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Propofol is widely used to sedate agitated patients in intensive care units. However, it can cause a rare but fatal complication, propofol-related infusion syndrome (PRIS). The pathophysiology of PRIS is not clear, and there is no definitive diagnosis and treatment. We report a successfully treated case of PRIS in a critically ill patient receiving low-dose propofol infusion. A 59-year-old male patient complaining of sudden chest pain repeatedly collapsed in an ambulance and the emergency room, and veno-arterial extracorporeal membrane oxygenation was delivered. He was diagnosed with a total occluded left anterior descending coronary artery in coronary angiography. On day 20, he showed arrhythmia, increased creatinine kinase (CK), and increased CK-MB and troponin I, accompanied by unstable hemodynamic status despite high-dose vasopressors. He was administered propofol for 20 days at an average dose of 1.3 mg/kg/hr owing to issues with agitation and ventilator synchrony. We strongly suspected PRIS and immediately discontinued propofol infusion, and he was successfully treated with aggressive supportive care. PRIS can occur in patients administered propofol for a prolonged period at low doses. Thus, clinicians should use propofol with caution for PRIS and change to alternative sedatives for long-term sedation.

Background: The objective of this study was to investigate the characteristics and clinical outcomes of critically ill cancer patients admitted to intensive care units (ICUs) in Korea. Methods: This was a retrospective cohort study that analyzed prospective collected data from the Validation of Simplified Acute Physiology Score 3 (SAPS3) in Korean ICU (VSKI) study, which is a nationwide, multicenter, and prospective study that considered 5,063 pa tients from 22 ICUs in Korea over a period of 7 months. Among them, patients older than 18 years of age who were diagnosed with solid or hematologic malignancies prior to admission to the ICU were included in the present study. Results: During the study period, a total of 1,762 cancer patients were admitted to the ICUs and 833 of them were deemed eligible for analysis. Six hundred fifty-eight (79%) had solid tumors and 175 (21%) had hematologic malignancies, respectively. Respiratory problems (30.1%) was the most common reason leading to ICU admission. Patients with hematologic malignancies had higher Sequential Organ Failure Assessment (12 vs. 8, P

Advances in podocytology and genetic techniques have expanded our understanding of the pathogenesis of hereditary steroid-resistant nephrotic syndrome (SRNS). In the past 20 years, over 45 genetic mutations have been identified in patients with hereditary SRNS. Genetic mutations on structural and functional molecules in podocytes can lead to serious injury in the podocytes themselves and in adjacent structures, causing sclerotic lesions such as focal segmental glomerulosclerosis or diffuse mesangial sclerosis. This paper provides an update on the current knowledge of podocyte genes involved in the development of hereditary nephrotic syndrome and, thereby, reviews genotype-phenotype correlations to propose an approach for appropriate mutational screening based on clinical aspects.

