Renal microvascular and tubular injuries in type II diabetic nephropathy

Abstract

To the Editor: We read Verzola et al.'s1 article with great interest. The authors have pointed out the significance of glomerular cell injury and a correlation between the renal microvascular injury and the magnitude of tubulointerstitial fibrosis in type II diabetic nephropathy. Such correlation is further supported by recent intrarenal hemodynamic study, which reveals a phenomenon the so-called hemodynamic maladjustment secondary to glomerular endothelial cell dysfunction, which is characterized by a preferential constriction of the efferent arteriole, and a subsequent reduction in peritubular capillary flow inducing a chronic ischemic injury to the tubulointerstitium.2 The peritubular capillary flow reduction correlates inversely with the magnitude of tubulointerstitial fibrosis, and it progressively decreases as the disease severity increases from normoalbuminuric to albuminuric type II diabetic nephropathy. Thus, renal microvascular injury has a significant impact on renal disease progression. In this regard, it is mandatory to recognize renal microvascular disease at an early stage of type II diabetic nephropathy in which the mechanism of vascular repair is still adequately maintained,3 and treatment at this early stage under favourable environment is capable of restoring renal perfusion and function.4 To accomplish an effective preventive strategy of renal disease progression in type II diabetic nephropathy, it would require a more sensitive diagnostic marker than microalbuminuria, such as fractional excretion of magnesium, to screen early stage of diabetic nephropathy.5