Published online Nov 6, 2013. doi: 10.5527/wjn.v2.i4.125
Revised: June 4, 2013
Accepted: September 3, 2013
Published online: November 6, 2013
Under common practice, the conventional diagnostic marker such as microalbuminuria determination does not recognized early stage of diabetic kidney disease (normoalbuminuria, chronic kidney disease stage 1, 2); due to the insensitiveness of the available marker. Treatment at later stage (microalbuminuria) simply slows the renal disease progression, but is rather difficult to restore the renal perfusion. Intrarenal hemodynamic study in these patients revealed an impaired renal perfusion and abnormally elevated renal arteriolar resistances. Treatment with vasodilators such as angiotensin converting enzyme inhibitor and angiotensin receptor blocker fails to correct the renal ischemia. Recent study on vascular homeostasis revealed a defective mechanism associated with an impaired nitric oxide production which would explain the therapeutic resistance to vasodilator treatment in microalbuminuric diabetic kidney disease. This study implies that the appropriate therapeutic strategy should be implemented at earlier stage before the appearance of microalbuminuria.
Core tip: This manuscript demonstrates the therapeutic resistance to vasodilator treatment in restoring the renal functions in microalbuminuric diabetic nephropathy. It is supported by the intrarenal hemodynamic study which reveals a decline in renal plasma flow, peritubular capillary flow and glomerular filtration rate following vasodilator treatment. The above finding concerns with the recent study on vascular homeostasis which reveals a defective angiogenesis associated with an impaired nitric oxide production, which explains the therapeutic resistance to vasodilator and clinical failure in restoring renal perfusion in late stage diabetic nephropathy.