[Acute obstructive nephropathy: A pathophysiological view]

Obstructive acute renal failure is a heterogeneous entity as the pathophysiology of intratubular obstruction is quite different from upper tract obstruction. In the former case, tubules are dilated due to a high hydrostatic pressure whereas pressures are normal in urinary upper tract. In the latter case, a high pressure above the ureteral obstacle is responsible for dilated renal cavities leading to extrinsic compression with no or only few dilated tubules though high hydrostatic pressure are recorded within tubules. Obstruction within tubules may be related to crystal formation, exfoliated cells, cellular debris and/or protein gels altogether with cell proliferation, proliferating cells, and recruitment of inflammatory cells. Though fibrosis may develop, the occurrence of atubular glomeruli in several nephrons due to an initial loss of tubular patency highlights the critical importance of maintaining a fluid flow within tubules in order to avoid uncontrolled tubular cell proliferation. The onset of tubular obstruction in few tubules, especially in crystal nephropathy is underestimated especially in chronic kidney disease patients, thus suggesting that some macromolecular solubilizing factors may be potential relevant therapy to prevent (and/or reverse) chronic kidney disease progression or decrease acute renal failure sequelae.