Check out this twitter feed I had done on the topic of Intravitreal Anti VEGF agents and the Kidney.
Showing posts with label VEGF. Show all posts
Showing posts with label VEGF. Show all posts
Saturday, March 30, 2024
Wednesday, September 28, 2011
In the NEWS: A novel treatment for Pre eclampsia- A renal method
Soluble fms-like tyrosine kinase 1 (sFlt-1), an alternatively spliced variant of the vascular endothelial growth factor receptor 1, induces a preeclampsia-like phenotype in experimental models and circulates at elevated levels in human preeclampsia. This is the factor that leads to decreased VEGF in pre eclampsia and causes the kidney related findings. Mice studies have shown that giving VEGF can alleviate the findings; but giving VEGF might pose significant risk to the fetus. Investigators at Harvard have shown for the first time that sFLT-1 can be removed via apheresis. Dextran sulfate apheresis lowered the levels of sFlt1 and reduced proteinuria, blood pressure and allowed for fetal growth in their observational paper. This pilot study is published in the August Circulation Issue and further testing is needed in a randomized fashion with more subjects to prove this will work.
Labels:
General Nephrology,
In The News,
pre eclampsia,
pregnancy,
sfLT-1,
VEGF
Tuesday, September 13, 2011
In The News:- HIV Nephropathy and other adverse risk factors
Incidence of HIV-associated
has been decreased significantly after advent of HAART. We hypothesized that
patients who has sustained podocyte HIV expression before the start of HAART
are vulnerable to develop HIV-associated nephropathy during the development of
adverse host factors such as the activation of renin-angiotensin-sytem (because
of the development of diabetes or loss of critical nephron mass as a result of
nephrotoxic drugs or trauma etc) , despite having undetectable viral load. Since
HIV patients are now living almost a normal life and are prone to develop
diabetes and hypertension, they are likely to develop the activation of the RAS
in their later life. To test our hypothesis, HIV transgenic Vpr mice (which display
doxycycline [Doxy] specific podocyte Vpr expression) with 2, 3, and 4
angiotensinogen (Agt) copies (Vpr-Agt-2, Vpr-Agt-3, and Vpr-Agt-4) were
administered Doxy for 3 weeks to manifest clinically occult (in situ) HIVAN
followed by Doxy-free water during the next 3 weeks. Subsequently, renal
biomarkers were collected and kidneys were harvested for renal histology. Vpr
mice with Agt copies did not develop proteinuria and blood pressure, and
displayed minimal glomerular and tubular lesions only, without any microcyst
formation. Vpr mice with 3 Agt copies showed mild glomeular and tubular lesions
and microcyst formation; whereas, Vp mice 4 Agt copies exhibited moderate
proteinuria, hypertension, glomerular sclerosis, tubular dilatation, microcysts
and expression of epithelial mesenchymal transition markers. Moreover, Vpr mice
4 Agt copies displayed enhanced renal tissue expression of Agt, renin, and ACE and
also showed higher (P<0.04) renal tissue concentration of Ang II. In
addition, renal cells in Vpr mice 4 Agt copies showed enhanced expression of
TGF-β, connective tissue growth factor, and vascular endothelial growth factor
(VEGF). These findings indicate that adverse host factors such as the
activation of the RAS, promotes the progression of clinically occult HIVAN to overt
HIVAN despite the absence of active viral activity. Thus, to prevent HIVAN
early detection of HIV infection (prior to renal cell infection) and treatment
would be important.
Post by Pravin Singhal, MD
Dr. Singhal is a NIH funded investigator in the Division of Kidney Diseases and Hypertension at the Hofstra NSLIJ School of Medicine, NY
Dr. Singhal is a NIH funded investigator in the Division of Kidney Diseases and Hypertension at the Hofstra NSLIJ School of Medicine, NY
Labels:
basic science,
glomerular diseases,
HIVAN,
In The News,
infections,
VEGF
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