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. Author manuscript; available in PMC: 2024 Nov 17.
Published in final edited form as: Kidney Int. 2023 Aug 19;104(5):1008–1017. doi: 10.1016/j.kint.2023.07.022

Association of HIV and viral suppression status with hospital acute kidney injury in the era of antiretroviral therapy

Molly C Fisher 1, Melissa J Fazzari 2, Uriel R Felsen 3, David B Hanna 2, Nataliya Tappan 2, Christina M Wyatt 4, Matthew K Abramowitz 1,6, Michael J Ross 1,5,6
PMCID: PMC11569715  NIHMSID: NIHMS2014835  PMID: 37598853

Abstract

In the modern era, it is unknown if people that are virally suppressed with HIV (PWH) are at increased risk for acute kidney injury (AKI) compared to people without HIV and no studies have compared the risk of AKI by viral suppression status. Here, we determined the associations of HIV status and AKI among PWH with and without viral suppression compared to people without HIV. An observational cohort study of PWH and people without HIV hospitalized in a large New York City health system between 2010–2019 was conducted. Multivariable Cox proportional hazards models were used to determine associations between HIV status and risk of AKI, severe AKI and development of chronic kidney disease (CKD). Among 173,884 hospitalized patients, 4,718 had HIV; 2,532 (53.7%) were virally suppressed and 2,186 (46.3%) were not suppressed. Compared to people without HIV, PWH with and without viral suppression were at increased risk of AKI (adjusted hazard ratio 1.27, 95% confidence interval 1.15, 1.40 and 1.73, 1.58, 1.90, respectively) and AKI requiring kidney replacement therapy (1.89, 1.27, 2.84 and 1.87, 1.23, 2.84, respectively). Incremental, graded associations were observed between HIV status and Stage 2 or 3 AKI, and among AKI survivors, and incident CKD. The elevated risk of AKI across ages of PWH was similar in magnitude to older people without HIV. Thus, regardless of virologic control, HIV is an independent risk factor for AKI among hospitalized patients. Future studies should determine the mechanisms by which HIV increases susceptibility to AKI and identify strategies to prevent AKI in PWH.

Lay Summary

In the modern era, it is unknown if people with HIV that is well controlled are at increased risk of acute kidney injury (AKI). Among 173,884 patients hospitalized in a New York City health system between 2010 and 2019, we determined the risk of AKI, including its severity and outcomes, among people with HIV based on viral suppression status compared with people without HIV. We showed that people with HIV were at increased risk of having AKI, including more severe AKI requiring kidney replacement therapy, and were at increased risk of developing chronic kidney disease after AKI compared with people without HIV. The risk of AKI persisted despite HIV viral suppression. Future studies should determine the mechanisms by which HIV increases susceptibility to AKI and identify strategies to prevent AKI in people with HIV.

Keywords: acute kidney injury, HIV, hospital, outcomes

Worldwide, an estimated 38.4 million people are living with HIV, and >84 million have been infected since the beginning of the epidemic.1 Widespread use of antiretroviral therapy (ART) has dramatically increased the lifespan of people with HIV (PWH).2,3 As a result of increased longevity, the prevalence of HIV has continued to increase, and non–AIDS-related comorbidities have become the most important causes of morbidity and mortality.4 The burden of non–AIDS-related comorbidities, including chronic kidney disease (CKD), is higher among PWH receiving ART compared with age-matched people without HIV.5–7 Although viral suppression with ART reduces systemic inflammation, PWH with undetectable plasma HIV RNA still have higher levels of biomarkers of inflammation and aging, highlighting the important role of immune system dysregulation in the development of chronic disease.8–10

Acute kidney injury (AKI) is a common complication among hospitalized patients that is associated with high mortality and incident and progressive CKD. In recent years, the incidence of hospital AKI has increased and now occurs in ≈20% of the general hospitalized population.11 Although prior observational studies have indicated a high incidence of AKI and poor outcomes following AKI among PWH, most of these studies were performed before widespread use of ART and may have been driven by uncontrolled HIV infection.12–14 Furthermore, most of these studies lacked a comparison group of people without HIV, making it difficult to determine if HIV is independently associated with AKI.13–16

The purpose of our study was to determine if the risk of AKI and its sequelae differ among a contemporary cohort of PWH compared with people without HIV. We hypothesized that even among those with viral suppression, PWH would be at increased risk for AKI and worse outcomes following AKI compared with people without HIV.

METHODS

Study design, population, and data source

The Bronx borough in New York City has a 5-fold higher prevalence of HIV compared with the national prevalence in the United States.17 Montefiore Medical Center (MMC) is an integrated health care system in the Bronx with 4 hospitals and >21 ambulatory care sites. The population that MMC serves is predominantly African American and Hispanic, reflecting the 2 largest racial and ethnic demographics in the Bronx. We performed an observational cohort study of PWH and people without HIV hospitalized within MMC between January 1, 2010, and December 31, 2019. We included patients aged at least 18 years who had at least 1 outpatient creatinine measurement during the year preceding hospitalization; if a patient was admitted more than once, we considered only the first hospitalization. Patients with end-stage kidney disease, missing creatinine measurement during hospitalization, and receipt of ART but unconfirmed HIV status, and those diagnosed with HIV after the index hospitalization were excluded (Figure 1). Patients were categorized as HIV positive or HIV negative and followed up until the earliest of in-hospital death, discharge, or administrative censoring on the study end date.

