Livin is associated with the invasive and oncogenic phenotypes of human hepatocellular carcinoma cells.

AIM: Livin, a member of the inhibitors of apoptosis proteins, is expressed in variable cancers, and its expression is considered a poor prognostic marker. The aims of this study were to observe the effect of Livin on the behaviors of hepatocellular carcinoma (HCC) cells and to evaluate its expression in HCC tissues and its relation to prognosis. METHODS: The biological effects of Livin on tumor cell behavior were investigated using siRNA in HepG2 and Chang cells. Migration, invasion and proliferation assays were performed. Flow cytometric analyses and western blotting were used to evaluate the impact of Livin on apoptosis and the cell cycle. In addition, western blotting and immunohistochemistry were used to investigate Livin expression in HCC tissues. RESULTS: Livin knockdown suppressed tumor cell migration, invasion and proliferation in HCC cells, and increased the proportion of apoptotic cells as compared with scrambled siRNA-transfected HCC cells. Furthermore, Livin knockdown resulted in the activation of caspases and increased apoptosis. In addition, Livin knockdown modulated cell cycle regulatory protein levels such as decrease of cyclins and cyclin-dependent kinase (CDK) level, and increase of CDK inhibitor (CDKI) level in HCC cells. The Livin protein level was significantly elevated in HCC tissues as compared with normal hepatic tissues. However, Livin expression was not found to be associated with clinicopathological parameters, which included patient survival. CONCLUSION: These results suggest that Livin is associated with invasive and oncogenic phenotypes of human HCC cells.

Diffuse metastasis to the thyroid: unique ultrasonographic finding and clinical correlation.

Cases of metastases to the thyroid gland seem to be increasing in recent years. The clinical and ultrasonographic findings of diffuse metastases have been sparsely reported. Thirteen cases of diffuse metastases to the thyroid gland were documented by thyroid ultrasonography-guided fine needle aspiration cytology between 2004 and 2013. We retrospectively reviewed the patients with diffuse thyroid metastases. The most common primary site was the lung (n=9), followed by unknown origin cancers (n=2), cholangiocarcinoma (n=1), and penile cancer (n=1). Eleven patients were incidentally found to have thyroid metastases via surveillance or staging FDG-PET. Other 2 patients were diagnosed during work-up for hypothyroidism and palpable cervical lymph nodes. On ultrasonography, the echogenicity of the enlarged thyroid gland was heterogeneously hypoechoic or isoechoic, and reticular pattern internal hypoechoic lines were observed without increased vascularity found by power Doppler ultrasonography (3 right lobe, 2 left lobe, and 8 both lobes). In the 8 patients who had involvement of both lobes, 3 had hypothyroidism. In conclusion, ultrasonographic finding of diffuse metastasis is a diffusely enlarged heterogeneous thyroid with reticular pattern internal hypoechoic lines. Thyroid function testing should be performed in all patients with diffuse thyroid metastases, especially those with bilateral lobe involvement.

Prevalence and associations for abnormal bleeding times in patients with renal insufficiency.

Platelet dysfunction and associated hemorrhagic complications are often encountered in patients with chronic kidney disease. This study aimed to evaluate the prevalence and associations for abnormal bleeding time (BT) in patients with renal dysfunction. Hemoglobin, hematocrit, platelet, blood urea nitrogen, creatinine, and parathyroid hormone levels were determined in 1716 patients (55.18 ± 17.19 years, men 50.8%). For these patients, BTs were estimated using a platelet function analyzer-100. Glomerular filtration rates (GFRs) were estimated using the Chronic Kidney Disease Epidemiology Collaboration equation. The study population was divided into six groups according to the estimated GFR (eGRF): group I, eGFR ≥ 90 ml/min/1.73 m(2); group II, 60 ≤ eGFR < 90 ml/min/1.73 m(2); group III, 30 ≤ eGFR < 60 ml/min/1.73 m(2); group IV, 15 ≤ eGFR < 30 ml/min/1.73 m(2); group V, eGFR < 15 ml/min/1.73 m(2); and group VI, undergoing regular hemodialysis. Renal insufficiency was defined as eGFR < 60 ml/min/1.73 m(2). To further investigate the role of inflammatory cytokines, nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) were measured in a 327-patient subset of the total patient population (52.82 ± 18.3 years, men 60.9%). Abnormal BT occurred in 11.8% of group I, 15.3% of group II, 29.1% of group III, 37.5% of group IV, 35.0% of group V, and 32.1% of group VI. By Pearson correlation coefficient, eGFR (r = -0.089), hemoglobin (r = -0.127), platelet (r = -0.054) were correlated with BT. Multivariate analysis revealed that age [odds ratio (OR), 1.013; 95% CI, 1.004-1.022], renal insufficiency (eGFR < 60 ml/min/1.73 m(2); OR, 2.271; 95% CI, 1.672-3.083), anemia (hemoglobin < 120 g/l; OR, 1.486; 95% CI, 1.089-2.027), and thrombocytopenia (platelet < 150 × 10(9)/l; OR, 1.445; 95% CI, 1.089-1.918) were independently associated with prolonged BT. Plasma levels of NO and TNF-α were increased in patients with renal insufficiency (eGFR < 60 ml/min/1.73 m(2)). Plasma levels of NO in renal insufficiency group were higher in prolonged BT than those in normal BT. A significant positive correlation was noted between BTs and NO levels (r = 0.152, p = 0.009) but not with TNF-α levels. The prevalence of abnormal BTs was higher as eGFR declined. Old age, renal insufficiency, anemia, and thrombocytopenia were independent associations for abnormal BT.

