Abstract 4370562: Association of High-Sensitivity C-Reactive Protein with Chronic Kidney Disease in Patients with Hypertension
Abstract
Background: Patients with chronic kidney disease (CKD) encounter with chronic inflammatory state; however, the magnitude of the association between high-sensitivity C-reactive protein (CRP) and the severity of CKD among those other inflammatory diseases such as hypertension (HTN) and obesity is unknown. We aim to examine the association between CRP and CKD stage in patients with varying HTN and obesity statuses. Method: A retrospective cross-sectional study utilizing data from the 2017 - 2020 NHANES included participants with available CRP. The association between the quartile (Q) of CRP and CKD stages (stages 1, 2, 3a, 3b, 4, and 5) stratified by self-reported HTN and obesity status defined by BMI of < or >/= 30 kg/m 2 were examined by multiple ordered logistic regression analyses. Results: Of 9,693 adult participants, the mean age+/-SD was 50±19 years and 51.33% were female. Median CRP (IQR) was 1.94 mg/L (0.83, 4.45) and median CRP of Q1-Q4 was 0.31 (0.21, 0.41), 0.85 (0.67, 1.08), 2.2 (1.72, 2.84), and 6.5 (4.73, 10.29), respectively (P trend <0.0001). Up to 37% of the study population had HTN. Hypertensive patients had significantly higher SBP and DBP compared to their non-hypertensive counterparts (SBP 133±21 vs. 119±16; mean±SEM diff 15±0.42 mmHg and DBP 77±13 vs. 73±10, mean diff 5±0.26). Median eGFR was 98 mL/min/1.73 m 2 (76, 123). After adjusting for age (< vs. ≥65), gender, race (non-Black vs. Black), BMI, HbA1c, mean SBP and DBP, total cholesterol, serum albumin, serum ferritin, level of education, the ratio of family income to poverty, and an interaction term between age and race, participants with CRP in Q2, 3, and 4 had higher odds of worsening one more consecutive CKD stage from all cumulative below CKD stages compared to participants with CRP in Q1 (adjusted OR Q2 1.450119 (1.20, 1.76), P <0.0001; OR Q3 1.46 (1.21, 1.78, P <0.0001; OR Q4 1.32 (1.07, 1.62), P 0.009). With subgroup analyses, only non-obese participants with HTN had worsening CKD stages with higher quartile of CRP (aOR Q2 1.53 (1.02, 2.28), P 0.038; aOR Q3 1.68 (1.129, 2.50), P 0.011; aOR Q4 1.77, (1.14, 2.75), P 0.011). Race was identified as an effect modifier with decreased odds of worsening CKD stages observed in Black participants ≥65 years old in non-obese participants with HTN (P interaction 0.038). Conclusions: CRP is positively associated with CKD stages in non-obese participants with HTN, especially Black elderly participants.
Article Details
Authors (26)
Ekamol Tantisattamo
University of California Irvine School of Medicine, Orange, California, United States
Panchanit Yongkiatkan
University of California Irvine School of Medicine, Orange, California, United States
Napat Wongmat
University of California Irvine School of Medicine, Orange, California, United States
Natanon Chamnarnphol
University of California Irvine School of Medicine, Orange, California, United States
Nicha Wareesawetsuwan
University of California Irvine School of Medicine, Orange, California, United States
Sorawis Ngaohirunpat
Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand
Weerinth Puyati
University of California Irvine School of Medicine, Orange, California, United States
Wanprapit Noree
University of California Irvine School of Medicine, Orange, California, United States
Nopavit Mohpichai
Mahidol University, Bangkok, Thailand
Vishwaas Gangeddula
University of California Irvine School of Medicine, Orange, California, United States
Seonghyeon Kim
Monique Massihians
Joe C. Wen School of Population&Public Health, University of California Irvine, Irvine, California, United States
Mary Lapadjyan
Joe C. Wen School of Population&Public Health, University of California Irvine, Irvine, California, United States
Christine Shahnazarian
Joe C. Wen School of Population&Public Health, University of California Irvine, Irvine, California, United States
Yangjiayi Liu
Joe C. Wen School of Population&Public Health, University of California Irvine, Irvine, California, United States
David Park
University of California Irvine School of Medicine, Orange, California, United States
Meghan Ho
Joe C. Wen School of Population&Public Health, University of California Irvine, Irvine, California, United States
Bahaar Ghaffarian
University of California Irvine School of Medicine, Orange, California, United States
Sarah Lee
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA
Vanessa Le
University of California Irvine School of Medicine, Orange, California, United States
Possawat Vutthikraivit
University of California Irvine School of Medicine, Orange, California, United States
Issaree Bunyawannukul
University of California Irvine School of Medicine, Orange, California, United States
Chutawat Kookanok
Narathorn Kulthamrongsri
University of California Irvine School of Medicine, Orange, California, United States
Phuuwadith Wattanachayakul
University of California Irvine School of Medicine, Orange, California, United States
Kyunghee Lee
University of California Irvine School of Medicine, Orange, California, United States