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Abstract: TH-PO744

Animal Models of Preeclampsia: A Renal Perspective

Session Information

Category: Women’s Health and Kidney Diseases

  • 2000 Women’s Health and Kidney Diseases

Authors

  • Garcia Valencia, Oscar Alejandro, Mayo Clinic, Rochester, Minnesota, United States
  • Weissgerber, Tracey L., Mayo Clinic, Rochester, Minnesota, United States
  • Savic, Marko, Medical Faculty, University of Belgrade, Belgrade, Serbia
  • Milin-Lazovic, Jelena, Medical Faculty, University of Belgrade, Belgrade, Serbia
  • Gonzalez Suarez, Maria Lourdes, University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Vallapureddy, Rangit R., Mayo Clinic, Rochester, Minnesota, United States
  • Wang, Diping, Mayo Clinic, Rochester, Minnesota, United States
  • Cubro, Hajrunisa, Mayo Clinic, Rochester, Minnesota, United States
  • Milic, Natasa, Medical Faculty, University of Belgrade, Belgrade, Serbia
  • Cipolla, Marilyn, University of Vermont Larner College of Medicine, Burlington, Vermont, United States
  • Garovic, Vesna D., Mayo Clinic, Rochester, Minnesota, United States
Background

Preeclampsia is a heterogeneous syndrome with different pathophysiological subtypes. Many animal models have been proposed, each based on different pathophysiology. The preeclampsia phenotype may differ depending on the model, the lab or personnel, or the animal supplier. Whereas some models reproduce the glomerular endotheliosis observed in preeclamptic women, others cause hypertensive renal injury. This systematic review examines the types of measurements performed to assess renal damage in papers that use animal models of preeclampsia.

Methods

PubMed and EMBASE were searched to identify articles using animal models of preeclampsia, published between January 2000 and September 2016. The search strategy included terms for hypertensive pregnancy disorders and term lists for identifying animal studies. Two independent reviewers followed standardized screening and abstraction protocols. Detailed information was abstracted from papers that included a common (>20 publications) model.

Results

364 papers included a common model (NOS inhibition: n=112 (22%), reduced uterine perfusion pressure or subrenal aortic coarctation: 101 (19.8%), sFlt-1: 35 (6.9%), low dose endotoxin: 33 (6.5%), NaCl administration: 28 (5.5%), transgenic human angiotensinogen renin: 25 (4.9%), agonistic autoantibodies against the angiotensin II type 1 receptor: 23 (4.5%), or NaCl and corticosteroids: 20 (3.9%). 80.5% of studies reported maternal blood pressure. 44.2% measured proteinuria. Renal histopathology was rarely examined (12.4%). The proportion of papers that measured each characteristic was highly variable among models (blood pressure: 43% to 100% (range), proteinuria: 21% to 95%, renal histopathology: 5% to 40%). The proportion of papers reporting proteinuria and renal histopathology did not differ between papers with vs. without a preclinical agent. 40 (11%) studies acknowledged that the model may not apply to all preeclamptic women.

Conclusion

Renal histopathology is rarely reported, suggesting a need for better characterization of renal changes caused by preeclampsia models and preclinical agents. This is particularly important given that hypertensive renal injury observed in some models differs from the glomerular endotheliosis observed in preeclamptic women.

Funding

  • Other NIH Support