HBV reactivation risk factors in patients with chronic HBV infection with low replicative state and resolved HBV infection undergoing hematopoietic stem cell transplantation in Korea.

PURPOSE: To elucidate the rate and risk factors of HBV reactivation in patients with chronic HBV infection with low replicative state and resolved HBV infection undergoing allogenic/autologous hematopoietic stem-cell transplantation (HSCT) in Korea. METHODS: The medical charts of 506 patients who underwent allogenic/autologous HSCT from January 2008 to December 2013 were analyzed retrospectively. We examined the reactivation rate and variables related to the risk of HBV reactivation, with a median follow-up period of 41.8 (1-245) months. Univariate analysis was used to identify any factors associated with HBV reactivation. Factors that were significant in the univariate analysis were entered into a stepwise multivariate analysis to find the most significant risk factors associated with HBV reactivation. RESULTS: The reactivation rate of HBV in patients who underwent HSCT was 4.2 % (21/506). In subgroup analysis, the HBV reactivation rate (14.3 %) was the highest among HBsAg(+) patients (5/35). The reactivation rate of HBV in patients with resolved HBV infection [HBsAg(-)/HBcAb(+) with or without anti-HBs antibody] was 5.9 % (10/171). In univariate analysis for risk factors of HBV reactivation in patients who underwent HSCT, initial detectable HBV DNA (p = 0.004), age (≥60 years) (p = 0.012), recipient hepatitis B surface antigen-positive (HbsAg)(+) before HSCT (p = 0.004), recipient hepatitis B surface antibody-negative (HBsAb)(-) before HSCT (p = 0.005), recipient hepatitis B core antibody-positive (HbcAb)(+) before HSCT (p = 0.013), and donor HBsAg(+) (p < 0.001) were associated with reactivation of HBV. In multivariate analysis, significant risk factors of HBV reactivation in patients who underwent HSCT were old age (≥60 years) (p = 0.032) and donor HBsAg(+) (p = 0.026). CONCLUSION: Old age (≥60 years) and donor HBsAg(+) were risk factors for HBV reactivation in HSCT patients. Preemptive antiviral treatment should be considered in these patients.

Impact of KITENIN on tumor angiogenesis and lymphangiogenesis in colorectal cancer.

Angiogenesis and lymphangiogenesis are involved in the dissemination of tumor cells from solid tumors to regional lymph nodes and various distant sites. KAI1 COOH-terminal interacting tetraspanin (KITENIN) contributes to tumor progression and poor clinical outcomes in various cancers including colorectal cancer. The aim of the present study was to evaluate whether KITENIN affects tumor angiogenesis and lymphangiogenesis in colorectal cancer. A KITENIN small interfering RNA vector was used to silence KITENIN expression in colorectal cancer cell lines including DLD1 and SW480 cells. To evaluate the ability of KITENIN to induce angiogenesis and lymphangiogenesis in human umbilical vein endothelial cells (HUVECs) and lymphatic endothelial cells (HLECs), we performed Matrigel invasion and tube formation assays. Immunohistochemistry was used to determine the expression of KITENIN in colorectal cancer tissues. Angiogenesis and lymphangiogenesis were evaluated by immunostaining with CD34 and D2-40 antibodies. KITENIN silencing inhibited both HUVEC invasion and tube formation in the DLD1 and SW480 cells. KITENIN silencing led to decreased expression of the angiogenic inducers vascular endothelial growth factor (VEGF)-A and hypoxia-inducible factor-1α and increased expression of the angiogenic inhibitor angiostatin. KITENIN silencing did not inhibit either HLEC invasion or tube formation in all tested cells, but it resulted in decreased expression of the lymphangiogenic inducer VEGF-C. KITENIN expression was significantly associated with tumor stage, depth of invasion, lymph node and distant metastases and poor survival. The mean microvessel density was significantly higher in the KITENIN-positive tumors than that in the KITENIN-negative tumors. However, the mean lymphatic vessel density of KITENIN-positive tumors was not significantly higher than that of the KITENIN-negative tumors. These results suggest that KITENIN promotes tumor progression by enhancing angiogenesis in colorectal cancer.

