172 32nd World Congress of Internal Medicine (October 24-28, 2014) WCIM 2014
PS 0485 Nephrology
Acute Kidney Injury Due to Povidone-Iodine Ingestion
Chang Seong KIM1, Sung Sun KIM2, Eun Hui BAE1, Seong Kwon MA1, Soo Wan KIM1 Department of Internal Medicine, Chonnam National University Hospital, Korea1, Department of Patholo- gy, Chonnam National University Hospital, Korea2
Povidone-iodine is a broad spectrum antiseptic for topical application in the treatment and prevention of infection in wound. There are few case reports of acute kidney injury (AKI) after povidone-iodine irrigation in burn patients and in patients with its irrigation for management of post-renal transplantation lymphocele. However, AKI has not been described in patients after ingestion of povidone-iodine. We report a case of a 47-year-old man who was suspected ingestion of povidone-iodine solution and presented with nausea, vomiting, and reduced urine output. Laboratory data revealed blood urea nitrogen of 124 mg/dl, serum creatinine of 6.3 mg/dl, impaired liver func- tion and leukocytosis. Urine iodine/creatinine ratio marked increased. The patient was admitted to the intensive care unit and performed continuous venovenous hemodiafi l- tration. The kidney biopsy was showed feature of acute tubular necrosis and intersti- tial nephritis. Unstained section showed to tan-colored pigmentations that suspected iodine cast in tubular lumen. Renal function recovered after hemodialysis and steroid mediation, but not recovered completely. We observed the fi rst case of biopsy proven AKI accompanied by increased urine iodine concentration after povidone-iodine inges- tion. Although a specifi c treatment for povidone-iodine intoxication is not available, the patients might be partially recovered from AKI in treatment with hemodialysis and steroid as in our case.
PS 0486 Nephrology
Futhan Inhibits Apoptosis of Kidney in Ischemia Reper- fusion Renal Injury Mice
Hong Jae JEON1, Jin Young JEONG1, Yoo Hyung KIM1, Ye Jin KIM1, Sarah CHUNG1, Dae Eun CHOI1, Ki Ryang NA1, Kang Wook LEE1
Chungnam National University Hospital, Korea1
Background: It has been reported that futhan(nafamostat mesylate) inhibited in- fl ammatory injury via inhibition of complementary activation in ischemic heart, liver and intestine. However, it has been little known that NM inhibits the apoptosis in ischemia-reperfusion (IR) injured kidney. We investigated whether NM attenuates IR renal injury and involves apoptosis inhibition.
Methods: We used HK-2 cell and male C57BL/6 mice. C57Bl/6 mice were divided into four groups; Sham, Nafamostat mesylate(NM,2mg/kg)+Sham, IR injury( IR injury;
reperfusion 27 minutes after clamping of both renal artery and vein), and NM+IR injury. Kidneys were harvested 24hr after IR injury. BUN and serum creatinine(s-Cr) were measured 24 hrs after IR injury. We performed real time RT-PCR and immunohis- tochemistry for molecular study and H&E stain and Masson trichrome (MT) stain for histologic examination. For in vitro study, HK-2 cell were divided as into three groups;
Control, IR-HK-2(HK-2 cells were incubated for 6 hours with mineral paraffi n oil for ischemic injury) and IR-HK-2+NM(2nM) groups. Cell survival and the magnitude of apoptosis were evaluated.
Results: BUN, serum creatinine level and renal tissue injury score in NM+IR injured mice were signifi cantly lower than those of control IR mice (all, p<0.01). NM treatment signifi cantly improved cell survival in ischemic HK-2 cells (p<0.01). Renal Bax protein and mRNA expression were signifi cantly increased in IR injured kidneys and ischemic HK-2 cells. NM treatment signifi cantly decreased renal Bax expression (p<0.05). Renal Bcl-2 protein and mRNA expression were significantly decreased in IR kidney and ischemic HK-2 cells compared to those of sham and control groups. NM treatment increased renal Bcl-2 expression in IR injured kidneys and ischemic HK-2 cells (p<0.05).
