Obstructive Uropathy

L‐carnitine improves oxidative stress and suppressed energy metabolism but not renal dysfunction following release of acute unilateral ureteral obstruction in rat

“…Complete ureteral obstruction causes a temporary increase of renal blood flow (RBF), followed by progressive vasoconstriction due to an imbalance between local production of vasoconstrictors and vasodilators, which results in a marked decline of glomerular filtration rate (GFR) and RBF by 24 hr after onset of obstruction 1. The decreased levels of RBF and GFR continued during early hours following the release of acute unilateral ureteral obstruction (UUO), such as 24 hr, in the post‐obstructed kidney (POK), which are also associated with largely reduced tubular transport of different solutes and water as well as urinary concentrating ability 2, 3. However, only slight renal structural and ultrastructural disruptions were observed at early time points following release of acute ureteral obstruction 4.…”

Pre- or post-treatment with aminoguanidine attenuates a renal distal acidification defect induced by acute ureteral obstruction in rats

“…It is probable that overproduction of NO by intensively induced iNOS expression in the early hours after release of a ureteral obstruction may inhibit eNOS activity, leading to unopposed vasoconstriction by pressor compounds, such as angiotensin-II and thromboxane-A 2 (Vaughan et al 2004;Klahr 2008), with the consequence of more hypofiltration of the POK. This suggestion is based on a peculiar phenomenon in the kidney that was previously addressed in various conditions, including ischemic acute renal failure (Noiri et al 1996), sepsis (Schwartz et al 1997), and tubulointerstitial nephritis (Gabbai et al 2002), in which the substantial concentration of NO produced by iNOS was hypothesized to autoinhibit eNOS but not iNOS, which required much higher NO concentrations to be inhibited (Griscavage et al 1993;Rengasamy and Johns 1993).…”

“…In addition, the contralateral normal kidney can perform a compensatory increase in function to prevent solute retention, volume expansion, acidemia, and uremia during the period of obstruction (Klahr 2008;Moosavi et al 2011;Frokiaer and Zeidel 2012). Following release of the UUO after 24 h, the large increases of urinary pH and fractional bicarbonate excretion in postobstructed kidney (POK) are in conjunction with the intensive declines of renal blood flow (RBF), glomerular filtration rate (GFR), sodium reabsorption, and urine osmolality (Klahr 2008;Moosavi et al 2011;Frokiaer and Zeidel 2012).…”

“…In addition, the contralateral normal kidney can perform a compensatory increase in function to prevent solute retention, volume expansion, acidemia, and uremia during the period of obstruction (Klahr 2008;Moosavi et al 2011;Frokiaer and Zeidel 2012). Following release of the UUO after 24 h, the large increases of urinary pH and fractional bicarbonate excretion in postobstructed kidney (POK) are in conjunction with the intensive declines of renal blood flow (RBF), glomerular filtration rate (GFR), sodium reabsorption, and urine osmolality (Klahr 2008;Moosavi et al 2011;Frokiaer and Zeidel 2012). The molecular mechanism of acute ureteral-obstruction-induced impairment in tubular transport of solutes and water was identified to be the suppressed membrane expression of several major Na + carriers, the Na + /K + -ATPase pump, urea transporters, and aquaporin water channels at different tubular segments (Li et al 2003a(Li et al , 2003b(Li et al , 2004Jensen et al 2006).…”

A case of acute kidney injury due to complex, partial, multifocal ureteral strictures

“…The differential diagnosis and pathogenesis of obstructive uropathy has been the subject of a number of review articles. [1][2][3][4] Differential diagnosis of acute kidney injury…”