Aim Extracorporeal cardiopulmonary resuscitation (ECPR) has been shown to have survival benefit in patients who had in-hospital cardiac arrest (IHCA). However, limited data are available on the role of extracorporeal membrane oxygenation (ECMO) for out-of-hospital cardiac arrest (OHCA). Therefore, we aimed to investigate clinical outcomes and predictors of in-hospital mortality in patients who had OHCA and who underwent ECPR. Methods From January 2004 to December 2013, 235 patients who received ECPR were enrolled in a retrospective, single-centre, observational registry. Among those, we studied 35 adult patients who had OHCA. The primary outcome was in-hospital mortality. Results Among 35 patients with a median age of 55 years (IQR 45–64), 29 (82.9%) of whom were male, ECMO implantation was successful in all and 10 patients (28.6%) lived to be discharged from the hospital. In 18 cases (51.4%), first monitored rhythms were identified as ventricular tachycardia/ventricular fibrillation, that is, shockable rhythm. There were no differences between in-hospital survivors and non-survivors regarding median time of arrest to cardiopulmonary resuscitation (CPR) (survivors: 23.5 min (IQR 18.8–27.3) vs non-survivors: 20.0 min (IQR 15.0–24.5); p=0.41) and median time of CPR to ECMO pump-on (survivors: 61.0 min (IQR 39.8–77.8) vs non-survivors 50.0 min (IQR 44.0–72.5); p=0.50). In 23 cases (65.7%), ischaemic heart disease was diagnosed and successful revascularisation was achieved in a significantly higher proportion of the survivor group (8/10 (80.0%)) than the non-survivor group (8/25 (32.0%)) (p=0.02). Witnessed arrest (HR=3.96; 95% CI 1.38 to 11.41; p=0.01), bystander CPR (HR=4.05; 95% CI 1.56 to 10.42; p=0.004) and successful revascularisation (HR=2.90; 95% CI 1.23 to 6.86; p=0.02) were independent predictors of survival-to-discharge in patients who had OHCA in univariate Cox regression analysis. Conclusion Survival rate for ECPR in the setting of OHCA remains poor. Our findings suggest that ECMO implantation should be very carefully considered in highly selected patients who had OHCA with little no-flow time and a reversible cause.

Mucormycosis is an uncommon opportunistic fungal infection mostly affecting immunocompromised patients and gastrointestinal mucormycosis is a rare and life-threatening. We describe a 31-year-old man with a history of idiopathic cyclic neutropenia who developed perforations of the stomach and intestine and intra-abdominal bleeding due to disseminated gastrointestinal mucormycosis after the initial operation.

Nephrotic syndrome (NS) is a common chronic disease in children; in 90 percent of cases, the condition is primary (idiopathic). Toxic nephropathy can be induced by herbal medicines, and is mainly manifested as tubulointerstitial nephritis and rarely, as glomerulopathy. Here in, we describe two cases of steroid-sensitive NS, which developed after the patients received herbal medicines. A 5-year-old boy and an 8-year-old girl were separately admitted within a short time period with acute onset of generalized edema, proteinuria, hypoalbuminemia, and hypercholesterolemia. Each patient had previously taken herbal medicine, which had been prescribed by different oriental medical clinics for different conditions. The patients were diagnosed with herbal medicine-induced NS and were treated empirically by a standard steroid therapy, with subsequent resolution of their NS. One patient relapsed, but her NS again responded to steroid therapy. We described two unusual cases of prototypical pediatric, steroid-sensitive NS, which was presumed to be minimal-change disease that developed after the administration of herbal medicines. We also reviewed the literature.

Background: The actin cytoskeleton in podocytes is essential for the maintenance of its normal structure and function. Its disruption is a feature of podocyte foot-process effacement and is associated with proteinuria. α-Actinin-4 in podocytes serves as a linker protein binding the actin filaments of the cytoskeleton. Methods: To investigate the effect of ginseng total saponin (GTS) on the pathological changes of podocyte α-actinin-4 induced by diabetic conditions, we cultured mouse podocytes under normal glucose (5mM) or high glucose (HG, 30mM) conditions, with or without the addition of advanced glycosylation end products (AGE), and treated with GTS. Results: In confocal imaging, α-actinin-4 colocalized with the ends of F-actin fibers in cytoplasm, but diabetic conditions disrupted F-actin fibers and concentrated α-actinin-4 molecules at the peripheral cytoplasm. GTS upregulated α-actinin protein in a time- and dose-dependent manner, and suppressed the receptor for AGE levels in western blotting. Diabetic conditions, including HG, AGE, and both together, decreased cellular α-actinin-4 protein levels at 24 h and 48 h. Such quantitative and qualitative changes of α-actinin-4 protein induced by diabetic conditions were mitigated by GTS. Conclusion: These findings imply that both HG and AGE have an influence on the distribution and amount of α-actinin-4 in podocytes that can be recovered by GTS.

