NATURE OF GLOMERULAR DYSFUNCTION IN PREECLAMPSIA

Citation
Ra. Lafayette et al., NATURE OF GLOMERULAR DYSFUNCTION IN PREECLAMPSIA, Kidney international, 54(4), 1998, pp. 1240-1249
Citations number
39
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
54
Issue
4
Year of publication
1998
Pages
1240 - 1249
Database
ISI
SICI code
0085-2538(1998)54:4<1240:NOGDIP>2.0.ZU;2-O
Abstract
Background. Pre-eclampsia is characterized by hypertension, proteinuri a and edema. Simultaneous studies of kidney function and structure hav e not been repel-red. We wished to explore the degree and nature of gl omerular dysfunction in pre-eclampsia. Methods. Physiologic techniques were used to estimate glomerular filtration rate (GFR, renal plasma f low and afferent oncotic pressure immediately after delivery in consec utive patients with pre-eclampsia (PET; N = 13). Healthy mothers compl eting an uncomplicated pregnancy served as functional controls (N = 12 ). A morphometric analysis of glomeruli obtained bl biopsy and mathema tical modeling were used to estimate the glomerular ultrafiltration co efficient (K-f). Glomeruli from healthy female kidney transplant donor s sen ed as structural controls ((N = 8). Results. The GFR in PET was depressed below the control level, 91 +/- 23 versus 149 +/- 34 ml/min/ 1.73 m(2), respectively (P < 0.0001). In contrast. renal plasma flow a nd oncotic pressure were similar in the two groups (P = NS). A reducti on in thr density and size of endothelial fenestrae and subendothelial accumulation of fibrinoid deposits lowered glomerular hydraulic perme ability in PET compared to controls. 1.81 Versus 2.58 x 10(-9) m/sec/P A. Mesangial cell interposition also curtailed effective filtration su rface area. Together. these changes lowered the computed single: nephr on It, in PET below control. 4.26 versus 6.78 nl/min . mm Hg. respecti vely. Conclusion. The proportionate (similar to 40%) depression of K-f for single nephrons and GFR suggests that hypofiltration in PET does not have a hemodynamic basis, but is a consequence of structural chang es that lead to impairment of intrinsic glomerular ultrafiltration cap acity.