Figure 1 |. Flowchart of the study population.

Figure 1 |

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AKI, acute kidney injury; ART, antiretroviral therapy; MMC, Montefiore Medical Center.

Data were extracted from the Einstein-Rockefeller-CUNY (City University of New York) Center for AIDS Research Clinical Cohort Database. The database contains data on PWH and people without HIV who are receiving care within MMC and combines data from the electronic health record, including inpatient and outpatient visits; laboratory test results; prescription data; and intake data from New York State’s AIDS Institute Reporting System.18,19 The study was approved by the Albert Einstein College of Medicine Institutional Review Board.

Exposure of interest

HIV positivity was defined by at least 1 of the following: positive HIV Western blot or multispot, detectable HIV-1 RNA viral load, or ≥3 undetectable HIV-1 RNA viral loads ordered simultaneously with a CD4 T-cell count to identify those with viral suppression undergoing routine monitoring.20 PWH were classified into those with viral suppression (<200 copies/ml) and those without viral suppression, according to their most recent HIV-1 RNA within 1 year before hospitalization. The remaining patients were classified as HIV negative, regardless of whether they were tested for HIV. The likelihood of misclassification of an individual with known or undiagnosed HIV as being HIV negative using this approach was low; a prior HIV sero-prevalence study found only 0.2% of 4990 patients visiting our emergency department to have undiagnosed HIV.21

Outcomes of interest

The primary outcome was incident hospital AKI. AKI was defined by Kidney Disease: Improving Global Outcomes (KDIGO) criteria: stage 1—increase in creatinine level by 0.3 mg/dl within 48 hours or 1.5× to 1.9× increase in creatinine level from baseline within 7 days; stage 2—2× to 2.9× increase in creatinine level within 7 days; and stage 3—≥3× increase in creatinine level within 7 days or initiation of kidney replacement therapy (KRT),22 defined by orders for dialysis or continuous KRT during the index hospitalization. AKI was staged at time of diagnosis and maximum stage achieved during hospitalization. In patients who presented with an elevated creatinine level, AKI was defined and staged by comparison to the baseline creatinine level. Baseline creatinine level was defined as the mean of all creatinine values 8 to 365 days prehospitalization.23 All patients had at least 1 outpatient creatinine measurement within 1 year of hospitalization. We assessed adverse outcomes following AKI, including the need for KRT and incident CKD. Incident CKD was defined as a new estimated glomerular filtration rate (eGFR) <60 ml/min per 1.73 m2 90 to 365 days after discharge.

Covariates

Data were extracted on comorbidities using International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), or International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM), diagnostic codes. Sociodemographic data included age, sex, health insurance, and self-reported race and ethnicity, categorized as non-Hispanic White, non-Hispanic Black, Hispanic, or other. In addition to ICD-9-CM and ICD-10-CM codes, CKD before hospitalization was defined as 2 consecutive eGFR measurements of <60 ml/min per 1.73 m2 at least 90 days apart, calculated using the 2021 CKD Epidemiology Collaboration creatinine equation.24 Among PWH, data were extracted on prescription for ART, including tenofovir disoproxil fumarate (TDF), and most recent CD4 cell count and HIV-1 RNA level within 1 year of hospitalization. Data were extracted on prescription for nonsteroidal anti-inflammatory agents, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers within 1 year of hospitalization. Extracted hospital data included invasive ventilation, KRT, surgery, intensive care unit admission, potentially nephrotoxic medication classes, and in-hospital death.

Statistical analysis

Descriptive analyses were used to compare the clinical characteristics between PWH with and without viral suppression and people without HIV. Continuous variables are expressed as median with interquartile range and mean with SD, and categorical variables are expressed as numbers with percentages. Among the 3 groups, we compared the proportion with AKI, severe AKI (stage 2 or 3), AKI requiring KRT, in-hospital death, and incident CKD among AKI survivors who were discharged.

Cause-specific Cox proportional hazards models were used to determine the relative hazard of AKI, stage 2 or 3 AKI, and requirement of KRT by HIV status and viral suppression status, treating the competing risks of death and discharge as censoring events. Our multivariable models adjusted for a priori predictors known to be associated with AKI and those on bivariate analyses that were statistically significant at an α of <0.05. Time-independent variables included in the full models included demographics, comorbidities, nephrotoxic medications, and intensive care unit admission. Development of CKD within 1 year of discharge among AKI survivors was also assessed by cause-specific Cox proportional hazards models, treating the competing risks of death and last follow-up within 1 year of discharge as censoring events. Similar variables were included in our multivariable model with the addition of need for invasive ventilation or surgery during hospitalization. There were no missing data for the variables included in our models.

