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The present study investigated the prognostic factors predicting survival of patients with sepsis and acute kidney injury (AKI) undergoing continuous renal replacement therapy (CRRT). This retrospective observational study included 165 sepsis patients treated with CRRT. The patients were divided into two groups; the survivor group (n=73, 44.2%) vs. the nonsurvivor group (n=92, 55.8%). AKI was defined by the 2012 Kidney Disease: Improving Global Outcomes Clinical Practice Guidelines. We analyzed medical histories, clinical characteristics and laboratory findings of the enrolled patients when they started CRRT. In addition, we performed binary logistic regression and cox regression analysis. In the survivor group, urine output during the first day was significantly higher compared with the nonsurvivor group (55.7±66.3 vs. 26.6±46.4, p=0.001). Patients with urine output

A 71-year-old woman was admitted complaining of left flank pain, and presented with oliguria and hypotension. Pyuria and severe sepsis led to the diagnosis of acute pyelonephritis. An abdominal computed tomography intravenous pyelogram revealed normal-sized kidneys, however, the differentiation between cortex and medulla was poorly determined. The left kidney showed an amorphic, low attenuation lesion that was consistent with acute pyelonephritis (Fig. 1A). Both kidneys were incompletely malrotated and anteriorly facing hila were observed. The renal vessels and ureter were located laterally. The right kidney was 5 cm lower than the left kidney, indicating renal ectopia. Mild dilation was found at the proximal ureter of the left kidney. Additionally, a three-dimensional computed tomography reconstruction image showed anteriorly rotated kidneys (Fig. 1B). The patient initially received piperacillin-tazobactam empirically, then switched to cefotaxime after detecting an E. coli infection in the bloodstream. Three days later, her hemodynamic state had improved, and she was released from the intensive care unit.

The present study investigated the changes that occurred in the mammalian target of rapamycin (mTOR) signaling pathway in the kidney as a result of deoxycorticosterone acetate (DOCA)-salt hypertension. Rats were implanted with DOCA strips (200 mg/kg) 1 week after unilateral nephrectomy and were then supplied with 0.9% saline to drink. Four weeks after DOCA implantation, systolic blood pressure (SBP) was measured by use of the tail-cuff method. The expression levels of phosphorylated phosphatidylinositol-3-kinase (PI3K), Akt, and mTOR, as well as the protein expression levels of ED-1 and cyclooxygenase-2 (COX-2), transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (SMA), caspase-3, Bax, and Bcl-2, were then examined in the kidney by semiquantitative immunoblotting. DOCA-salt hypertensive rats were found to have significantly increased SBP as well as an increased kidney weight-to-body weight ratio. Moreover, the phosphorylation of PI3K, Akt, and mTOR was increased in the kidney of DOCA-salt hypertensive rats compared with the control, as was the protein expression of ED-1, COX-2, TGF-β1, and α-SMA. The expression levels of caspase-3 and Bax were increased significantly, whereas Bcl-2 expression was decreased. In conclusion, the phosphorylation of PI3K/Akt/mTOR was increased in the kidney of DOCA-salt hypertensive rats.