Hepatic Hemangioma with Kasabach-Merritt Syndrome in an Adult Patient.

Hemangiomas are the most common benign tumors of the liver. They are generally asymptomatic, but giant hemangiomas can lead to abdominal discomfort, bleeding, or obstructive symptoms. Kasabach-Merritt syndrome is a rare but life-threatening complication of hemangioma, characterized by consumptive coagulopathy with large vascular tumors. More than 80% of Kasabach-Merritt syndrome cases occur within the first year of life. However, there are few reports of Kasabach-Merritt syndrome with giant hepatic hemangioma in adults and, as far as we know, no reports of Kasabach-Merritt syndrome with hepatic hemangioma treated with first line medical treatment only. The most important treatment for this syndrome is removal of the large vascular tumor. However, surgical treatment entails risk of bleeding, and the patient's condition can mitigate against surgery. We herein present a case of unresectable giant hepatic hemangioma with disseminated intravascular coagulopathy. The patient was a 60-year-old woman who complained of hematochezia, ecchymosis, and abdominal distension. She refused all surgical management and was therefore treated with systemic glucocorticoids and beta-blockers. After two weeks of steroid therapy, she responded partially to the treatment. Her laboratory findings and hematochezia improved. She was discharged on hospital day 33 and observed without signs of bleeding for three months.

Impact of prospero homeobox-1 on tumor cell behavior and prognosis in colorectal cancer.

Prospero homeobox 1 (PROX1) is up-regulated in colorectal cancer and plays an oncogenic role. In the present study, we sought to investigate the impact of PROX1 on oncogenic processes and to assess the prognostic value of PROX1 expression in colorectal cancer. A small interfering RNA or pcDNA6-myc vector was used to control PROX1 gene expression in colorectal cancer DLD1 and SW480 cell lines. The expression of PROX1 in colorectal cancer tissues was investigated by immunohistochemistry. Angiogenesis, lymphangiogenesis, and tumor cell proliferation were assessed by analyzing the expression of respective markers of these phenomena, CD34, D2-40, and Ki-67 after immunohistochemical staining. PROX1 knockdown decreased both umbilical vein endothelial cell invasion and tube formation, down-regulated the expression of VEGF-A and HIF-1α, and up-regulated the expression of angiostatin. Lymphatic endothelial cell invasion and tube formation as well as the expression of VEGF-C were also suppressed by PROX1 knockdown. PROX1 knockdown suppressed tumor cell proliferation, migration, invasion, and epithelial-mesenchymal transition. In contrast, PROX1 overexpression enhanced tumor cell angiogenesis, lymphangiogenesis, proliferation, migration, invasion, and epithelial-mesenchymal transition. Levels of phosphorylated Akt, GSK3ß, and MAPK were decreased by PROX1 knockdown and increased by PROX1 overexpression. PROX1 expression positively correlated with tumor size, extent of differentiation, lymphovascular invasion, depth of invasion, lymph node metastasis, stage, and poor survival. The mean microvessel density and Ki-67 labeling index values of PROX1-positive tumors were significantly higher than those of PROX1-negative tumors. However, there was no significant correlation between PROX1 expression and lymphatic vessel density. These results indicate that PROX1 influences tumor progression in colorectal cancer by regulating angiogenesis and tumor cell proliferation.

Endoscopic ultrasonographic characteristics of gastric schwannoma distinguished from gastrointestinal stromal tumor.