Because previous studies have shown that PWH develop comorbidities associated with chronic disease decades earlier than people without HIV, we hypothesized that HIV status would modify the association between age and AKI. Interaction testing between HIV status and age was performed. We categorized PWH and people without HIV by age tertiles (<40, 40–59, and ≥60 years) and performed multivariable Cox regression to determine differences in the risk of AKI across age groups among PWH and people without HIV. Furthermore, we compared differences in the unadjusted and adjusted mean age at AKI diagnosis between the groups using multivariable linear regression.

Two-sided P < 0.05 was considered statistically significant. Stata, version 17.0 (Stata Corp), was used for all analyses.

RESULTS

Baseline characteristics

From 2010–2019, 173,884 patients were hospitalized at MMC who met our inclusion criteria (Figure 1). Among these patients, 4718 had HIV; 2532 (53.7%) were virally suppressed, and 2186 (46.3%) were not virally suppressed. Compared with people without HIV, PWH were younger and more likely to be men and Hispanic or non-Hispanic Black (Table 1). PWH with viral suppression had a similar prevalence of diabetes, hypertension, hyperlipidemia, cerebrovascular disease, and CKD and a similar baseline eGFR as people without HIV. As expected, PWH had a higher prevalence of hepatitis C virus infection compared with people without HIV. People without HIV were more likely to be obese and to have cardiovascular disease compared with PWH. Median hospital length of stay was longest among PWH (3.9 and 3.4 days among virally unsuppressed and suppressed patients, respectively, compared with 3.2 days in people without HIV). Compared with those without viral suppression, PWH with viral suppression had longer duration of HIV, had higher CD4 cell counts (538 vs. 189 cells/mm3), and were more likely to have a prescription for ART within the past year.

Table 1 |.

Characteristics of hospitalized patients by HIV status between January 1, 2010, and December 31, 2019

Variable HIV-negative patients
(n = 169,166)		 HIV-positive patients, viral
suppression (n = 2532)		 HIV-positive patients, no viral
suppression (n = 2186)
Sociodemographics
 Age at index, median (IQR), yr 59 (43–72) 53 (46–60) 48 (38–54)
 Sex, n (%)
 Male 63,110 (37.3) 1328 (52.5) 1180 (54.0)
 Female 106,056 (62.7) 1204 (47.5) 1006 (46.0)
 Race/ethnicity, n (%)
 Hispanic 64,032 (37.9) 1146 (45.3) 882 (40.4)
 Non-Hispanic Black 53,104 (31.4) 1047 (41.4) 1023 (46.8)
 Non-Hispanic White 24,213 (14.3) 133 (5.3) 90 (4.1)
 Other 27,817 (16.4) 206 (8.1) 191 (8.7)
 Insurance status, n (%)
 Commercial 36,692 (21.7) 278 (11.0) 221 (10.1)
 Government 129,510 (76.6) 2235 (88.2) 1955 (89.5)
 Self-pay 48 (0.0) 0 (0.0) 0 (0.0)
 Unknown 2916 (1.7) 19 (0.8) 10 (0.5)
Comorbidities, n (%)
 Obesity (BMI ≥30 kg/m2) 69,357 (43.2) 818 (33.2) 465 (22.3)
 BMI, mean (SD), kg/m2a 30.3 (8.5) 28.2 (7.7) 25.8 (7.3)
 Diabetes mellitus 55,132 (32.6) 702 (27.7) 367 (16.8)
 Hypertension 101,764 (60.2) 1480 (58.5) 869 (39.8)
 Hyperlipidemia 67,575 (40.0) 993 (39.2) 375 (17.2)
 Pulmonary disease 42,154 (24.9) 1188 (46.9) 864 (39.5)
 Cardiovascular disease 44,561 (26.3) 475 (18.8) 251 (11.5)
 Cerebrovascular disease 8,993 (5.3) 117 (4.6) 61 (2.8)
 Chronic kidney disease 23,702 (14.0) 333 (13.2) 168 (7.7)
 Hepatis C infection 4,637 (2.5) 567 (21.4) 471 (20.7)
 Hepatitis B infection 378 (0.2) 64 (2.5) 77 (3.5)
 Baseline eGFR, median (IQR), ml/min per 1.73 m2 88.3 (63.8–106.6) 84.9 (67.4–100.6) 93.9 (75.1–108.0)
 Baseline creatinine, median (IQR), mg/dl 0.9 (0.7–1.1) 1.0 (0.8–1.2) 0.9 (0.8–1.1)
Home medications, n (%)
 ACE-I or ARB 41,821 (24.7) 624 (24.6) 291 (13.3)
 NSAIDs 35,396 (20.9) 947 (37.4) 531 (24.3)
Laboratory values at admission
 eGFR, median (IQR), ml/min per 1.73 m2 86.8 (66.3–104.8) 84.4 (63.7–102.8) 90.8 (68.3–108.5)
 Creatinine, median (IQR), mg/dl 0.9 (0.7–1.1) 1.0 (0.8–1.2) 0.9 (0.8–1.2)
 Serum albumin, mean (SD), g/dla 3.9 (0.6) 3.9 (0.6) 3.6 (0.6)
Medications administered during
 hospitalization, n (%)
 ACE-I or ARB 46,241 (24.3) 506 (20.0) 297 (13.6)
 Diuretics 41,800 (24.7) 489 (19.3) 312 (14.3)
 I.v. antibioticsb 80,118 (47.4) 1199 (47.4) 1113 (50.9)
 Proton pump inhibitors 52,764 (31.2) 629 (24.8) 523 (23.9)
 NSAIDs 47,265 (27.9) 615 (24.3) 501 (22.9)
Procedures during hospitalization, n (%)
 Surgery 50,726 (30.0) 505 (19.9) 274 (12.5)
 Invasive ventilation 5634 (3.3) 64 (2.5) 67 (3.1)
 Intensive care unit care 44,835 (26.5) 435 (17.2) 322 (14.7)
Hospital outcomes
 Length of stay, d, median (IQR) 3.2 (1.2–5.7) 3.4 (2.0–6.1) 3.9 (2.3–7.0)
 Death, n (%) 2818 (1.7) 26 (1.0) 42 (1.9)
HIV-related characteristics
 HIV duration, median (IQR), yr N/A 7.5 (2.5–12.8) 3.7 (0.6–9.7)
 HIV RNA, median (IQR), copies/ml N/A N/A 16,909 (2641–82,843)
 CD4 nadir, median (IQR), cells/mm3a N/A 225 (94–398) 130 (34–297)
 Current CD4, median (IQR), cells/mm3 N/A 538 (345–770) 189 (62–375)
 ART prescription within past year, n (%) N/A 2073 (81.9) 1275 (58.3)
 TDF prescription within past year, n (%) N/A 724 (28.6) 585 (26.8)
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ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; ART, antiretroviral therapy; BMI, body mass index; eGFR, estimated glomerular filtration rate; IQR, interquartile range; N/A, not applicable; NSAID, nonsteroidal anti-inflammatory drug; TDF, tenofovir disoproxil fumarate.