TUNEL positive cells were signifi cantly lower in NM+IR injured kidneys, comparing to control IR injured mice (p<0.05).
Conclusions: futhan attenuates ischemia-reperfusion renal injury via inhibition of ap- optosis.
PS 0487 Nephrology
Renin Angiotensin System Induces Renal Infl ammation via Renal TLR2 Activation in Experimental Unilateral Ureteral Obstruction
Sarah CHUNG1, Jin Young JEONG1, Ye Jin KIM1, Dae Eun CHOI1, Yoon Kyung CHANG1, Ki Ryang NA1, Kang Wook LEE1
Chungnam National University Hospital, Korea1
Background: Although Toll-like receptor 2(TLR2) may play an important role, inhibi- tion of TLR2 has not shown consistent results of amelioration in renal infl ammation of obstructed kidney. There have been some reports that renin angiotensin system (RAS) may affect the activation of TLR signaling. However, there was few study for the re- lationship between RAS and renal TLR2 activation in experimental unilateral ureteral obstruction(UUO).
Methods: Male wild type and TLR2 knokout(KO) mice backgrounded C57BL/6 were divided into the 8 groups; 1)Sham, 2)Angiotensin II(Ang II)+ Sham, 3)AngII+TLR2 KO, 4)Aliskiren+Sham, 5)Aliskiren+TLR2 KO, 6)UUO only 7)TLR2 KO UUO, and 8)Aliskiren + TLR2 KO UUO. We performed realtime RT PCR and immunohistochemistry for molec- ular study and H&E stain and Masson trichrome (MT) stain for histologic examination of kidneys.
Results: Ang II increased the renal mRNA expression of TLR2 in wild type mice (p <
0.05). Ang II-infused TLR2 KO mice kidney showed signifi cantly lower mRNA expres- sions of osteopontin(OPN) and TGF-ß compared to those of Ang II-infused wild type mice. In TLR2 KO UUO kidneys, there were no differences of MCP-1, OPN and TGF-ß mRNA expressions and renal histology compared with UUO kidneys of wild type mice(p < 0.05, p < 0.05, respectively). The renal renin mRNA expression in TLR2 KO UUO was signifi cantly higher than that of UUO kidneys of wild type mice (p < 0.05).
Renin inhibition by aliskiren decreased the mRNA expressions of MCP-1, OPN and TGF-ß, all of which were upregulated in TLR2 KO UUO kidneys (all, p < 0.05). Aliskiren also signifi cantly reduced renal tissue injury score (p < 0.05).
Conclusions: Inhibition of RAS attenuates renal infl ammation in TLR2 KO UUO kid- neys. It is speculated that RAS may modulate renal TLR2 activation in experimental unilateral ureteral obstruction.
PS 0488 Nephrology
Cyclophosphamide for the Treatment of Acute Inter- stitial Nephritis: Case Series
Ji Yeon MIN1, Su Kil PARK1
Department of Nephrology, Asan Medical Center, Korea1
Background: Acute interstitial nephritis (AIN) is common cause of patients undergo- ing renal biopsy for unexplained AKI. The mainstay of treatment for AIN is steroid, but many patients are refractory to or intolerant of steroid treatment. Moreover, some patients are unable to discontinue therapy without clinical relapse. In order to help to treat the patients whom are hard to cure with steroid treatment we attempted to use different way to cure AIN. Here, we are going to report three cases of AIN that were treated successfully with cyclophosphamide at our center.
Methods: We retrospectively reviewed the medical records and renal biopsy fi ndings in these three patients at Asan Medical Center who had biopsy proven AIN and were treated with cyclophosphamide.
Results: All patients presented with renal insuffi ciency. Baseline creatinine levels were higher in all patients. The mean serum creatinine was 5.5 mg/dl (range 2.2 to 11.3 mg/
dl). A 24-h urine protein collection was available for two of them, whom had a 24-h urine protein of
Conclusions: Cyclophosphamide can be a powerful fi rst-line therapy in the patients with AIN.