BACKGROUND/AIMS: Gastric schwannoma (GS), a rare neurogenic mesenchymal tumor, is usually benign, slow-growing, and asymptomatic. However, GS is often misdiagnosed as gastrointestinal stromal tumors (GIST) on endoscopic and radiological examinations. The purpose of this study was to evaluate EUS characteristics of GS distinguished from GIST. METHODS: A total of 119 gastric subepithelial lesions, including 31 GSs and 88 GISTs, who were histologically identified and underwent EUS, were enrolled in this study. We evaluated the EUS characteristics, including location, size, gross morphology, mucosal lesion, layer of origin, border, echogenic pattern, marginal halo, and presence of an internal echoic lesion by retrospective review of the medical records. RESULTS: GS patients comprised nine males and 22 females, indicating female predominance. In the gross morphology according to Yamada's classification, type I was predominant in GS and type III was predominant in GIST. In location, GSs were predominantly located in the gastric body and GISTs were predominantly located in the cardia or fundus. The frequency of 4th layer origin and isoechogenicity as compared to the echogenicity of proper muscle layer was significantly more common in GS than GIST. Although not statistically significant, marginal halo was more frequent in GS than GIST. The presence of an internal echoic lesion was significantly more common in GIST than GS. CONCLUSIONS: The EUS characteristics, including tumor location, gross morphology, layer of origin, echogenicity in comparison with the normal muscle layer, and presence of an internal echoic lesion may be useful in distinguishing between GS and GIST.

Clinical impact of prophylactic antibiotic treatment for self-expandable metallic stent insertion in patients with malignant colorectal obstruction.

Purpose. The aim of this study was to determine the efficacy of prophylactic antibiotics (PA) for reducing the infectious complications and the potential risk factors responsible for the infectious complications after stent insertion for malignant colorectal obstruction. Methods. We performed a retrospective review of 224 patients who underwent self-expandable metallic stent (SEMS) insertion for malignant colorectal obstruction from May 2004 to December 2012. Results. There were 145 patients in the PA group and 79 in non-PA group. The CRP level in PA group was significantly higher than that in non-PA. Abdominal tenderness and mechanical ileus were significantly more frequent in PA group than those in non-PA. The frequency of post-SEMS insertion fever, systemic inflammatory response syndrome (SIRS), and bacteremia was not significantly different between PA and non-PA groups. In multivariate analysis, the CRP level was risk factor related to post-SEMS insertion SIRS. However, in propensity score matching analysis, there was no independent risk factor related to post-SEMS insertion fever, SIRS, and bacteremia. Conclusion. The use of PA in patients with malignant colorectal obstruction may be not effective to prevent the development of infectious complications after SEMS insertion.

Myeloid cell leukemia-1 promotes epithelial-mesenchymal transition of human gastric cancer cells.

Epithelial-mesenchymal transition (EMT) is a critical process that occurs during cancer progression, and cancer stem cells have been shown to acquire the EMT phenotype. Myeloid cell leukemia-1 (Mcl-1) has been implicated in cancer progression and is overexpressed in a variety of human cancers. However, the interaction between Mcl-1 and EMT in human gastric cancer (GC) is unclear. We investigated the impact of Mcl-1 expression levels on EMT and the underlying signaling pathways in human GC cells. We used the human GC cell lines, AGS and SNU638, and small interfering RNAs (siRNAs) to evaluate the effects of Mcl-1 knockdown on cell adhesion, migration and invasion. Expression of Mcl-1 and other target genes was determined using reverse transcription-polymerase chain reaction assays and western blotting. The results revealed that expression levels of Mcl-1 mRNA and protein in the AGS and SNU638 cells were reduced following transfection with Mcl-1 siRNAs. Knockdown of Mcl-1 led to increased cellular adhesion to fibronectin and collagen. Expression levels of vimentin, MMP-2, MMP-9 and Snail protein were decreased following knockdown of Mcl-1. However, expression of E-cadherin was increased in the AGS cells following knockdown of Mcl-1. The expression of cancer stemness markers, such as CD44 and CD133, was not altered by knockdown of Mcl-1. Knockdown of Mcl-1 suppressed tumor cell migration and invasion in both human GC cell lines. Signaling cascades, including the ß-catenin, MEK1/2, ERK1/2 and p38 pathways, were significantly blocked by knockdown of Mcl-1. Our results indicate that Mcl-1 expression induces EMT via ß-catenin, MEK1/2 and MAPK signaling pathways, which subsequently stimulates the invasive and migratory capacity of human GC cells.

Myeloid cell leukemia-1 is associated with tumor progression by inhibiting apoptosis and enhancing angiogenesis in colorectal cancer.

