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10.2215/CJN.12811213

http://scihub22266oqcxt.onion/10.2215/CJN.12811213
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suck abstract from ncbi


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pmid25035270      Clin+J+Am+Soc+Nephrol 2014 ; 9 (8): 1377-85
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  • Association of preeclampsia with podocyte turnover #MMPMID25035270
  • Penning ME; Bloemenkamp KW; van der Zon T; Zandbergen M; Schutte JM; Bruijn JA; Bajema IM; Baelde HJ
  • Clin J Am Soc Nephrol 2014[Aug]; 9 (8): 1377-85 PMID25035270show ga
  • 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.
  • |*Cell Proliferation[MESH]
  • |Adult[MESH]
  • |Autopsy[MESH]
  • |Biomarkers/analysis[MESH]
  • |Case-Control Studies[MESH]
  • |Cause of Death[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Hyaluronan Receptors/analysis[MESH]
  • |Ki-67 Antigen/analysis[MESH]
  • |Kidney Diseases/etiology/metabolism/mortality/*pathology[MESH]
  • |Netherlands[MESH]
  • |Podocytes/chemistry/*pathology[MESH]
  • |Pre-Eclampsia/metabolism/mortality/*pathology[MESH]
  • |Pregnancy[MESH]


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