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Abstract Angiogenesis, a physiological response to ischemia, is regulated by many angiogenic inducers and antiogenic inhibitors . Imbalance between these angiogenic factors results in various pathologic condition. The aim of the work to review the possible role of angiogenesis in the development and \ or progression of various renal disorders and its implications. In kidney, impaired angiogenesis may cause development and /or progression of renal disease e g: During the healing phase of acute and chronic inflammatory renal disease, deficiency of EPCs results in cell death and development of CKD In stenotic kidney [RAS] , reduction of VEGF causes microvascular loss and progression of renal injury. In stenotic kidney [RAS] , intrarenal administration of VEGF prevent MV rarefaction thereby contributing to preservation of the blood supply and renal perfusion, and filtration function and a decreaPse in fibrosis .These findings underscore the role of VECF in the stenotic kidney and indicate feasibility and potential of a novel therapeutic approach for management of patients with chronic renovascular disease. In ADPKD , angiogenesis stimulates cyst cell proliferation and cyst growth replacing the native tissue conducting to renal failure. In CKD, imbalance in the expression of angiogenic factors [i e .loss of intrinsic VEGF expression and an increase in local TSp-1 expression] contribute to loss of microvascular and progressive renal disease. The therapeutic value of angiogenesis in treating renal diseases is a new target in recent years. Rcently, modulation of angiogenic factors is a new target in treating renal diseases as : Stimulation of angiogenesis by direct transfere of EPCs, or VEGF into the kidney can stabilize renal function, slow histologic progression and prevent renal detoriation in early stage of CKD and in chronic renovascular disease. Inhbition of angiogenesis exhibites therapeutic effects on diabetic nephropathy and on ADPKD. On the other hand, the use of angiogenesis inhibitors is not without risk. Sorafenib [anti-antigenic agent] cause a unique combination of acute thrombotic microangiopathy and minimal change disease [MCD] resulting in renal failure and nephrotic syndrome. |