Chronic kidney fibrosis is the unifying pathological feature of diverse renal disease leading to a progressive decline in renal function and eventually end-stage kidney failure. Many growth factors are able to induce an imbalance of extracellular matrix production and degradation, leading to excessive matrix and fibrosis in both glomeruli and in the tubulointerstitium. Over the last decade the role of connective tissue growth factor (CTGF) in renal fibrosis has been intensively studied. CTGF participates in cell proliferation, migration, and differentiation and mediates profibrotic activity by acting either directly, or as a co-factor for TGF beta 1, which is well characterised as a key cytokine mediating both the induction and promotion of fibrogenesis. CTGF also has the potential to modulate factors such as VEGF and bone morphogenic proteins, which are integral to both the development and repair process inherent in renal fibrogenesis. This review focuses on the role of CTGF in renal fibrosis and specifically its role in inducing fibrosis by factors integrally involved in the development of diabetic nephropathy, namely high glucose, angiotensin II, TGF beta 1 and AGEs.