Myeloid cell leukemia-1 (Mcl-1) is a highly expressed anti-apoptotic Bcl-2 protein in cancer. Therefore, inhibition of its expression induces apoptosis in cancer cells and enhances sensitivity to cancer treatment. The aims of this study were to evaluate whether Mcl-1 affects the oncogenic behaviors of colorectal cancer cells, and to document the relationship of its expression with various clinicopathological parameters in colorectal cancer. Mcl-1 knockdown induced apoptosis by activating cleaved caspase-3 and -9, and increasing the expression of the pro-apoptotic protein, PUMA. Mcl-1 knockdown induced cell cycle arrest by decreasing cyclin D1, CDK4 and 6, and by increasing p27 expression. Mcl-1 knockdown decreased both endothelial cell invasion and tube formation, and decreased the expression of VEGF. The phosphorylation level of STAT3 was decreased by Mcl-1 knockdown. The mean apoptotic index value of Mcl-1 positive tumors was significantly lower than that of Mcl-1 negative tumors. The mean microvessel density value of Mcl-1 positive tumors was significantly higher than that of negative tumors. Mcl-1 expression was significantly increased in colorectal cancer, also associated with tumor stage, lymph node metastasis, and poor survival. These results indicate Mcl-1 is associated with tumor progression through its inhibition of apoptosis and enhancement of angiogenesis in colorectal cancer.

Association between interleukin-18 gene polymorphism and Helicobacter pylori infection in the Korean population.

Interleukin-18 (IL-18) is a pleiotropic, pro-inflammatory cytokine that is capable of promoting the Th1 response. A predominant Th1 response induces chronic and persistent inflammatory changes in the gastric mucosa in response to Helicobacter pylori (H. pylori) infection. The aim of this study was to investigate the potential association between IL-18 gene polymorphisms and susceptibility to H. pylori infection in the Korean population. A total of 678 subjects who underwent a routine health check-up were enrolled. The IL-18 gene polymorphisms at positions -656, -607, -137, +113, and +127 were genotyped. H. pylori positivity was demonstrated in 456 subjects (67.3%). The allele frequencies of IL-18 gene polymorphisms at position -137 (rs187238) were different based on the status of H. pylori infection (G vs. C, adjusted OR 0.64 CI: 0.47-0.87, P = 0.005). The results indicate that the genetic variants in the IL-18 gene may be associated with susceptibility to H. pylori infection in the Korean population, suggesting that IL-18 plays a role in the pathogenesis of H. pylori-associated diseases. However, this finding requires further replication and validation.

Myeloid cell leukemia-1 regulates the cell growth and predicts prognosis in gastric cancer.

The expression of myeloid cell leukemia-1 (Mcl­1), a member of the anti-apoptotic Bcl-2 protein family, has been associated with tumor progression and adverse patient outcome. The aims of current study were to evaluate whether Mcl-1 affects the survival or death of gastric cancer cells, and to investigate the prognostic value of its expression in gastric cancer. PcDNA3.1-Mcl-1 expression and Mcl-1 siRNA vectors were used to overexpress and silence Mcl-1 expression in gastric cancer cell lines including SNU638 and TMK1, respectively. Immunohistochemistry was used to determine the expression of Mcl-1 in gastric cancer tissues. Apoptosis was determined by the TUNEL assay, and cell proliferation was determined by immunostaining with a Ki-67 antibody. Mcl-1 knockdown induced apoptosis through the upregulation of caspase-3, and -7, and PARP activity, and the release of Smac/DIABLO and Omi/HtrA2 into the cytoplasm. Additionally, cell cycle arrest occurred due to decrease of cyclin D1, cell division cycle gene 2 (cdc2), and cyclin-dependent kinase 4 and 6. In contrast, overexpression of Mcl-1 inhibited apoptosis and cell cycle arrest. Mcl-1 knockdown did not suppress tumor cell proliferation in gastric cancer cells, whereas overexpression of Mcl-1 enhanced tumor cell proliferation. The JAK2 and STAT3 signaling cascades were significantly blocked by Mcl-1 knockdown. The mean Ki-67 labeling index (KI) value of Mcl-1 positive tumors was significantly lower than that of Mcl-1 negative tumors. However, there was no significant difference between Mcl-1 expression and the apoptotic index (AI). Mcl-1 expression was significantly increased in gastric cancer tissues compared to normal gastric mucosa tissues, and was associated with age, tumor size, stage, depth of invasion, lymph node metastasis and poor survival. Our study showed that Mcl-1 regulates the cell growth and might be a potential prognostic marker for gastric cancer.

Relation of serum potassium level to long-term outcomes in patients with acute myocardial infarction.

