OBJECTIVE: To investigate the association of mild renal impairment and coronary plaque in people living with HIV (PLHIV). METHODS: PLHIV and non-HIV controls with serum creatinine less than 1.5 mg/dl were investigated. Estimated glomerular filtration rate (eGFR) (calculated by CKD-EPI formula) was related to coronary plaque indices obtained by CT angiography. RESULTS: One hundred and eighty-four PLHIV [HIV viral load, 49 (47,49) copies/ml, CD4+ cell count, median 536 (370, 770) cells/μl, duration HIV, 15 ± 7 years] and 72 HIV-negative controls without known cardiovascular disease (CVD) were studied. The two groups were well matched for traditional CVD risk factors. Serum creatinine (0.9 ± 0.2 vs. 0.9 ± 0.2 mg/dl, P = 0.96) and eGFR (96 ± 22 vs. 96 ± 24 ml/min per 1.73 m(2), P = 0.99) were similar between PLHIV and non-HIV, respectively. In PLHIV, eGFR inversely related to total severity of coronary plaque score (r = -0.27, P = 0.002), total coronary segments with plaque (r = -0.21, P = 0.005), calcified plaque segments (r = -0.15, P = 0.045), and Agatston score (r = -0.21, P = 0.006). Adjusting for total Framingham point score, BMI, and HIV parameters, eGFR remained significantly associated with calcified plaque and Agatston score in PLHIV. In HIV negative controls, eGFR did not correlate with calcified plaque (r = -0.20, P = 0.10) or Agatston score (r = -0.13, P = 0.29). Among PLHIV, those with eGFR less than 90 ml/min per 1.73 m(2) demonstrated increased total severity of coronary plaque score compared with those with eGFR greater than or equal to 90, P = 0.02). This relationship was stronger in PLHIV than the non-HIV group. CONCLUSION: Our data highlight a robust relationship between subclinical renal impairment and coronary artery disease among PLHIV. Further research is needed to understand the relationship between mild renal impairment and CVD in HIV.
OBJECTIVE: To investigate the association of mild renal impairment and coronary plaque in people living with HIV (PLHIV). METHODS: PLHIV and non-HIV controls with serum creatinine less than 1.5 mg/dl were investigated. Estimated glomerular filtration rate (eGFR) (calculated by CKD-EPI formula) was related to coronary plaque indices obtained by CT angiography. RESULTS: One hundred and eighty-four PLHIV [HIV viral load, 49 (47,49) copies/ml, CD4+ cell count, median 536 (370, 770) cells/μl, duration HIV, 15 ± 7 years] and 72 HIV-negative controls without known cardiovascular disease (CVD) were studied. The two groups were well matched for traditional CVD risk factors. Serum creatinine (0.9 ± 0.2 vs. 0.9 ± 0.2 mg/dl, P = 0.96) and eGFR (96 ± 22 vs. 96 ± 24 ml/min per 1.73 m(2), P = 0.99) were similar between PLHIV and non-HIV, respectively. In PLHIV, eGFR inversely related to total severity of coronary plaque score (r = -0.27, P = 0.002), total coronary segments with plaque (r = -0.21, P = 0.005), calcified plaque segments (r = -0.15, P = 0.045), and Agatston score (r = -0.21, P = 0.006). Adjusting for total Framingham point score, BMI, and HIV parameters, eGFR remained significantly associated with calcified plaque and Agatston score in PLHIV. In HIV negative controls, eGFR did not correlate with calcified plaque (r = -0.20, P = 0.10) or Agatston score (r = -0.13, P = 0.29). Among PLHIV, those with eGFR less than 90 ml/min per 1.73 m(2) demonstrated increased total severity of coronary plaque score compared with those with eGFR greater than or equal to 90, P = 0.02). This relationship was stronger in PLHIV than the non-HIV group. CONCLUSION: Our data highlight a robust relationship between subclinical renal impairment and coronary artery disease among PLHIV. Further research is needed to understand the relationship between mild renal impairment and CVD in HIV.
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