a

Missing data: BMI (N = 8917), admission albumin (N = 25,090), and CD4 nadir (N = 99).

b

I.v. vancomycin, aminoglycosides, penicillins, and/or cephalosporins.

AKI incidence

Among 31,054 hospitalized patients with AKI, 47.1% were diagnosed with AKI at admission, whereas the remaining 52.9% developed AKI during hospitalization (Table 2). Among patients who developed AKI during hospitalization, median time to onset was 72 hours (interquartile range, 24–96 hours). Compared with people without HIV, the incidence of AKI was higher among PWH both without and with viral suppression (25.2% and 19.7%, respectively, vs. 17.7%). The incremental, graded association based on HIV viral suppression status was unchanged after multivariable adjustment (adjusted hazard ratio [aHR], 1.27 [95% confidence interval {CI}, 1.15–1.40] and aHR, 1.73 [95% CI, 1.58–1.90] for HIV virally suppressed and unsuppressed patients, respectively; Table 3; Supplementary Table S1).

Table 2 |. Incidence, severity, and outcomes of hospital AKI by HIV status.

Variable HIV-negative patients HIV-positive patients, viral suppression HIV-positive patients, no viral suppression P value
AKI incidence, n (%) 30,005 (17.7) 499 (19.7) 550 (25.2) <0.0001
Proportions below reflective of those with AKI*
 AKI stage at diagnosis, n (%)
  1 23,365 (77.9) 370 (74.2) 423 (76.9)
  2  3163 (10.5)  65 (13.0)  57 (10.4)  0.28
  3 3477 (11.6) 64 (12.8) 70 (12.7)
 Maximum AKI stage, n (%)
  1 21,234 (70.9) 348 (69.9) 365 (66.4)
  2 4766 (15.9) 81 (16.2) 96 (17.5) 0.17
  3 3941 (13.2) 69 (13.9) 89 (16.1)
 Severe AKI (stage 2 or 3), n (%) 8944 (29.8) 153 (30.7) 186 (33.8) 0.12
 Need for KRT, n (%) 1283 (4.3) 29 (5.8) 27 (4.9) 0.004
 In-hospital death after AKI, n (%) 2270 (7.6) 21 (4.2) 40 (7.3) 0.02
 Length of stay, d, median (IQR) 6.7 (3.8–12.2) 6.9 (4.0–13.1) 6.9 (3.9–13.1) 0.24
 Incident CKD after AKI, n (%)a 3342 (29.8) 74 (24.2) 64 (20.6) <0.0001
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AKI, acute kidney injury; CKD, chronic kidney disease; IQR, interquartile range; KRT, kidney replacement therapy.

a

Incident CKD defined as new estimated glomerular filtration rate <60 ml/min per 1.73 m2 within 90 to 365 days after hospital discharge. Data available for 61% of the cohort with AKI after excluding death during hospitalization (n = 2331), death within 90 days of hospital discharge (n = 1599), and CKD before hospitalization (n = 7746).

Group comparisons reflect those with hospital AKI; 3 group comparisons made using analysis of variance, Kruskal-Wallis, and χ2 tests.

Table 3 |. Risk of in-hospital AKI by HIV status and viral suppression status.

