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.