Literature DB >> 25035270

Association of preeclampsia with podocyte turnover.

Marlies E Penning1, Kitty W M Bloemenkamp2, Tom van der Zon3, Malu Zandbergen3, Joke M Schutte4, Jan A Bruijn3, Ingeborg M Bajema3, Hans J Baelde3.   

Abstract

BACKGROUND AND OBJECTIVES: Preeclampsia is characterized by hypertension and proteinuria, and increased shedding of podocytes into the urine is a common finding. This finding raises the question of whether preeclamptic nephropathy involves podocyte damage. This study examined podocyte-related changes in a unique sample of renal tissues obtained from women who died of preeclampsia. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: All patients with preeclampsia who died in The Netherlands since 1990 and had available autopsy tissue were identified using a nationwide database of the Dutch Pathology Registry (PALGA). This resulted in a cohort of 11 women who died from preeclampsia. Three control groups were also identified during the same time period, and consisted of normotensive women who died during pregnancy (n=25), and nonpregnant controls either with (n=14) or without (n=13) chronic hypertension. Glomerular lesions, including podocyte numbers, podocyte proliferation, and parietal cell activation, were measured.
RESULTS: Patients with preeclampsia had prominent characteristic glomerular lesions. The results showed that the number of podocytes per glomerulus did not differ significantly between the patients with preeclampsia and the control groups. However, preeclampsia was associated with a significant increase in intraglomerular cell proliferation (7.3% [SD 9.4] of the glomeruli of patients with preeclampsia had Ki-67-positive cells versus 1.6% [SD 3.3] of the glomeruli of hypertensive controls and 1.1% [SD 1.3] of nonpregnant controls; P=0.004) and activated parietal epithelial cells on a podocyte location (34% [SD 13.1] of the glomeruli of patients with preeclampsia versus 18.0% [SD 15.3] of pregnant controls, 11.9% [SD 13.2] of hypertensive controls, and 10.8% [SD 13.4] of nonpregnant controls; P=0.01).
CONCLUSIONS: These findings suggest that the recently described mechanisms of podocyte replacement play a role in preeclampsia. These results provide key new insights into the pathogenesis of preeclamptic nephropathy, and they open new possibilities for developing therapeutic modalities.
Copyright © 2014 by the American Society of Nephrology.

Entities:  

Keywords:  kidney; podocyte; renal epithelial cell; target organ damage

Mesh:

Substances:

Year:  2014        PMID: 25035270      PMCID: PMC4123409          DOI: 10.2215/CJN.12811213

Source DB:  PubMed          Journal:  Clin J Am Soc Nephrol        ISSN: 1555-9041            Impact factor:   8.237


  32 in total

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3.  Glomerular expression of nephrin and synaptopodin, but not podocin, is decreased in kidney sections from women with preeclampsia.

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5.  Urinary podocyte excretion as a marker for preeclampsia.

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9.  Podocyte Regeneration Driven by Renal Progenitors Determines Glomerular Disease Remission and Can Be Pharmacologically Enhanced.

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10.  Diagnosis of proteinuria using a random urine protein-creatinine ratio and its correlation with adverse outcomes in pregnancy with preeclampsia characterized by renal damage.

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