CKD is reported commonly in people with HIV infection, although estimates of the prevalence of renal disease vary according to study design, location and the definition of renal impairment used¹¹. A global prevalence of CKD of 6.4% in HIV-infected patients using the MDRD formula, or 4.8% using the CKD-EPI formula, has been reported in a systematic review of studies from 60 countries world-wide; however, the African continent demonstrated the highest prevalence of CKD with 7.9% of HIV-infected patients affected overall, according to the MDRD formula¹².  Some studies have reported a much higher prevalence of CKD within Africa, with 44.4% of HIV-infected patients affected by CKD in Cameroon using the CKD-EPI formula. The variability of prevalence may relate to true differences in disease patterns, but may also reflect variability in the methods used to estimate renal function in the clinic and in the equations used to estimate a patient’s renal function¹³. The reported prevalence of CKD, defined as a glomerular filtration rate (GFR) <60 mL/min on two separate occasions 6 months apart, ranges from 4.7 – 9.7% in the United States of America (USA) and Europe¹⁴. Rates of up to 30% are reported in some studies¹⁵. As well, proteinuria is common in these patients with rates of up to 10% reported in the Australian population¹⁶.

The higher prevalence of CKD in HIV-infected patients in Africa may be explained by the 18- to 50-fold higher risk of patients of African descent world-wide developing HIV-related end-stage renal disease (ESRD) compared to Caucasian patients¹⁴. The susceptibility to the development of kidney disease in these patients is primarily due to genetic factors⁷.  Black African patients in the Western and Southern African continent are more likely to carry certain polymorphisms of the apolipoprotein-1 (APOL-1) gene that have been linked to an aggressive course of HIVAN¹⁷.  More recently, this genetic marker has also been linked to susceptibility to a wide-range of renal conditions, such as hypertension-related renal disease and Focal Segmental Glomerulosclerosis (FSGS) in HIV-negative individuals⁷. The risk alleles G1 and G2 of the APOL-1 gene, located on chromosome 22, have not only been strongly associated with the development of HIVAN but may be a pre-requisite for the development of HIVAN¹⁸.  These APOL-1 gene risk alleles are found in 70-80% of persons of African origin¹⁷.

Importantly, the prevalence of NICMs, particularly hypertension and diabetes, are significantly associated with the prevalence of CKD in HIV-infected patients; the higher the prevalence of NICMs, the higher the prevalence of CKD¹⁹.