Cumulative proportion of participants with progressive kidney disease.

<p>Cumulative proportion of participants with progressive kidney disease.</p

Baseline characteristics associated with progressive CKD in univariate and multivariate analysis.

<p>Baseline characteristics associated with progressive CKD in univariate and multivariate analysis.</p

Baseline characteristics of study participants, stratified by the development of progressive chronic kidney disease (CKD).

<p>Baseline was defined at randomization into the parent trial (SMART or ESPRIT).</p><p>Categorical variables are presented as N (%) and continuous variables presented as median (interquartile range).</p>1<p>Data on HIV RNA and Hepatitis B surface antigen were available for 3435 participants (99.8%).</p>2<p>Data on Hepatitis C antibody status were available for 3436 participants (99.8%).</p>3<p>Among 473 participants with positive Hepatitis C antibody, RNA viral load was available for 471 (99.6%) and genotype was available for 353 (74.6%).</p><p>eGFR, estimated GFR calculated using the CKD-EPI formula; BMI, body mass index.</p

Association of Hepatitis C viremia with progressive kidney disease.

<p>Hepatitis C (HCV)-RNA was further stratified by quartiles to determine whether there is clinically useful threshold HCV-RNA level associated with increased risk of progressive kidney disease. The number of patients (events) included for HCV antibody negative and for increasing quartiles of HCV-RNA were 2963 (102), 108 (4), 154 (7), 102 (7), and 107 (7), respectively. Final models were adjusted for trial, age, race, infection through same sex exposure, prior AIDS diagnosis, CD4, CD4 nadir, previous exposure to antiretrovirals, previous exposure to indinavir, treatment with antihypertensives, treatment with lipid lowering therapy, estimated glomerular filtration rate, year of randomization, and Hepatitis B surface antigen status, all measured at randomization into the parent trial.</p

Markers of hepatic fibrosis as proposed mediators of progressive chronic kidney disease (CKD).

<p>Data available for¹n = 827,</p>2<p>n = 1421,</p>3<p>n = 1268.</p><p>The number of participants who developed progressive kidney disease was ¹n = 42,</p>2<p>n = 73,</p>3<p>n = 63.</p><p>APRI, aspartate aminotransferase platelet ratio index.</p

Association of Hepatitis B and C viremia and Hepatitis C genotype with progressive kidney disease.

<p>Final models were adjusted for trial, age, race, infection through same sex exposure, prior AIDS diagnosis, CD4, CD4 nadir, previous exposure to antiretrovirals, previous exposure to indinavir, treatment with antihypertensives, treatment with lipid lowering therapy, estimated glomerular filtration rate, and year of randomization, all measured at randomization into the parent trial. As appropriate, analyses were also adjusted for ¹Hepatitis C (HCV) antibody status or ² Hepatitis B surface antigen (HBsAg) status. Participants with positive HBsAg were further stratified by the presence or absence of detectable HBV DNA, with a cutoff of <357 IU/ml. The number of patients (events) for HBsAg negative, positive with HBV DNA <357 IU/mL, and positive with HBV DNA ≥357 IU/ml were 3321 (113), 44 (6), and 70 (8), respectively. Participants with positive HCV antibody were further stratified into those with undetectable HCV RNA, low HCV RNA (≤800,000 IU/ml), and high HCV RNA (>800,000 IU/ml). The number of patients (events) for HCV antibody negative, positive with undetectable HCV RNA, low HCV RNA, and high HCV RNA were 2963 (102), 108 (4), 212 (9), and 151 (12), respectively. The analysis of HCV genotype was limited to participants with positive HCV antibody and known HCV genotype, stratified as genotype 1 (258 patients, 18 events) or other (95 patients, 3 events).</p

Use of potentially nephrotoxic antiretrovirals during follow-up in among 17,954 individuals in the D:A:D study.

<p>All individuals were naïve to these antiretrovirals at baseline.</p><p>/r, ritonavir boosted; ARV, antiretroviral; PI, protease inhibitor.</p><p>Use of potentially nephrotoxic antiretrovirals during follow-up in among 17,954 individuals in the D:A:D study.</p

Baseline characteristics of patient population.

<p>¹Baseline haemoglobin known for 13,568 (75.6%) overall: 13,067 (75.5%) among those who did not develop CKD, and 501 (78.2%) among those who developed CKD.</p><p>²First eGFR > 60 ml/min/1.73 m² after later of 1 January 2004 or enrolment into the D:A:D study.</p><p>Baseline characteristics of patient population.</p

Comparison of the risk score model in the derivation and validation cohorts.

<p>Comparison of the risk score model in the derivation and validation cohorts.</p

Number needed to harm among those at low (risk score < 0), medium (risk score 0–4), or high risk (risk score ≥ 5) of CKD.

<p>ATV, atazanavir; ATV/r, atazanavir/ritonavir; BPI, other ritonavir-boosted protease inhibitor (excluding lopinavir/ritonavir and atazanavir/ritonavir); LPV/r, lopinavir/ritonavir; TDF, tenofovir.</p