What determines glomerular capillary permeability?

Abstract

There have been exciting recent advances in our understanding of the structural and molecular biology of the glomerular slit diaphragm, as described in a report in this issue of the JCI (see the related article beginning on page 1475). These findings, combined with data on the permeability of the basement membrane and evidence that the endothelium may be a more important barrier than often supposed, are allowing a clearer understanding to emerge of how the 3 parts of the glomerular capillary wall jointly determine its functional properties.

Association of Bone Mineral Density with Albuminuria and Estimated Glomerular Filtration Rate : The Dong-gu Study

“…Endothelial dysfunction of the glomerular basement membrane can modify glomerular barrier permeability in the kidneys, leading to excretion of albumin into the urine [16]. Therefore, albuminuria is a marker of endothelial dysfunction, plays a key role in the initiation and progression of atherosclerosis [15], and is associated with increased levels of inflammatory markers [29].…”

“…Moreover, endothelial dysfunction plays a key role in the initiation and progression of atherosclerosis [15]. Endothelial dysfunction of the glomerular basement membrane can modify glomerular barrier permeability in the kidneys, leading to excretion of albumin into the urine [16]. Atherosclerotic vascular disease may also directly impact bone metabolism and contribute to the development of osteoporosis [17].…”

Effects of maternal serum on permeability of glomerular endothelial cell membrane

“…The pathophysiology of preeclampsia involves the abnormal development of the placenta, imbalance of immunity and gene susceptibility, in which the injury of vascular endothelial cells has been proposed to play an important role [3][4][5] . It is the traditional opinion that the lesion of endothelial cells is the key mechanism of renal lesion in patients with preeclampsia and the main position of renal lesion is the glomerulus that is characterized by glomerular endothelial swelling with loss of endothelial fenestrae and occlusion of the capillary lumens [6,7] . Recent evidence suggests that over-expression of sFlt-1 in the maternal circulation has been found to contribute to endothelial dysfunction, hypertension and proteinuria in preeclampsia by blocking the effects of VEGF [8][9][10] .…”

“…The subjects were classified into 3 groups according to the results of final diagnosis after parturition: normotensive group (NP group, n=24), mild preeclampsia group (mPE group, n=12) and severe preeclampsia group (sPE group, n=12). Patients in the PE groups fulfilled the diagnosis criteria set in Williams Obstetrics [7] as follows:(1) blood pressure ≥140/90 mmHg after 20 weeks of gestation;(2) proteinuria (presence of 300 mg or more of protein in a 24-h urine collection); (3) disappearance of hypertension and proteinuria 12 weeks post partum; (4) no previous history of hypertension. The exclusion criteria included pre-existing chronic hypertension, diabetes, multiple pregnancies and any chronic renal or liver disease.…”

“…The subjects were classified into 3 groups according to the results of final diagnosis after parturition: normotensive group (NP group, n=24), mild preeclampsia group (mPE group, n=12) and severe preeclampsia group (sPE group, n=12). Patients in the PE groups fulfilled the diagnosis criteria set in Williams Obstetrics [7] as follows:…”