Cystatin-C not only detects the beginning of the deterioration of renal function, but also correlates well with structural changes such as renal glomerular endotheliosis
.10 Cystatin-C, in terms of its diagnostic performance, has proven itself to be a better indicator of early decline in renal functions because of its independence from height, weight, age, gender, race and varying muscle mass.
This angiogenic imbalance linked with maternal endothelial dysfunction, blood coagulation and renal endotheliosis
, manifests as increased blood pressure and proteinuria (2).
Second, RUPP does not mimic all the pathological features of preeclampsia, such as glomerular endotheliosis
and changes in hemoglobin, platelets, and liver function (10).
Biopsy-proven cases of glomerular disease in anti-VEGF therapy are few; however, most have demonstrated changes in keeping with glomerular thrombotic microangiopathy (TMA) histology, with predominant endotheliosis
and membranoproliferative changes [30, 31].
In addition, adenoviral transfer of sFlt-1 in mice induced proteinuria and caused glomerular endotheliosis
similar to VEGF-A-deficient glomeruli .
The only consistently found pathological lesion in PE is the renal lesion termed glomerular endotheliosis
, which has been regarded as pathognomic for the condition.
The predominant target organ may be the brain (seizures or eclampsia), the liver (HELLP syndrome), or the kidney (glomerular endotheliosis
Targeted heterozygous deletion of VEGF in podocytes results in renal pathology manifested by loss of endothelial fenestrations in glomerular capillaries, proliferation of glomerular endothelial cells (endotheliosis
), loss of podocytes, and proteinuria in mice [6,7].
In line with this, C1q-deficient pregnant [C1q (-/-)] rats present the main findings of human preeclampsia: hypertension, albuminuria, endotheliosis
, diminished placental VEGF, and elevated levels of soluble VEGF receptor 1 (sFlt-1), with high fetal mortality.
(5,6) The proteinuria of preeclampsia is associated with a pathognomonic renal lesion known as glomerular endotheliosis
, in which the endothelial cells of the glomerulus swell and endothelial fenestrations are lost.