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Related Experiment Videos

Collapsing glomerulopathy.

Joshua A Schwimmer1, Glen S Markowitz, Anthony Valeri

  • 1Division of Nephrology, Department of Medicine, Columbia College of Physicians and Surgeons, New York, NY, USA.

Seminars in Nephrology
|April 22, 2003
PubMed
Summary
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Collapsing glomerulopathy, a severe kidney disease, involves glomerular capillary collapse and podocyte damage. Its causes are unclear, but it often leads to rapid kidney failure and may recur after transplantation.

Area of Science:

  • Nephrology
  • Pathology
  • Genetics

Background:

  • Collapsing glomerulopathy is a severe morphologic variant of focal segmental glomerulosclerosis (FSGS).
  • It is characterized by glomerular capillary collapse, podocyte hypertrophy/hyperplasia, and tubulointerstitial disease.
  • Identical findings occur in idiopathic collapsing glomerulopathy and HIV-associated nephropathy, with associations to parvovirus B19 and pamidronate treatment.

Purpose of the Study:

  • To review the pathology, clinical presentation, and treatment of collapsing glomerulopathy.
  • To highlight the unknown etiology and pathogenesis involving visceral epithelial cell injury and cell cycle dysregulation.
  • To discuss clinical characteristics, transplant outcomes, and potential therapeutic strategies.

Main Methods:

Related Experiment Videos

  • Literature review of collapsing glomerulopathy.
  • Analysis of pathological findings, clinical features, and treatment outcomes.
  • Discussion of pathogenetic mechanisms including podocyte cell cycle dysregulation.

    • Main Results:

    • Collapsing glomerulopathy presents with glomerular collapse, podocyte proliferation, and severe tubulointerstitial damage.
    • Clinical features include nephrotic syndrome, rapid renal failure, and a predilection for Black individuals.
    • The condition can recur post-transplant, leading to graft loss.

    Conclusions:

    • Optimal treatment for collapsing glomerulopathy remains undefined.
    • Potential treatments include steroids, calcineurin inhibitors, blood pressure control, ACE inhibitors/ARBs, and lipid-lowering agents.
    • Further clinical trials are necessary to establish effective therapies for this aggressive FSGS variant.