Kidney Week

Abstract: PUB325

High Serum Vascular Endothelial Growth Factor (VEGF) Level Is Associated with Vascular Lesions in Glomerular Diseases

Session Information

• Publication Only

Category: Glomerular Diseases

• 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

• Braga Barbosa, Gessica Sabrine, Universidade de Sao Paulo, Sao Paulo, Brazil

Gessica Sabrine Braga Barbosa, MD

• Zen, Renata De cassia, Universidade de Sao Paulo, Sao Paulo, Brazil

Renata De cassia Zen

• Dominguez, Wagner, Universidade de Sao Paulo, Sao Paulo, Brazil

Wagner Dominguez, MBChB

• Woronik, Viktoria, Universidade de Sao Paulo, Sao Paulo, Brazil

Viktoria Woronik, MD

• Dias, Cristiane B., Universidade de Sao Paulo, Sao Paulo, Brazil

Cristiane B. Dias, MD

Background

Vascular endothelial growth factor (VEGF) is a pro-angiogenic factor essential for vascular homeostasis. However, it has been pathogenically involved in tumor growth and diabetic retinopathy, which can be treated with VEGF inhibitors (VEGFi). The implication of VEGFi and kidney damage is well described, but the association between serum VEGF level (sVEGF) and histological vascular lesions in glomerular diseases is limited.

Methods

We evaluated sVEGF in patients with primary glomerular disease, including IgA nephropathy, focal segmental glomerulosclerosis, minimal change disease and membranous nephropathy at the time of kidney biopsy. We then analyzed the sVEGF in two comparative groups regarding the presence or absence of vascular lesions (VL) on renal histology. Patients under 50 years of age were included and those with diabetes, systemic autoimmune diseases and chronic infections were excluded.

Results

Of all patients with glomerular diseases (N=20), the median age was 31.5 years [27.2;43.5], with a predominance of females (55%) and white ethnicity (75%). Most patients had vascular lesions at the time of kidney biopsy (85%). The arterial intimal fibrosis/thickening was the most common lesion (88.2%), followed by arteriolar hyalinosis (29.4%) and thrombotic microangiopathy (5.8%). A higher sVEGF was detected in the group with VL (568.8 ± 97.0 vs 77.4 ± 13.8, p = 0.0001). Other laboratory findings at the time of kidney biopsy were as follows: proteinuria level 4.8g/g or g/24h [1.9;6.0], albumin level 2.4g/dL [1.7;3.2], serum creatinine level 1.24 mg/dL [0.88;2.6], hemoglobin level 11.8 g/dL [10.7;13.7], C3 level 125.5mg/dL [100.3;136.3], and C4 level 29.1mg/dL [22.3;40.2], no difference between the groups, except for the platelet level, which was higher in the VL group (337,000/mm³ vs 190,000/mm³, p = 0.019). There was no difference in the sVEGF or in the presence of VL between patients with a history of hypertension and those without.

Conclusion

Serum VEGF level is higher in glomerular diseases with histologic vascular lesions. More studies are needed to define the mechanisms of this increase and the relationship with glomerulopathies, whether it is a reparative effect, secondary or involved in the development of vascular lesion.

Funding

• Government Support – Non-U.S.