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Plasma apolipoprotein L1 levels do not correlate with CKD.

Leslie A Bruggeman1, John F O'Toole, Michael D Ross

  • 1Division of Nephrology and.

Journal of the American Society of Nephrology : JASN
|November 16, 2013
PubMed
Summary
This summary is machine-generated.

Apolipoprotein L1 (APOL1) gene variants, not circulating APOL1 levels, are linked to chronic kidney disease (CKD) in HIV-infected African Americans. APOL1 risk variants accelerate kidney function decline in these patients.

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Area of Science:

  • Nephrology
  • Genetics
  • Infectious Diseases

Background:

  • Polymorphisms in the apolipoprotein L1 (APOL1) gene are a significant risk factor for chronic kidney disease (CKD), particularly in individuals of African ancestry.
  • The precise role of APOL1's location, whether circulating or within kidney cells, in the pathogenesis of CKD remains incompletely understood.
  • HIV-associated nephropathy (HIVAN) is a major cause of CKD in HIV-infected individuals of African descent, with APOL1 genotype being a key determinant.

Purpose of the Study:

  • To investigate the association between plasma APOL1 levels and CKD in HIV-infected African Americans.
  • To examine the relationship of circulating APOL1 levels with APOL1 genotype, cytokine profiles, and lipid levels.
  • To determine whether APOL1 genotype or circulating APOL1 levels are more strongly associated with the progression of CKD in this population.

Main Methods:

  • A nested case-control study of 270 HIV-infected African Americans from a multicenter prospective observational study.
  • Patients were categorized into CKD groups based on estimated glomerular filtration rate (eGFR <60 ml/min/1.73 m²) or nephrotic proteinuria (>3.5 g/g).
  • Measurements included plasma APOL1 levels, APOL1 genotype, plasma cytokine levels, lipid profiles, and longitudinal eGFR and proteinuria assessments.

Main Results:

  • Plasma APOL1 levels did not correlate with APOL1 genotype, CKD status, or pro-inflammatory cytokines, but were associated with cholesterol and triglyceride levels.
  • APOL1 risk variants were associated with the reduced eGFR cohort, and cases with two risk variants showed significant eGFR decline over 4 years.
  • Higher circulating pro-inflammatory cytokine levels were independently associated with CKD, irrespective of APOL1 genotype.

Conclusions:

  • The level of circulating APOL1 does not appear to mediate APOL1-associated kidney disease in HIV-infected African Americans.
  • The function of APOL1 proteins, either circulating or synthesized within kidney cells, likely plays a crucial role in disease pathogenesis.
  • APOL1 risk variants are significant predictors of kidney function decline in HIV-infected individuals of African ancestry, independent of circulating APOL1 levels.