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Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of...
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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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APOL1 genotype-associated morphologic changes among patients with focal segmental glomerulosclerosis.

Jarcy Zee1, Michelle T McNulty2, Jeffrey B Hodgin3

  • 1Department of Biostatistics, Epidemiology, and Informatics, University of Pennsylvania Perelman School of Medicine and Children's Hospital of Philadelphia, 423 Guardian Drive, Philadelphia, PA, 19104, USA. Jarcy.Zee@Pennmedicine.upenn.edu.

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Apolipoprotein L1 (APOL1) risk variants are linked to kidney changes in Black individuals with focal segmental glomerulosclerosis (FSGS). These variants correlate with specific cellular and structural alterations in kidney biopsies, but not in minimal change disease (MCD).

Keywords:
APOL1Focal segmental glomerulosclerosisMinimal change diseaseMorphologyPediatric

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Area of Science:

  • Nephrology
  • Genetics
  • Pathology

Background:

  • The G1 and G2 alleles of apolipoprotein L1 (APOL1) are prevalent in the Black population and are associated with an elevated risk of focal segmental glomerulosclerosis (FSGS).
  • The precise molecular mechanisms connecting APOL1 risk variants to FSGS remain unclear, compounded by the absence of APOL1 in laboratory animals, hindering pathobiological studies.

Purpose of the Study:

  • To investigate the tissue-based consequences of APOL1 risk variants and gene expression in Black patients with FSGS and minimal change disease (MCD).
  • To identify correlations between APOL1 risk alleles or glomerular APOL1 mRNA expression and kidney biopsy morphologic traits.

Main Methods:

  • Analysis of kidney biopsy traits from 90 Black patients (58% pediatric onset) with FSGS or MCD within the Nephrotic Syndrome Study Network.
  • Testing associations between APOL1 risk alleles/mRNA expression and 83 light- or electron-microscopy determined kidney structural and cellular changes.

Main Results:

  • In FSGS patients, APOL1 risk variants significantly correlated with reduced mesangial hypercellularity, decreased cytoskeleton condensation, and increased tubular microcysts under both recessive and dominant models.
  • No significant correlations were found in the minimal change disease (MCD) cohort.
  • Glomerular APOL1 expression in FSGS patients did not correlate with morphologic features, independent of risk alleles.

Conclusions:

  • Both one and two APOL1 risk alleles are associated with cellular/tissue changes in FSGS patients, extending beyond the presence of two risk alleles.
  • The limited discovery of tissue differences and lack of significant findings in MCD may indicate a need for increased statistical power or the application of machine learning methods for more sensitive detection of APOL1-associated changes.