Background: Adenosine monophosphate-activated protein kinases (AMPKs), as a sensor of cellular energy status, have been known to play an important role in the pathophysiology of diabetes and its complications. Because AMPKs are known to be expressed in podocytes, it is possible that podocyte AMPKs could be an important contributing factor in the development of diabetic proteinuria. We investigated the roles of AMPKs in the pathological changes in podocytes induced by high-glucose (HG) and advanced glycosylation end products (AGEs) in diabetic proteinuria. Methods: We prepared streptozotocin-induced diabetic renal tissues and cultured rat and mouse podocytes under diabetic conditions with AMPK-modulating agents. The changes in AMPKα were analyzed with confocal imaging and Western blotting under the following conditions: (1) normal glucose (5mM, =control); (2) HG (30mM); (3) AGE-added; or (4) HG plus AGE-added. Results: The density of glomerularphospho-AMPKα in experimental diabetic nephropathy decreased as a function of the diabetic duration. Diabetic conditions including HG and AGE changed the localization of phospho-AMPKα from peripheral cytoplasm to internal cytoplasm and peri- and intranuclear areas in podocytes. HG reduced the AMPKα (Thr172) phosphorylation of rat podocytes, and similarly, AGEs reduced the AMPKα (Thr172) phosphorylation of mouse podocytes. The distributional and quantitative changes in phospho-AMPKα caused by diabetic conditions were preventable using AMPK activators, metformin, and 5-aminoimidazole-4-carboxamide-1β-riboside. Conclusion: We suggest that diabetic conditions induce the relocation and suppression of podocyte AMPKα, which would be a suggestive mechanism in diabetic podocyte injury.

The aim of this study was to compare the efficacy of combination therapy with desmopressin and an anticholinergic to desmopressin monotherapy for the first-line treatment of children with primary monosymptomatic nocturnal enuresis (PMNE).A total of 98 children with PMNE (male:female 71:27) aged 5-16 (mean age 7.18 ± 1.8) years were retrospectively analyzed. The patients were divided into two groups: the monotherapy group (n = 49) was given oral desmopressin alone, and the combination therapy group (n = 49) was given desmopressin plus an anticholinergic (propiverine 10 mg) as a first-line treatment. The two groups were matched according to the following criteria: age, gender, and baseline frequency of nocturnal enuresis. The efficacy was evaluated by International Children's Continence Society criteria at 1 and 3 months after treatment initiation.The combination therapy group showed a higher rate of complete response than the monotherapy group (20.4 vs. 6.1% at 1 month of treatment; 46.9 vs. 22.4% at 3 months of treatment). In terms of success (response and complete response), there was a significant difference between the two groups after 3 months of treatment (P = 0.002).Our results indicate that combination therapy with desmopressin plus an anticholinergic is quicker and more effective than desmopressin monotherapy in reducing PMNE.

Type I (distal) renal tubular acidosis (RTA) is a disorder associated with the failure to excrete hydrogen ions from the distal renal tubule. It is characterized by hyperchloremic metabolic acidosis, an abnormal increase in urine pH, reduced urinary excretion of ammonium and bicarbonate ions, and mild deterioration in renal function. Hypercalciuria is common in distal RTA because of bone resorption, which increases as a buffer against metabolic acidosis. This can result in intractable rickets. We describe a case of distal RTA with nephrocalcinosis during follow-up of rickets in a patient who presented with clinical manifestations of short stature, failure to thrive, recurrent vomiting, dehydration, and irritability.

