Background. The pathogenesis and natural history of HIV-associated immune complex kidney disease (HIVICK) is not well understood. Key questions remain unanswered, including the role of HIV infection and replication in disease development and the efficacy of antiretroviral therapy (ART) in the prevention and treatment of disease. Methods. In this multicentre study, we describe the renal pathology of HIVICK and compare the clinical characteristics of patients with HIVICK with those with IgA nephropathy and HIV-associated nephropathy (HIVAN). Poisson regression models were used to identify risk factors for each of these pathologies. Results. Between 1998 and 2012, 65 patients were diagnosed with HIVICK, 27 with IgA nephropathy and 70 with HIVAN. Black ethnicity and HIV RNA were associated with HIVICK, receipt of ART with IgA nephropathy and black ethnicity and CD4 cell count with HIVAN. HIVICK was associated with lower rates of progression to end-stage kidney disease compared with HIVAN and IgA nephropathy (P < 0.0001). Patients with HIVICK who initiated ART and achieved suppression of HIV RNA experienced improvements in estimated glomerular filtration rate and proteinuria. Conclusions. These findings suggest a pathogenic role for HIV replication in the development of HIVICK and that ART may improve kidney function in patients who have detectable HIV RNA at the time of HIVICK diagnosis. Our data also suggest that IgA nephropathy should be viewed as a separate entity and not included in the HIVICK spectrum.
Bibliographical noteFunding Information:
The UK CHIC Study is funded by the Medical Research Council, UK (grant numbers G0000199, G0600337, G0900274 and M004236). The views expressed in this article are those of the researchers and not necessarily those of the MRC.
J.W.B. has received conference funding from Shire Pharmaceuticals. L.H. is the recipient of a National Institute for Health Research (NIHR) Doctoral Research Fellowship Award. B.M.H. has received honoraria and/or conference funding from Gilead Sciences, AbbVie, Janssen and ViiV Healthcare. C.S. has received honoraria participation in data safety and monitoring boards and advisory boards, for preparation on educational materials and from membership on speaker panels from Gilead Sciences, Bristol-Myers Squibb, GlaxoSmithKline/ ViiV Healthcare, Janssen-Cilag and AbbVie. R.J. has received funding to attend conferences or educational meetings, honoraria and/or research grants from Gilead Sciences, Bristol-Myers Squibb, Janssen-Cilag, GlaxoSmithKline/ViiV Healthcare and Merck. J.L. has received funding to attend educational meetings and honoraria from Gilead Sciences and ViiV Healthcare. F.A.P. has received funding to attend conferences or educational meetings, honoraria and/or research grants from Gilead Sciences, Bristol-Myers Squibb, Janssen-Cilag, GlaxoSmithK-line/ViiV Healthcare and Merck. S.J., S.M., P.D., C.H., P.O, E. A.K., T.T.-S., N.K., C.N., D.W., E.K., N.M., R.H. and J.C.: no conflict. This study was presented in abstract form at the American Society of Nephrology, Atlanta, GA, USA, 5–10 November 2014 (Abstract SA-PO854) and the Conference on Retroviruses and Opportunistic Infections, Boston, MA, USA, 3–6 March 2014 (Abstract 793). The results presented in this article have not previously been published in whole or part other than in abstract form.
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- Immune complex kidney disease