Variable Cause-specific hazard ratio (95% CI) P value
Unadjusted
 HIV(−) [Reference]
 HIV(+), viral suppression 1.08 (0.99–1.18) 0.08
 HIV(+), no viral suppression 1.37 (1.26–1.49) <0.0001
Adjusted for demographics
 HIV(−) [Reference]
 HIV(+), viral suppression 1.20 (1.10–1.33) <0.0001
 HIV(+), no viral suppression 1.60 (1.47–1.74) <0.0001
Adjusted for demographics + comorbidities, home medications, and ICU admissiona
 HIV(−) [Reference]
 HIV(+), viral suppression 1.27 (1.15–1.40) <0.0001
 HIV(+), no viral suppression 1.73 (1.58–1.90) <0.0001
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AKI, acute kidney injury; CI, confidence interval; ICU, intensive care unit; Reference, reference group.

a

Adjusted for demographics (age, sex, and race and ethnicity), comorbidities (chronic kidney disease, hypertension, diabetes, cardiovascular disease, hyperlipidemia, hepatitis C, and pulmonary disease), and home medications (angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, nonsteroidal anti-inflammatory drug, and tenofovir disoproxil fumarate).

Number with incident AKI: 31,054.

Factors associated with AKI

Compared with PWH without AKI, PWH with hospital AKI were older, less likely to be women, and more likely to have diabetes, hypertension, cardiovascular disease, hepatitis C, and CKD. HIV-related factors associated with AKI included current CD4 cell count of <200 cells/mm3, shorter duration of HIV infection, unsuppressed HIV RNA viral load, and lower admission albumin levels. PWH with AKI were less likely to have a prescription for ART, including TDF, in the year before hospitalization compared with those without AKI (Supplementary Table S2). Use of TDF was not associated with AKI after multivariable adjustment (Supplementary Table S3). The magnitude of the independent association between HIV and AKI varied by HIV viral suppression status, with a more pronounced effect of HIV compared with some traditional risk factors among those without viral suppression and a similar magnitude in those with viral suppression (Figure 2).

Figure 2 |. Independent factors associated with hospital acute kidney injury.

Figure 2 |

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Data adjusted for age, sex, Black race, chronic kidney disease (CKD), diabetes, hypertension, hyperlipidemia, cardiovascular disease, hepatitis C infection, pulmonary disease, intensive care unit (ICU) admission, and prescription for angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, nonsteroidal anti-inflammatory drug, or tenofovir disoproxil fumarate. Adjusted hazard ratios (aHRs) (95% confidence intervals [CIs]) are as follows: HIV(+) suppressed, 1.27 (1.15–1.40); HIV(+) unsuppressed, 1.73 (1.58–1.90); female sex, 0.88 (0.86–0.90); diabetes, 1.26 (1.23–1.29); hypertension, 1.21 (1.17–1.25); cardiovascular disease, 1.11 (1.09–1.14); CKD, 1.60 (1.56–1.65); hepatitis C, 1.27 (1.20–1.34); and ICU admission, 1.58 (1.54–1.62).

Severe AKI

Proportionally, the incidence of stage 2 or 3 AKI was higher among PWH both without and with viral suppression (33.8% and 30.7% vs. 29.8%; Table 2). After multivariable adjustment, PWH with and without viral suppression remained at higher risk of stage 2 or 3 AKI (aHR, 1.32 [95% CI, 1.12–1.58] and aHR, 1.96 [95% CI, 1.67–2.30] for HIV virally suppressed and unsuppressed patients, respectively; Table 4). Compared with people without HIV, the incidence of AKI requiring KRT was higher among PWH both with and without viral suppression (5.8% and 4.9%, respectively, vs. 4.3%). The association of AKI requiring KRT with HIV viral suppression status increased after multivariable adjustment (aHR, 1.89 [95% CI, 1.27–2.84] and aHR, 1.87 [95% CI, 1.23–2.84] for HIV virally suppressed and unsuppressed patients, respectively; Table 5). Notably, among patients who developed AKI requiring KRT, those with HIV were significantly younger than those without HIV (54 [interquartile range, 45–59.5] vs. 65 [interquartile range, 54–75] years; P < 0.0001).

Table 4 |. Risk of stage 2 or 3 in-hospital AKI by HIV status and viral suppression status.

Variable Cause-specific hazard ratio (95% CI) P value
Unadjusted
 HIV(−) [Reference]
 HIV(+), viral suppression 1.12 (0.95–1.31)  0.17
 HIV(+), no viral suppression 1.51 (1.31–1.75)  <0.0001
Adjusted for demographics
 HIV(−) [Reference]
 HIV(+), viral suppression 1.26 (1.07–1.48)  0.005
 HIV(+), no viral suppression 1.88 (1.62–2.18)  <0.0001
Adjusted for demographics + comorbidities, home medications, and ICU admissiona
 HIV(−) [Reference]
 HIV(+), viral suppression 1.32 (1.12–1.58) <0.0001
 HIV(+), no viral suppression 1.96 (1.67–2.30) <0.0001
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AKI, acute kidney injury; CI, confidence interval; ICU, intensive care unit; Reference, reference group.

a

Adjusted for demographics (age, sex, and race and ethnicity), comorbidities (chronic kidney disease, hypertension, diabetes, cardiovascular disease, hyperlipidemia, hepatitis C, and pulmonary disease), and home medications (angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, nonsteroidal anti-inflammatory drug, and tenofovir disoproxil fumarate).