Proteinuric conditions demonstrate structural and compositional changes of the foot processes and slit diaphragms between podocytes. p130Cas in podocytes serves as an adapter protein anchoring glomerular basement membrane to actin filaments of podocyte cytoskeleton. To investigate the effect of ginseng total saponin (GTS) on the pathologic changes of podocyte p130Cas induced by diabetic conditions, we cultured mouse podocytes under: 1) normal glucose (5 mM, control); 2) high glucose (HG, 30 mM); 3) advanced glycosylation endproducts (AGE)-added; or 4) HG plus AGE-added conditions and treated with GTS. In confocal imaging, p130Cas colocalized with zonula occludens-1 and synaptopodin connecting to F-actin. However, diabetic conditions relocalized p130Cas molecules at perinuclear cytoplasmic area and reduced the intensity of p130Cas. In Western blotting, diabetic conditions, especially HG plus AGE-added condition, decreased cellular p130Cas protein levels at 24 and 48 h. GTS improved such quantitative and qualitative changes. These findings imply that HG and AGE have an influence on the redistribution and amount of p130Cas of podocytes, which can be reversed by GTS.

Since 1998, urine screening tests have been performed on school children in Korea. We report the findings of the screening program that analyzed patients with proteinuria and/or hematuria. Between 1999 and 2008, 5,114 children were referred to pediatric nephrologists at seven nationwide hospitals. Renal biopsies were performed on 1,478 children [28.79 % of total subjects; 26.77 % for isolated hematuria (IH), 9.09 % for isolated proteinuria (IP), and 51.19 % for combined hematuria and proteinuria (CHP)] who showed abnormal renal function, persistent hematuria and/or proteinuria for more than 6 months, nephrotic-range proteinuria, or those with underlying systemic diseases. Chronic glomerulonephritis (GN) was detected in 25 % of all visiting subjects. The most common findings in renal biopsies were immunoglobulin A (IgA) nephropathy in 38.97 %, mesangial proliferative GN in 24.29 %, and thin basement membrane nephropathy in 13.13 %. Compared with the relative frequency of renal diseases associated with urinary abnormalities, CHP (46.90 %) and nephrotic-range proteinuria (69.96 %) groups had more frequent GN than the others. Abnormal findings on renal ultrasound with or without Doppler scan were noted in 462 cases (suspected nutcracker phenomenon, 159; increased parenchymal echogenicity, 92; hydronephrosis, 75; simple cyst, 47). Mass urine screening tests could detect asymptomatic GN in its early stages. Initial aggressive diagnosis and treatment for CHP and nephrotic-range groups may prove helpful as interventions that delay chronic kidney disease progression. These findings may assist in the development of diagnostic and management guidelines for relatively mild urinary abnormalities, such as IH or low-grade IP.

Adenosine monophosphate (AMP)-activated protein kinase (AMPK), as a sensor of cellular energy status, has been known to play an important role in the pathophysiology of diabetes and its complications. As AMPK is also expressed in podocytes, it is possible that podocyte AMPK would be an important contributing factor in the development of diabetic proteinuria. We investigated the roles of AMPK in the pathological changes of podocytes induced by angiotensin II (Ang II), a major injury inducer in diabetic proteinuria. Mouse podocytes were incubated in media containing various concentrations of Ang II and AMPK-modulating agents. The changes of AMPKα were analyzed by confocal imaging and Western blotting in response to Ang II. Ang II changed the localization of AMPKα from peripheral cytoplasm into internal cytoplasm and peri- and intranuclear areas in podocytes. Ang II also reduced AMPKα (Thr172) phosphorylation in time- and dose-sensitive manners. In particular, 10−7 M Ang II reduced phospho-AMPKα significantly and continuously at 6, 24, and 48 h. AMPK activators, metformin and 5-aminoimidazole-4-carboxamide-1β-riboside, restored the suppressed AMPKα (Thr172) phosphorylation. Losartan, an Ang II type 1 receptor antagonist, also recovered the suppression and the mal-localization of AMPKα, which were induced by Ang II. PD98059, a mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor, also restored the AMPKα (Thr172) phosphorylation suppressed by Ang II. We suggest that Ang II induces the relocation and suppression of podocyte AMPKα via Ang II type 1 receptor and MAPK signaling pathway, which would be an important mechanism in Ang II-induced podocyte injury.

