WCIM 2014 SEOUL KOREA 175
Poster Session
The Korean Journal of Internal Medicine Vol. 29, No. 5 (Suppl. 1)
PS 0496 Nephrology
Hemorrhagic Fever with Renal Syndrome in Korean Tertiary Military Hospital: The Clinical and Molecular Features
Yong Chul KIM1, Min-Jeong SON1 The Armed Forces Capital Hospital, Korea1
Background: Hantavirus, a rodent-borne virus, is the etiologic agent for hemorrhagic fever with renal syndrome (HFRS). HFRS is characterized by fever, thrombocytopenia and acute kidney injury. However, there are few recent studies on clinical and molecu- lar epidemiologic trends of HFRS in Korea.
Methods: Medical records of HFRS patients, who were admitted to a tertiary military hospital during January 2012 to December 2013, were reviewed. Sera from patients were tested for Hantaan virus (HTNV) RNA using RT-PCR.
Results: Among 21 patients, mean age was 21.7 ± 4.82, all of them were male solders.
Initial serum creatinine was 1.10 ± 0.40 mg/dL, and acute kidney injury was developed in 19 patients (90%). Peak creatinine during admission was 2.47 ± 1.99 mg/dL, two patients had emergent hemodialysis (9.5%) and one patient died (4.8%). Mean du- ration of admission was 11.2 ± 2.4 days and there were no sequlae of chronic kidney disease. Phylogenic tree of the viruses showed there was no major variation compared with previous HTNV sequences, and the viruses which was used to make HTNV vac- cines.
Conclusions: There are still large numbers of HFRS patients in Korean civilians and military croups. More efforts are necessary to establish accurate diagnosis, effective prevention including vaccines and proper treatment for hantavirus infection.
PS 0497 Nephrology
Paricalcitol Pretreatment Attenuates Apoptosis and Infl ammation in Renal Ischemia-Reperfusion Injury via Prostaglandin E2 Receptor Ep4
Hyeon Seok HWANG1, Keum Jin YANG2, Sung Eun KIM2, Ki Cheol PARK2, Hyun Soo CHOI2, Jeong Min OH2, Yoon Kyung CHANG1, Cheol Whee PARK1, Chul Woo YANG1, Suk Young KIM1 Division of Nephrology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Korea1, Daejeon St. Mary`s Hospital, Korea2
Background: Paricalcitol has protective effects against renal ischemia-reperfusion (IR) injury, but the mechanism by which this occurs remains unclear. We investigated whether paricalcitol attenuates apoptosis and infl ammation in renal IR injury through the prostaglandin E2 (PGE2) receptor EP4.
Methods: Human proximal tubular cell line (HK-2) was exposed to LPS and ischemia by mineral oil monolayer. Male C57BL/6 mice were subjected to 23 min of bilateral kidney ischemia and 24 h reperfusion. The effects paricalcitol pretreatment with or without antagonist was investigated in both in vitro and in vivo models.
Results: Paricalcitol treatment upregulated the signaling pathway of cyclooxygenase (COX)-2 and PGE2, and it increased the expression of EP4 in HK-2 cells. Paricalcitol pretreatment prevented the HK-2 cell death induced by IR and LPS exposure, and the cotreatment of EP4-specifi c antagonist offset the cell protective effects of parical- citol. The phosphorylation of Akt and cAMP-responsive element binding protein was increased after paricalcitol pretreatment in IR-exposed cells. EP4 antagonist blunted the phosphorylation of these cell survival signals. EP4 antagonist also reversed the inhibitory effects of paricalcitol on p65 NF-κB phosphorylation and nuclear translo- cation in LPS-exposed cell. In mice kidneys with IR injury, EP4 blockade restored serum creatinine levels and tubular necrosis, which was reduced by paricalcitol pretreatment.
Decreased TUNEL-positive cells, decreased Bax levels and increased Bcl-2 expression were observed in paricalcitol-treated mice kidney with IR injury. These apoptotic effects of paricalcitol were abolished by EP4 antagonist. Paricalcitol attenuated the infiltration of inflammatory cells (T-cells and macrophages) and the production of proinfl ammatory cytokines (RANTES, tumor necrosis factor-a, interleukin-1ß and in- terferon-γ, MIP-1a). The cotreatment with EP4 antagonist reversed the infl ammatory cells infi ltration and proinfl ammatory cytokines expressions.