Number with stage 2 or 3 AKI: 9283.

Table 5 |. Risk of AKI requiring kidney replacement therapy by HIV status and viral suppression status.

Variable Cause-specific hazard ratio (95% CI) P value
Unadjusted
 HIV(−) [Reference]
 HIV(+), viral suppression 1.61 (1.10–2.34)  0.01
 HIV(+), no viral suppression 1.45 (0.97–2.15)  0.07
Adjusted for demographics
 HIV(−) [Reference]
 HIV(+), viral suppression 1.63 (1.12–2.37) 0.01
 HIV(+), no viral suppression 1.53 (1.03–2.29) 0.04
Adjusted for demographics + comorbidities, home medications,
and ICU admissiona
 HIV(−) [Reference]
 HIV(+), viral suppression 1.89 (1.27–2.84) 0.002
 HIV(+), no viral suppression 1.87 (1.23–2.84) 0.003
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AKI, acute kidney injury; CI, confidence interval; ICU, intensive care unit; Reference, reference group.

a

Adjusted for demographics (age, sex, and race and ethnicity), comorbidities (chronic kidney disease, hypertension, diabetes, cardiovascular disease, hyperlipidemia, hepatitis C, and pulmonary disease), and home medications (angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, nonsteroidal anti-inflammatory drug, and tenofovir disoproxil fumarate).

Number with AKI requiring kidney replacement therapy: 1339.

Incident CKD among AKI survivors

Among AKI survivors, there was no association between HIV and incident CKD within 1 year in unadjusted analysis (Table 6). After adjustment for age, PWH with and without viral suppression were at increased risk of developing CKD following AKI. This risk persisted after multivariable adjustment (aHR, 1.35 [95% CI, 1.07–1.72] and aHR, 1.46 [95% CI, 1.13–1.88] for HIV virally suppressed and unsuppressed patients, respectively).

Table 6 |. Risk of incident CKD after hospital AKI by HIV status and viral suppression status.

Variable Cause-specific hazard ratio (95% CI) P value
Unadjusted
 HIV(−) [Reference]
 HIV(+), viral suppression 0.99 (0.78–1.24) 0.92
 HIV(+), no viral suppression 0.78 (0.61–1.00) 0.05
Adjusted for demographics
 HIV(−) [Reference]
 HIV(+), viral suppression 1.32 (1.05–1.67) 0.02
 HIV(+), no viral suppression 1.35 (1.05–1.73) 0.02
Adjusted for demographics + comorbidities + severity of illness + hospital medicationsa
 HIV(−) [Reference]
 HIV(+), viral suppression 1.35 (1.07–1.72) 0.01
 HIV(+), no viral suppression 1.46 (1.13–1.88) 0.004
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AKI, acute kidney injury; CI, confidence interval; CKD, chronic kidney disease; Reference, reference group.

a

Adjusted for demographics (age, sex, and race and ethnicity), comorbidities (chronic kidney disease, hypertension, diabetes, cardiovascular disease, and hepatitis C), severity of illness (invasive ventilation, surgery, or intensive care unit care), and hospital medications (diuretics, proton pump inhibitors, nonsteroidal anti-inflammatory drugs, and antibiotics).

Number with incident CKD (new estimated glomerular filtration rate <60 ml/min per 1.73 m2 90–365 days after hospital discharge): 3480.

Relationship between age and AKI by HIV status

Finally, because PWH develop comorbidities, including CKD, earlier than people without HIV, we sought to determine whether HIV status modified the association of age with risk of AKI. Because of limited sample size, we did not stratify by viral suppression status. Interaction testing between HIV status and age was statistically significant (P < 0.0001). As expected, increasing age was associated with AKI among people without HIV. Remarkably, the estimated risk of AKI after multivariable adjustment was markedly and similarly elevated across all age groups in PWH (Figure 3). Overall, the risk of AKI among PWH regardless of age was similar to older people without HIV. Virally unsuppressed and suppressed PWH with AKI were significantly younger compared with people without HIV and AKI (48.1 and 54.7 years old compared with 64.3 years old), and a significant difference in age persisted after multivariable adjustment (Supplementary Table S4).

Figure 3 |. Risk of hospital acute kidney injury by HIV status across age tertiles.

Figure 3 |

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Data are adjusted for sex, Black race, chronic kidney disease, diabetes, hypertension, cardiovascular disease, hepatitis C infection, and intensive care unit admission. Adjusted hazard ratios (aHRs) (95% confidence intervals [CIs]) are as follows: HIV(–) for those aged <40 years, reference; HIV(–) for those aged 40 to 59 years, 1.27 (1.22–1.33); HIV(–) for those aged ≥60 years, 1.63 (1.57–1.70); HIV(+) for those aged <40 years, 1.82 (1.60–2.07); HIV(+) for those aged 40 to 59 years, 1.80 (1.65–1.97); and HIV(+) for those aged ≥60 years, 1.84 (1.58–2.15).