Serum lactate clearance (LC) during initial resuscitation is a potentially useful prognostic marker in patients with severe sepsis or septic shock. However, it is unclear whether LC is also associated with the outcome in septic patients with hepatic dysfunction that may impair lactate elimination, which may contribute to elevated serum lactate levels or decreased LC.The relationships between LC measured within 6 and 24h after initial resuscitation and hospital mortality were evaluated with multiple logistic regression analysis.Of 770 patients with severe sepsis or septic shock, 208 (27%) with hepatic dysfunction were included in the analysis. The median LC within 6h in survivors (31.4%) was significantly higher than that of non-survivors (9.3%) (P=.010). In addition, the median LC within 24h was also significantly different between groups (51% vs. 12%, P.001). Low LCs, defined as less than 10% of clearance, at 6 and 24h were associated with in-hospital mortality. After adjusting for potential confounding factors, low LCs at 6 and 24h remained associated with hospital mortality (adjusted OR 4.940, 95% CI 1.762-13.854 at 6h; adjusted OR 5.997, 95% CI 2.149-16.737 at 24h). However, LC at 24h (area under the curve of 0.704) had higher discriminatory power to predict hospital mortality than LC at 6h (area under the curve of 0.608) (P=.033).LC may be useful for predicting outcomes in septic patients with hepatic dysfunction.

Objectives To evaluate the prevalence of abnormal voiding and bowel habits in healthy children, and to identify possible relationships between personal and familial factors and voiding and/or bowel habits. Methods A randomly selected cross-sectional study was conducted in 19 240 children (5-13 years old) nationwide in the Republic of Korea. Parents were asked to complete questionnaires, which included items about nocturnal enuresis, daytime dysfunctional voiding symptoms (DVSs), and abnormal bowel habits (ABHs). Rates and associated factors were investigated. Results The overall rates of DVS, ABH, and of both were 46.4%, 31.3%, and 18.4%, respectively, and nocturnal enuresis was reported in 919 (5.6%). Daytime dysfunctional voiding symptoms were as follows: increased voiding frequency in 419 (2.5%), decreased voiding frequency in 720 (4.4%), urgency in 2740 (16.6%), daytime incontinence in 1854 (11.2%), urge incontinence in 2775 (16.8%), and holding maneuvers or postponed voiding in 3888 (23.5%). ABHs were as follows: constipation by frequency in 1103 (6.7%), constipation by the Bristol scale in 1941 (11.8%), fecal incontinence in 1293 (7.8%), and difficult or painful defecation in 2609 (15.8%). Delayed stool control, history of urinary tract infection, and a double-income family were positively associated with DVS or ABH or both. Furthermore, fathers with a low level of education and a low income were found to be associated with higher risk of ABH or DVS or both. Conclusions Delayed stool control, a history of urinary tract infection, a low paternal level of education, a double-income family, and a lower family income had a negative effect on voiding or bowel habits in children.

Aim: Henoch-Schonlein purpura (HSP) is a common childhood systemic vasculitis involving the skin, gastrointestinal tract, joint, kidneys and even scrotum. Methods: We retrospectively reviewed the clinical and laboratory data of 120 male patients with HSP and also evaluated the risk factors for scrotal involvement and the relation between scrotal involvement and other clinical features. Twenty-six out of 120 boys (21.7%) diagnosed with HSP had scrotal involvement. Results: Scrotal symptoms manifested as swelling in 88.5% and pain (or tenderness) in 69.2% of HSP patients with scrotal involvement. Neurologic symptoms, mainly headache and localized edema among various manifestations and high serum C3 level of laboratory profiles were more frequently observed in scrotal-involved group than in those of non-involved group. However, there was no difference in the outcomes of scrotal symptoms according to therapeutic modalities and the occurrence of scrotal involvement had no correlation with renal involvement from acute to chronic phase. Conclusions: We found that neurologic symptoms, localized edema and high serum C3 level show a significant relation with scrotal involvement in male HSP patients. Because scrotal involvement in male HSP patients is not rare, the accurate early diagnosis of HSP is mandatory by the early notification of purpura and imaging evaluations in order to avoid unnecessary procedures.

