective of baseline kidney function.