An insight into chronic kidney diseas (CKD) through an unbalanced angiogenesis

Elham Farsi


EMAN Research and Testing Laboratory, Department of Pharmacology, School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia

*Corresponding Author. E-mail:


Angiotherapy, 2017, 1(1), 036–038. (Received 11 September 2016, Published 10 May 2017).


Citation: Elham Farsi. (2017). An insight into chronic kidney disease (CKD) through balanced angiogenesis , 1(1), pages 036-038.


Recent research data and supporting animal studies have shown that acute kidney injury (AKI) can eventually lead to chronic kidney disease (CKD). Moreover, the frequency of kidney transplants as result of CKD have been increasing daily. Various renal disorders result in end stage renal failure (ESRF) including glomerulonephritis, hypertensive nephrosclerosis and diabetic nephropathy (Levey and Coresh 2012). Chronic kidney disease involves conditions such as glomerulonephritis, glomerular endothelial cell injuries accompanies mesangial alterations or extracapillary lesions. To retrieve the glomerular endothelial cells in these models, angiogenesis stimulation is required to promote glomerular endothelial repair in association with accelerated resolution of nephritic alterations. The level of angiogenic signal should be adjusted according to the type and the stage of disease, to avoid an imbalance of pro / antigrowth and promotion of other pathologic condition as result of excessive angiogenesis (Goligorsky 2015; Levey and Coresh 2012) . The development of new blood vessels, termed angiogenesis is responsible for several physiological and pathological events such as tumor growth and metastasis, proliferative retinopathy, rheumatoid arthritis, psoriasis and neointimal formation (Risau 1997). This process is controlled by pro and anti- growth factors and it is directly associated with the development of renal failure. Consequently, balanced ratios of these factors control severe renal conditions (Carmeliet 2003) The deregulated expression of factorsinhibitors ends in pathological conditions, like inflammation. Although findings about the biological role of angiogenesis factors in CKD are relatively limited, therapeutic effects have been reported for angiogenesis factors in experimental diabetic nephropathy models. Angiogenesis inhibitors exhibit therapeutic effects on diabetic nephropathy by anti-angiogenic and anti-inflammatory mechanisms. These effects highlight the importance of a tight regulation of angiogenic factors and inhibitors (Tanaka and Nangaku 2013).


Keywords: Chronic Kidney Disease, Angiogenesis