Introduction Angiotensin II (Ang II) contributes to the pathological process of vascular structures, including renal glomeruli by hemodynamic and nonhemodynamic direct effects. On renal effects, Ang II plays an important role in the development of proteinuria and glomerulosclerosis by the modification of podocyte molecules and cell survival. In the present study, we investigated the effect of Ang II on endoplasmic reticulum (ER) stress in podocytes. Methods We cultured mouse podocytes with increasing doses of Ang II and evaluated ER stress markers by Western blotting. Results Ang II increased Bip protein, an ER chaperone, in a dose-dependent manner at 24 h, which was ameliorated by losartan, an angiotensin II type 1 receptor antagonist. Ang II also increased ER stress markers, such as phospho-PERK, phospho-eIF2α, and ATF4 proteins of podocyte, significantly in a dose-dependent manner at 24 h. Increased phospho-PERK and ATF4 proteins were further augmented by phosphoinositide 3 (PI3)-kinase inhibitor, LY294002, which suggested that Ang II could induce podocyte ER stress of PERK-eIF2α-ATF4 axis via PI3-kinase pathway. Discussion These studies suggest that Ang II could induce podocyte ER stress of PERK-eIF2α-ATF4 axis via PI3-kinase pathway, which would contribute to the development of podocyte injury induced by Ang II, and the augmentation of PI3-kinase would be a therapeutic target.

Left renal vein entrapment syndrome (nutcracker syndrome) was documented by magnetic resonance angiography (MRA) as a cause of orthostatic proteinuria in a 14-year-old girl female adolescent. Because of continuous proteinuria we performed a left renal biopsy which showed moderate mesangial hypercellularity. Her overt orthostatic proteinuria disappeared after a treatment of angiotensin-converting enzyme (ACE) inhibition. Nutcracker syndrome remains a rare but important cause of elevated protein excretion, which can induce mesangial changes and be improved by ACE inhibitor treatment.

Henoch-Schonlein purpura (HSP) is one of the most common types of vasculitis disorders in childhood and is characterized by a rash, arthritis, abdominal pain, and renal involvement. The factors that determine and mediate the severity of HSP and its renal involvement remain poorly understood, although it is likely that pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), are involved in the pathogenesis. Serum and urine levels of TNF-alpha were measured in children with HSP in the acute and convalescent phases by ELISA. Serum TNF-alpha levels were significantly higher in proteinuric HSP in the acute phase (36.6+/-8.5 pg/ml) compared with those with HSP without renal involvement and those with hematuric HSP (25.4+/-4.5 and 27.1+/-3.9 pg/ml) (P

Perlecan is one of major heparan sulfate proteoglycans in the glomerular basement membrane and is reduced in the renal parenchyma of diabetic patients and animals with proteinuria. To examine the effects of glucose and advanced glycosylated end-products (AGE) on perlecan, we cultured rat glomerular epithelial cells (GEpC) on AGE- or bovine serum albumin (BSA)-coated plates under normal (NG, 5 mM) and high-glucose (HG, 30 mM) conditions and measured the change in perlecan core protein production by a sandwich ELISA and northern blot analysis. We observed significant decreases of perlecan core protein under HG conditions at 1 week incubation, specifically on the AGE-coated compared with the BSA-coated surface, by 22.2% and 4.7%, respectively. The expression of mRNA for perlecan promoter was decreased under HG conditions on AGE-coated surfaces by 19.7% at 2 days and 61.1% at 1 week. Even under NG condition, the expression of mRNA was reduced by 30% at 1 week if GEpC were grown on an AGE-coated surface. In conclusion, HG and AGE have an additive effect in reducing the production of perlecan core protein by GEpC in vitro. AGE had a greater effect than HG, implying that the inhibition of AGE formation may be more effective than short-term glucose control in the prevention of diabetic proteinuria.