DISCUSSION

We evaluated the incidence and outcomes of hospital AKI among a contemporary cohort of PWH and people without HIV in a large New York City health system. We observed graded, independent associations between the incidence, severity, and outcomes of AKI by HIV viral suppression status. The most severe outcomes were observed among virally unsuppressed PWH, but more important, even in the setting of viral suppression, HIV remained an independent risk factor for AKI, including severe AKI requiring KRTand transition to CKD. To our knowledge, this is the first study to compare the incidence and outcomes of hospital AKI by HIV and viral suppression status in the modern era of ART. Notably, we observed a similarly elevated risk of AKI associated with HIV irrespective of age, and of a magnitude at least as large as that observed in older adults without HIV. This highlights that HIV is an important risk factor for AKI, even among young adults, and that HIV infection may promote premature development of age-related chronic comorbidities, such as CKD, and hospitalization-related events, including AKI.

The coronavirus disease 2019 (COVID-19) era has been a reminder that viral infections are an important risk factor for kidney injury, particularly among hospitalized patients.25–27 Prior observational studies have consistently identified low CD4 cell count, unsuppressed viral load, and coinfection with hepatitis C as risk factors for AKI among PWH.13,28,29 Although case reports and small series have described AKI among PWH receiving TDF,30 this association has not been found in epidemiologic studies. A recent study evaluating risk factors for AKI among >1400 ART-treated PWH found no association between TDF use and AKI.28 We similarly did not identify an association between TDF use and AKI. Only 1 study directly compared differences in AKI incidence by HIV status. Wyatt et al. used billing codes among hospitalized patients in New York State in 1995 and 2003 to determine differences in AKI incidence in pre-ART and post-ART eras. The incidence of AKI was higher among PWH compared with those without HIV during both years but decreased by ≈2-fold in 2003.12 CD4 cell count and HIV viral load were unknown in that study, but the reduction in AKI incidence shortly after the rollout of ART suggests that viral control reduces the risk of AKI.12 Consistent with this observation, we found that PWH without viral suppression were at the highest risk for hospital AKI. However, despite viral suppression, HIV remained independently associated with AKI.

Compared with people without HIV, PWH were more likely to develop severe AKI and had an ≈2-fold higher risk of requiring KRT irrespective of viral suppression status. Observational studies in the modern era have indicated an increase in the severity of AKI among PWH.13,16 A prospective Veterans Administration study of >56,000 PWH observed a doubling in the incidence of AKI requiring KRT between 2000 and 2006.13 Similarly, a national US sample of >1.8 million hospitalizations of PWH observed a 2-fold increase in the incidence of dialysis-requiring AKI from 2002 to 2010.16 These findings were attributed to an aging HIV population with increased comorbidities. However, the burden of comorbidities cannot completely explain the increased risk of AKI requiring KRT among PWH. In our study, the prevalence of comorbidities was similar among PWH with viral suppression and people without HIV but was significantly lower among those without viral suppression. We also found that PWH with AKI requiring KRT were significantly younger than people without HIV with AKI requiring KRT. These findings suggest that HIV is a more potent risk factor for severe AKI than many traditional risk factors.

AKI is associated with poor long-term kidney outcomes, including incident and progressive CKD, and risk of developing CKD increases with worsening stage of AKI.31,32 Consistent with our findings of increased risk of AKI and severe AKI among PWH, we also found that PWH were more likely to subsequently develop CKD following AKI compared with people without HIV. These findings underscore the need for diligent monitoring of kidney function after hospital discharge among PWH with hospital AKI, because transition to CKD may have important implications for ART selection and dose adjustment.

As expected, the magnitude of the risk of AKI incrementally increased with increasing age tertile among people without HIV. Conversely, the risk of AKI in PWH was markedly elevated in all age tertiles and not meaningfully different among young and old adults. Because older age is a strong risk factor for AKI, the relative homogeneity of risk of AKI across age tertiles of PWH was striking. Across age tertiles, the risk of AKI among PWH was similar to the oldest adults without HIV, supporting the hypothesis that HIV is a disease of accentuated aging.33 This finding is supported by other studies indicating that ART-treated PWH develop non–AIDS-related comorbidities, including CKD, 10 to 20 years earlier than people without HIV.5,6

The mechanisms by which HIV increases the risk of AKI remain unclear. The most well-studied cause of HIV-induced kidney injury is HIV-associated nephropathy. HIV-associated nephropathy is nearly exclusive to individuals with African ancestry and is strongly associated with apolipoprotein L1 risk variants.34–36 Although ART is effective at treating HIV-associated nephropathy, it does not eradicate HIV-1 RNA expression in the kidney.37 HIV-1 infects kidney tubular epithelial cells, leading to activation of proinflammatory mediators, including nuclear factor-kB and interleukin 6.38 Systemic inflammation plays an important role in the pathogenesis of several forms of AKI, including sepsis. Even virally suppressed PWH have significantly higher circulating levels of plasma biomarkers of inflammation compared with age-matched HIV-seronegative persons.8,10,39–41 Increased levels of proinflammatory cytokines have been shown to be predictive of AKI as well as nonrecovery from AKI.42,43 We speculate that long-term expression of HIV genes in kidney tubular epithelial cells promotes inflammation and kidney aging, which may partially explain increased risk of AKI and progression to CKD among PWH. Future studies are needed to determine the mechanisms by which HIV promotes AKI and progression to CKD.