Potassium plays a key role in normal myocardial function, and current guidelines recommend that serum potassium levels be maintained from 4.0 to 5.0 mEq/L in patients with acute myocardial infarction (AMI). However, the impact of serum potassium levels on long-term mortality has not been evaluated. We retrospectively studied 1,924 patients diagnosed with AMI. The average serum potassium levels measured throughout the hospitalization were obtained and statistically analyzed. Patients were categorized into 5 groups to determine the relation between mean serum potassium and long-term mortality: <3.5, 3.5 to <4.0, 4.0 to <4.5, 4.5 to <5.0, and ≥5 mEq/L. The long-term mortality was lowest in the group of patients with potassium levels of 3.5 to <4.0 mEq/L, whereas mortality was higher in the patients with potassium levels≥4.5 or <3.5 mEq/L. In a multivariate Cox-proportional regression analysis, the mortality risk was greater for serum potassium levels of >4.5 mEq/L (hazard ratio [HR] 1.71, 95% confidence interval [CI] 1.04 to 2.81 and HR 4.78, 95% CI 2.14 to 10.69, for patients with potassium levels of 4.5 to <5.0 mEq/L and ≥5.0, respectively) compared with patients with potassium levels of 3.5 to <4.0 mEq/L. The mortality risk was also higher for patients with potassium levels<3.5 mEq/L (HR 1.55, 95% CI 0.94 to 2.56). In contrast to the association with long-term mortality, there was no relation between serum potassium levels and the occurrence of ventricular arrhythmias. The results of the current analysis suggest that there is a need for change in our current concepts of the ideal serum potassium levels in patients with AMI.

Benign teratoma of the thyroid gland.

Although pathology reports of thyroid tissue in ovarian teratomas are abundant, benign teratomas of the thyroid are extremely rare in adolescents and adults. Therefore, their clinical characteristics are still not well characterized. We report a case of a 54-year-old woman with a growing mass in her neck. Left lobectomy of the thyroid revealed it to be a benign thyroid teratoma composed of tissues from all three germ layers. Preoperative evaluations included thyroid ultrasonography (US), ultrasound-guided fine needle aspiration cytology (FNAC), and computed tomography (CT) of the neck. A 4.7-cm, well defined, predominantly hypoechoic mass intermingled with hyperechoic internal lesions, was observed in the inferior portion of the left thyroid lobe with substernal extension on US. The posterior extent of the nodule was not visualized due to deep attenuation of the echo. US-guided FNAC failed to reveal any thyroid follicular cells, but suggested a benign cystic tumor. Neck CT hinted at the diagnosis of teratoma because the mass contained large amounts of fat, and the margin was well defined. Extrathyroidal extension and cervical lymphadenopathy were not seen. She underwent left thyroid lobectomy, and histologic examination confirmed benign thyroid teratoma. To the best of our knowledge, this is the first case report of benign thyroid teratoma in Korea.

Incidence, predictive factors, and clinical outcomes of acute kidney injury after gastric surgery for gastric cancer.

BACKGROUND: Postoperative acute kidney injury (AKI), a serious surgical complication, is common after cardiac surgery; however, reports on AKI after noncardiac surgery are limited. We sought to determine the incidence and predictive factors of AKI after gastric surgery for gastric cancer and its effects on the clinical outcomes. METHODS: We conducted a retrospective study of 4718 patients with normal renal function who underwent partial or total gastrectomy for gastric cancer between June 2002 and December 2011. Postoperative AKI was defined by serum creatinine change, as per the Kidney Disease Improving Global Outcomes guideline. RESULTS: Of the 4718 patients, 679 (14.4%) developed AKI. Length of hospital stay, intensive care unit admission rates, and in-hospital mortality rate (3.5% versus 0.2%) were significantly higher in patients with AKI than in those without. AKI was also associated with requirement of renal replacement therapy. Multivariate analysis revealed that male gender; hypertension; chronic obstructive pulmonary disease; hypoalbuminemia (<4 g/dl); use of diuretics, vasopressors, and contrast agents; and packed red blood cell transfusion were independent predictors for AKI after gastric surgery. Postoperative AKI and vasopressor use entailed a high risk of 3-month mortality after multiple adjustments. CONCLUSIONS: AKI was common after gastric surgery for gastric cancer and associated with adverse outcomes. We identified several factors associated with postoperative AKI; recognition of these predictive factors may help reduce the incidence of AKI after gastric surgery. Furthermore, postoperative AKI in patients with gastric cancer is an important risk factor for short-term mortality.