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Spectrum of chronic kidney disease in HIV-infected patients
L J Campbell1, F Ibrahim, M Fisher
1Academic Department of HIV/GU Medicine, King's College London, London, France.
Insights
Chronic kidney disease (CKD) affects 2.4% of HIV patients, often linked to metabolic diseases. Certain HIV medications, indinavir (IDV) and tenofovir (TFV), accelerate kidney function decline in those with CKD.
Area of Science:
- Nephrology
- Infectious Diseases
- Pharmacology
Background:
- Chronic kidney disease (CKD) is a significant concern in the human immunodeficiency virus (HIV)-infected population.
- Understanding the prevalence, causes, and renal function trends in HIV patients is crucial for effective management.
Purpose of the Study:
- To investigate the prevalence and aetiology of CKD in HIV-infected patients.
- To analyze trends in estimated glomerular filtration rate (eGFR) in this cohort.
- To assess the impact of specific antiretroviral drugs on renal function.
Main Methods:
- A review of CKD cases was conducted at King's College and Brighton Hospitals, UK.
- CKD was defined as eGFR <60 mL/min for ≥3 months.
- Longitudinal eGFR slopes were analyzed in relation to exposure to indinavir (IDV) or tenofovir (TFV).
Main Results:
- CKD prevalence was 2.4% among HIV patients.
- Aetiology varied by ethnicity: HIV-associated nephropathy in Black patients, and metabolic/vascular diseases in White/other patients.
- Exposure to IDV and TFV was associated with accelerated eGFR decline (4.6-fold and 3.7-fold, respectively).
- Older age (≥50 years) and baseline eGFR were risk factors for CKD development with IDV or TFV exposure.
Conclusions:
- Metabolic and vascular diseases contribute significantly to CKD burden in aging HIV patients.
- Treatment with IDV or TFV is linked to a faster decline in renal function among HIV patients who develop CKD.
Objectives:
The aim of the study was to investigate the prevalence and aetiology of chronic kidney disease (CKD) and trends in estimated glomerular filtration rate (eGFR) in HIV-infected patients.
Methods:
Ascertainment and review of CKD cases among patients attending King's College and Brighton Hospitals, UK were carried out. CKD was defined as eGFR <60 mL/min for > or =3 months. Longitudinal eGFR slopes were produced to examine trends in renal function before, during and after exposure to indinavir (IDV) or tenofovir (TFV).
Results:
CKD prevalence was 2.4%. While HIV-associated nephropathy accounted for 62% of CKD in black patients, 95% of CKD in white/other patients was associated with diabetes mellitus, hypertension, atherosclerosis and/or drug toxicity. Exposure to IDV or TFV was associated with an accelerated decline in renal function (4.6-fold and 3.7-fold, respectively) in patients with CKD. In patients initiating IDV, age > or =50 years increased the odds of CKD [odds ratio (OR) 4.9], while in patients initiating TFV, age > or =50 years (OR 5.4) and eGFR 60-75 mL/min (OR 17.2) were associated with developing CKD.
Conclusion:
This study highlights the importance of metabolic and vascular disease to the burden of CKD in an ageing HIV-infected cohort. In patients who developed CKD, treatment with IDV or TFV was associated with an accelerated decline in renal function.
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