This was the first study to determine the association between HIV viral suppression status and AKI. Major strengths include our large sample size of PWH, comparison with an HIV-negative group, and inclusion of a racially and ethnically diverse population, including a large proportion of women with HIV. Our definition of AKI is consistent with international guidelines, and we had no missing data on baseline creatinine level before hospitalization. Although our study spans a period that includes evolving recommendations for the initiation of ARTs, the time frame is representative of an era characterized by high rates of accessibility to modern ART regimens for PWH, but persistent disparities in virologic suppression. Ten years have passed since the World Health Organization’s recommendation that all PWH be initiated on ART irrespective of CD4 cell count. Despite this recommendation, one-third of PWH in the United States are not virally suppressed.44 Our findings underscore the urgent need to address barriers to ART uptake and adherence among PWH.

Our study also has limitations. First, the cause of AKI was unknown; and if there were significant differences by HIV status, this may have affected the incidence of AKI and its outcomes. We tried to account for this by adjusting for pre-admission and hospitalization risk factors known to be associated with AKI and its sequelae. Second, we were unable to confirm HIV-seronegative status among all people without HIV in our cohort. To avoid misclassification, we excluded individuals who received ART if we could not confirm an HIV diagnosis. Misclassification would more likely bias our results to the null. Third, we did not have follow-up eGFR data on all AKI survivors, which restricts the association of HIV with incident CKD after AKI to those with follow-up data in our health system. In addition, the definition of incident CKD after AKI was based on a single eGFR value of <60 ml/min per 1.73 m2. Although this may inflate the incidence of CKD, it has been shown to predict clinically important outcomes, including CKD progression, need for dialysis, and death.45 Finally, as with any observational study, there is the possibility of unmeasured confounding. For example, we did not have complete data on social determinants of health, such as income, food insecurity, substance use, and unstable housing, which have been shown to be associated with AKI and CKD,46 and HIV viral suppression status,47 despite our catchment area in 1 of the poorest urban counties in the United States. However, most of our study population has government insurance; therefore, we believe there to be less socioeconomic variability than other studies of PWH, and our results remained consistent after adjustment for health insurance.

CONCLUSION

Among a contemporary cohort of PWH and people without HIV, HIV is an independent risk factor for AKI, severe AKI, and poor long-term kidney outcomes following AKI, even among those with viral suppression. Moreover, HIV is independently associated with development of AKI at younger ages, suggesting that HIV may lead to premature kidney aging. Future studies are needed to examine the role of HIV in the development of AKI and to identify strategies to prevent AKI in PWH.

Supplementary Material

Supplementary File

Supplementary Table S1. Sensitivity analysis of risk of hospital acute kidney injury (AKI) by HIV status and viral suppression status with additional adjustment for health insurance.

Supplementary Table S2. Clinical characteristics among people with HIV with and without hospital acute kidney injury (AKI).

Supplementary Table S3. Unadjusted and adjusted risk factors associated with hospital acute kidney injury (AKI).

Supplementary Table S4. Unadjusted and adjusted mean difference in age at time of acute kidney injury (AKI) diagnosis. Supplementary File (.do)

Data_code

Supplementary data_code.do.

FUNDING

The research of MCF was supported by the National Institutes of Health (NIH)/National Center for Advancing Translational Science Einstein-Montefiore Clinical and Translational Science Awards grant UL1TR001073. The Einstein-Rockefeller-CUNY (City University of New York) Center for AIDS Research (P30-AI-124414; principal investigator: Harris Goldstein, MD) is supported by the following NIH cofunding and participating institutes and centers: National Institute of Allergy and Infectious Diseases, National Cancer Institute, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Heart, Lung, and Blood Institute, National Institute on Drug Abuse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of General Medical Sciences, National Institute of Mental Health, National Institute on Minority Health and Health Disparities, National Institute on Aging, Fogarty International Center (FIC), and Office of AIDS Research (OAR).

Footnotes

DISCLOSURE

All the authors declared no competing interests.

DATA STATEMENT

The code used in the analyses is available in Supplementary data_code.do.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplementary File

Supplementary Table S1. Sensitivity analysis of risk of hospital acute kidney injury (AKI) by HIV status and viral suppression status with additional adjustment for health insurance.

Supplementary Table S2. Clinical characteristics among people with HIV with and without hospital acute kidney injury (AKI).

Supplementary Table S3. Unadjusted and adjusted risk factors associated with hospital acute kidney injury (AKI).

Supplementary Table S4. Unadjusted and adjusted mean difference in age at time of acute kidney injury (AKI) diagnosis. Supplementary File (.do)

NIHMS2014835-supplement-Supplementary_File.docx (24.5KB, docx)
Data_code

Supplementary data_code.do.

NIHMS2014835-supplement-Data_code.do (4.7KB, do)

Data Availability Statement

The code used in the analyses is available in Supplementary data_code.do.

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