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Abstract Number: 380

Active Rheumatoid Arthritis Is An Independent Risk Factor Of Chronic Kidney Disease

Ryosuke Hanaoka1,2, Kazuhiro Kurasawa3, Ayae Tanaka4 and Harutsugu Okada5, 1Department of Rheumatology, Kamitsuga General Hospital, Kanuma, Japan, 2Department of Rheumatology, Kamitsuga General Hospital, Kanuma, Tochigi, Japan, 3Clinical Immunology, Dokkyo Medical University, Mibu-machi, Shimotsuga-gun, Tochigi-ken, Japan, 4Clinical Immunology, Dokkyo Medical University, Mibu, Tochigi, Japan, 5Clinical Immunology, Dokkyo Medical University, Mibu-machi, Tochigi-ken, Japan

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Disease Activity, Kidney and rheumatoid arthritis (RA)

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects I: Comorbidities in Rheumatoid Arthritis

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Rheumatoid arthritis (RA) is a systemic inflammatory disease that affects not only joints but also many organs. RA causes vascular damages to contribute to progression of atherosclerosis. RA itself is a risk factor for cardiovascular diseases as well as hypertension and/or hyperlipidemia that could be induced by medication for RA. However, it has not been determined whether RA itself is a risk factor for chronic kidney disease (CKD). The aim of this study is to determine whether RA is an independent risk factor for CKD.  And if so, to determine whether the disease activity contributes to renal function in RA patients.

Methods:

A prospective cohort study was performed. The study included 134 RA patients who met ACR criteria 1987 and were treated at our hospital, and 1156 non-RA individuals who received annual medical screening at the same hospital. Demographic data, general risk factors for CKD, laboratory data, medications and data for RA activity were collected. Estimated glomerular filtration rate (eGFR) was calculated as follows; eGFR= 1.94x Cr (mg/dl)-1.094x age (year)-0.287x(1.0 if male/0.739 if female). When patients showed eGFR less than 60 ml/min/1.73m2 or positive for urinary protein test, they were judged as having CKD. To identify risk factors, univariate and multivariate analysis were conducted.

Results:

RA patients were 38 male, and 96 female, mean age; 65.3 year, mean disease duration; 100.1 months, and DAS28 CRP; 2.41. Control individual were 768 male and 388 female and mean age; 53.4 year. At baseline, eGFR were 71.5 ml/min/1.73m2 in RA and 77.7 ml/min/1.73m2 in controls, and CKD was found in 33.6 % of RA patients, while 12.6 % of controls had CKD. Annual decline of eGFR was greater in RA group compared with control (-5.81 %, 95%CI. -7.82 to -3.79 vs. 0.71 %, 95%CI. 0.22 to 1.20). Annual incidence of CKD was significantly higher in RA group compared with control (15.7 % vs. 4.6 %, relative risk 1.210, 95%CI. 1.051 to 1.393). Univariate analysis for identification of risk factors for CKD development revealed RA is a risk factor for CKD (p<0.001) as well as hypertension, hypercholesterolemia, and anemia. Multivariate analysis using logistic regression analysis showed RA is an independent risk factor of incident of CKD (P = 0.005, relative risk = 2.968, 95%CI. =1.393 to 6.327) as well as hypertension.

Among RA patients, active RA patients showed greater annual decline of eGFR compared to those in remission (-8.89 %, 95%CI. -10.38 to-7.40 in active disease vs. -3.52 %, 95%CI. -4.86 to 2.18 in remision). Significant correlation was found between DAS28CRP at baseline and annual decline of eGFR (correlation coefficient -0.238, P = 0.006). Active group had significantly greater annual decline of eGFR compared to remission group (-8.89 %, 95%CI. -10.38 to -7.40 vs. -3.52 %, 95%CI. -4.86 to 2.18). Multiple regression analysis showed that high DAS28 CRP is correlated with annual decline of eGFR in the patients with RA (coefficients -2.026, 95%CI. -3.909 to -0.142).

Conclusion:

RA is an independent risk factors of CKD incident. RA activity is correlated with annual decline of eGFR in patients with RA, suggesting that RA activity, presumably systemic inflammation, could contribute to development of CKD.


Disclosure:

R. Hanaoka,
None;

K. Kurasawa,
None;

A. Tanaka,
None;

H. Okada,
None.

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