For CKD other than HIVAN, there is limited information on the natural history per se and on whether ART confers renal benefit. Immunodeficiency is a potent risk factor for CKD [8, 9]. The majority of patients with CKD have (nadir) CD4 cell counts <350 cells/μL and thus qualify for ART as per current treatment guidelines. There are no data to provide guidance on whether HIV-positive patients with (or at risk of developing) CKD benefit from earlier ART initiation. None the less, HIV replication, immune activation and inflammation may play a role in the pathogenesis of kidney diseases or contribute to kidney disease progression in some patients [10]. For this reason, ART should be considered

in those presenting with CKD other than HIVAN. Renal transplantation is the treatment of choice for those requiring renal replacement therapy. Patients to be considered for renal transplantation are required to have suppressed HIV RNA selleck products levels and to have CD4 cell counts >200 cells/μL [11], and

should start ART, irrespective of CD4 cell count. We recommend against the use of ARV drugs that are potentially nephrotoxic in patients with stages 3–5 CKD if acceptable alternative ARV agents are available (GPP). We recommend dose adjustment of renally cleared ARV drugs in patients with reduced renal function (GPP). Number of patients with CKD stages 3–5 on ARVs that MG 132 are potentially nephrotoxic and a record of the rationale. Record in patient’s notes of calculated dose of renally cleared ARVs Mannose-binding protein-associated serine protease in patients with CKD stage 3 or greater. There are no data from clinical RCTs to inform ART decisions in patients with

CKD. The risk of CKD is increased with older age, reduced estimated glomerular filtration rate (eGFR), hypertension, diabetes and with cumulative exposure to indinavir, TDF, ATV and, to a lesser extent, LPV [12, 13]. Indinavir use is no longer recommended in view of the high incidence of renal complications: crystalluria and pyuria are reported in 20–67% [14-16] and nephrolithiasis, tubulointerstitial nephritis and gradual loss of renal function in 4–33% of patients [14, 17-20]. TDF has been associated with falls in eGFR [12, 21, 22], accelerated decline in eGFR [9], acute renal failure [23], tubulointerstitial nephritis [24], CKD [9, 12], renal tubular dysfunction [13, 25] and Fanconi syndrome [26, 27]. The incidence of TDF-associated renal toxicity is low in clinical trials and cohort studies of the general HIV population [28, 29]. Older age, pre-existing renal impairment, co-administration of didanosine or (ritonavir-boosted) PIs, advanced HIV infection and low body mass appear to increase the risk of renal complications [9, 13, 25, 27, 30, 31]. ATV has been associated with reductions in eGFR [32], nephrolithiasis and tubulointerstitial nephritis [13, 24, 33], and CKD [12].