Conclusions: Paricalcitol attenuates apoptosis and infl ammation through the EP4 de- pendent pathway in renal IR injury.
PS 0498 Nephrology
Endothelial Dysfunction According to Classifi cation of Serum Phosphorus Level within Normal Range in Chronic Kidney Disease
Shina LEE1, Jung-Hwa RYU1, Hee Sung GO1, Seung-Jung KIM1, Duk-Hee KANG1, Dong-Ryeol RYU1, Kyu Bok CHOI1
Ewha Womans University Mokdong Hospital, Korea1
Background: Hyperphosphatemia is important problem because of its affect on en- dothelial dysfunction as well as homeostasis of bone. Chronic kidney disease(CKD) pa- tients tend to have higher serum phosphorus values than those in healthy population due to their positive balance of phosphorus in kidney. There are a few studies which reported that serum phosphorus level was correlated with endothelial function. Re- cently it has been reported the patients with higher serum phosphorus level revealed the more endothelial dysfunction in healthy population. Thus, the following study was carried out in an effort to redefi ne the relationship between serum phosphorus level and endothelial dysfunction to those on chronic kidney disease.
Methods: This is a cross-sectional study and the enrolled 79 CKD patients with ex- ception of CKD stage 5 or receiving renal replacement therapy. They were subjected to the measurement with iontophoresis, and endoPAT, ankle brachial index, which repre- sented endothelial function assessment. And also the average serum phosphrous level in patients was measured for the last three months including examination month. The Pearson’s correlation coeffi cient analysis was performed to defi ne the association of serum phosphorus and endothelial function.
Results: When participants were divided into four groups according to estimated GFR, serum phosphorus level had signifi cant higher values in CKD stage 4. From univariate analysis, higher phosphorus level was associated with better endoPAT values(r=0.296, p=0.008). Multivariate analysis adjusted by PTH, TG showed significant correlation between the serum phophorus level and endoPAT.
Conclusions: This study showed that serum phosphorus level may associate with en- dothelial function even in CKD. Furthermore, it is required a prospective study of larger population to identify the relationship between phosphorus and endothelial function and to establish optimal reference range of phosphorus level for protection from en- dothelial dysfunction.
PS 0499 Nephrology
Omega-3 Fatty Acids Up-Regulate Elongase and Down-Regulate 9-Desaturase in Cyclosporine Induced Rat Model
Su Mi LEE1, Dongyeol LEE1, Young Ki SON1, Seong Eun KIM1, Won Suk AN1 Dong-A University, Korea1
Background: Previous studies have reported that omega-3 fatty acid (FA) supplemen- tation can modify erythrocyte membrane FA content, including oleic acid decrease.
Stearoyl-CoA desaturases (SCD) and elongase are related with oleic acid synthesis but little is known of the effect of omega-3 FA on these enzymes. In this study, we evalu- ated the effect of omega-3 FA on the activity of SCD and elongase in CsA-induced rat model.
Methods: Male Sprague-Dawley rats fed a low-sodium diet were divided into three groups: control (0.9% saline injection; n = 6), CsA (15 mg/kg/day by subcutaneous injection; n = 6), CsA + Omega-3 FA (300 mg/kg/day by gastric gavage; n = 6). We measured erythrocyte membrane FA contents with gas chromatography. The activity of elongase and SCD were examined by using western blot analysis.
Results: The omega-3, EPA, DHA, and omega-3 index levels were increased in CsA with omega-3 FA supplemented group compared to CsA group. The ratio of AA to EPA and omega-6 to omega-3 were signifi cantly decreased in CsA with omega-3 FA supplemented group compared to CsA group. Oleic acid levels in CsA with omega-3 FA group were lower than in CsA group. Compared with the control group, CsA group showed signifi cant elevation of SCD expression and decrement of elongase expression (P = 0.029, P = 0.006, respectively). Omega-3 FA with CsA supplementation signif- icantly up-regulated expression of elongase and down-regulated expression of SCD compared with CsA group (P = 0.001, P = 0.057, respectively).
Conclusions: Omega-3 FA may decrease erythrocyte membrane oleic acid contents by inhibiting SCD acitivity and activating elongase activity. Future studies are necessary to elucidate the effect of omega-3 FA on desaturase and elongase activities.
