The incidences of acquired immunodeficiency syndrome (AIDS) associated events and death among people living with HIV (PLWH) have reduced over the last two decades due to increasing HIV testing and antiretroviral therapy (ART) [
1]. However, non-AIDS-defining diseases (NADs), such as cardiovascular disease and kidney disease, were more prevalent in PLWH than HIV-uninfected individuals, which have become the main causes of death among PLWH in the era of modern ART [
2,
3]. In a cohort of PLWH in China during 2010–2019, the incidence of advanced kidney disease was 270 per 100,000 person-years of follow-up after initiation of ART, which has become the second common NADs [
4]. ART, infections (including HIV, BK virus, et.al), HIV-associated nephropathy, HIV-immune complex disease, and HIV-thrombotic thrombocytopenic purpura / hemolytic uremic syndrome may result in renal lesions and may eventually progress to end-stage renal disease (ESRD) which need dialysis treatment [
5‐
7]. The number of PLWH on dialysis is increasing and survival rates of these patients are similar to those in the HIV-negative dialysis population [
5,
8]. However, in another clinical trial, the one-year survival of HIV-positive hemodialysis (HD) patients seems to be lower compared to their HIV-negative counterparts [
9] and the hemoglobin (Hgb) of HIV-positive dialysis patients was lower than that of HIV-negative people [
10].
Anemia is a common complication of chronic kidney disease (CKD) and HIV infection [
11,
12] and is associated with an increased risk of cardiovascular events, and all-cause mortality [
13]. Thus, correction of anemia is an important task in the management of CKD complications. There are many reasons for anemia in HIV-HD patients. HIV infection may cause defective myelopoiesis/erythropoiesis, as well as the accumulation of myeloid/erythroid precursors, and may increase levels of inflammatory cytokines, affecting dynamics and functions or inducing Fas-mediated apoptosis of hematopoietic stem/progenitor cells, which consist of progenitors for all blood cell lineages including erythroid progenitors [
14]. Opportunistic infections, antiretroviral drugs, other drugs administered to treat infection, and malignancies in HIV-positive patients could exacerbate the severity of anemia [
15]. Relative erythropoietin deficiency, shortened erythrocyte lifespan, increased blood loss, chronic inflammation, iron deficiency, copper deficiency, vitamin B12 deficiency, folate deficiency, and aluminum overload result in anemia in HD patients [
12]. Therefore, anemia in HIV-HD patients is theoretically more difficult to control. In fact, the Hgb of HIV-positive dialysis patients was lower than that of HIV-negative patients in a previous clinical trial [
10]. Therapy with erythropoiesis-stimulating agents (ESAs) is an appropriate treatment for anemia in HIV-HD patients. Iron may be important in the activation of HIV-1 and high iron stores may also adversely influence the outcome of HIV-infected patients. Closely monitoring HIV disease progression in patients receiving intravenous iron by measuring plasma viral loads and CD4 + T cell counts is essential. Blood transfusions in HIV-infected patients with CKD should be avoided as some studies have shown increased activation of HIV-1 after transfusion, which could potentially accelerate HIV disease.[
15]. The response to erythropoietin in HIV-infected patients appears to be similar to HIV-negative patients in a small study of HIV-HD patients [
16]. However, in another study, there was a statistically significant higher erythropoietin dosage used in the HIV-HD patients as compared to the control group [
17]. Up to now, there is no research on anemia and its treatment in HD patients with HIV infection in China. This study focused on anemia and its therapeutic strategy in southwestern areas of China and further explored the current status of anemia in HIV-HD patients and the optimization of treatment options.