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Changes in renal function associated with indinavir

K Boubaker1, P Sudre, F Bally

  • 1Division of Infectious Diseases, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

AIDS (London, England)
|January 6, 1999
PubMed
Summary
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Indinavir therapy can cause crystal nephropathy, leading to elevated creatinine and urinary issues. Risk factors include long-term use, low BMI, and trimethoprim-sulfamethoxazole, but abnormalities are reversible.

Area of Science:

  • Nephrology
  • Infectious Diseases
  • Pharmacology

Background:

  • Indinavir is known to cause renal and urinary complications like nephrolithiasis and crystalluria.
  • A distinct form of indinavir-associated nephropathy has not been previously well-characterized.

Purpose of the Study:

  • To determine the frequency and risk factors of indinavir-associated nephropathy and urinary complications.
  • To compare indinavir's renal effects with other protease inhibitors like ritonavir and nelfinavir.

Main Methods:

  • Retrospective analysis of 106 HIV-infected individuals on indinavir.
  • Comparison group received ritonavir or nelfinavir.
  • Identified risk factors including duration of treatment, body mass index, and concurrent medications.

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Main Results:

  • 18.6% of indinavir recipients developed elevated creatinine, not seen in controls.
  • Risk factors for elevated creatinine included treatment >54 weeks, BMI ≤20 kg/m², and use of trimethoprim-sulfamethoxazole (TMP-SMX).
  • Renal complications occurred in 12.3% of patients, often associated with elevated creatinine; abnormalities were reversible upon drug discontinuation.

Conclusions:

  • Crystal nephropathy is a frequent complication of indinavir, marked by creatinine elevation, impaired kidney concentrating ability, leukocyturia, and renal imaging abnormalities.
  • Identifying patients at risk (low BMI, TMP-SMX use) can guide the choice between indinavir and alternative protease inhibitors to prevent adverse renal events.