A retrospective genotype and phenotype analysis of X-linked congenital nephrogenic diabetes insipidus (NDI) was conducted on a nationwide cohort of 25 (24 male, 1 female) Korean children with AVPR2 gene mutations, comparing non-truncating and truncating mutations. In an analysis of male patients, the median age at diagnosis was 0.9 years old. At a median follow-up of 5.4 years, urinary tract dilatations were evident in 62% of patients and their median glomerular filtration rate was 72 mL/min/1.73 m2. Weights and heights were under the 3rd percentile in 22% and 33% of patients, respectively. One patient had low intelligence quotient and another developed end-stage renal disease. No statistically significant genotype-phenotype correlation was found between non-truncating and truncating mutations. One patient was female; she was analyzed separately because inactivation and mosaicism of the X chromosome may influence clinical manifestations in female patients. Current unsatisfactory long-term outcome of congenital NDI necessitates a novel therapeutic strategy.

Revised JPN guidelines for the management of acute pancreatitis: JPN guidelines 2015 Toshihiko Mayumi, Tadahiro Takada, Masamichi Yokoe, Masahiro Yoshida University of Occupational and Environmental Health, Japan Teikyo University School of Medicine, Japan Japanese Red Cross Nagoya Daini Hospital, Japan Clinical Research Center Kaken Hospital, International University of Health and Welfare, Japan Background/Purpose: JPN guidelines for the management of acute pancreatitis were published in 2003 and revised in 2007 and 2009 that the severity assessment score has been highly regarded all over the world. Since the classification and the definition of acute pancreatitis had been changed significantly in the New Atlanta classification of acute pancreatitis 2012, the working group of JPN guidelines revised JPN guidelines with making new meta-analysis and using the GRADE system. Methods: The working group of revising JPN guidelines consists of 28 specialists, surgeons, gastroenterologists, endoscopists, radiologists, and epidemiologists. Results: JPNguidelines 2015 containmajor topics as described below: (1) epidemiology and etiology, (2) diagnostic criteria, (3) severity scoring system, (4) fundamental and intensive care with flowcharts, (5) therapeutic intervention and surgery, (6) post-ERCP pancreatitis, (7) treatment strategy, (8) clinical indicator andpancreatitis bundles, and (9) imaging. JPN guidelines also released mobile applications for the management of acute pancreatitis. Meta-analyses were performed on prophylactic antibiotic use for the prevention of necrotizing pancreatitis and reduction of mortality and on prophylactic pancreatic stent placement for the prevention of post-ERCP pancreatitis. These metaanalysis data have the results that significant effects are expected to each setting. JPN guidelines 2015 take advantage of this brand-new evidence for the new idea for the treatment of acute pancreatitis. Conclusions: Revised JPN guidelines 2015 achieve further evolution with new meta-analysis data and contain a lot of recommendations using the GRADE system for clinical use.

Background Proteinuria results from increased glomerular permeability and is associated with retraction and effacement of the highly specialized interdigitating podocyte foot processes. In podocytes (glomerular epithelial cells [GECs]), p130Cas localizes diffusely to the cytoplasm and connects focal adhesion proteins and kinases to the glomerular basement membrane and adapter proteins of slit diaphragm insertion sites. Methods To investigate whether high-glucose (HG) and advanced glycosylation end products (AGEs) induce quantitative and distributional changes of podocyte p130Cas protein, a docking protein connecting F-actin fibers to the glomerular basement membrane and adapter proteins, we cultured rat GECs (r-GECs) and mouse GECs (m-GECs) under (i) normal glucose (5 mM = control), (ii) HG (30 mM), (iii) AGE-added or (iv) HG plus AGE-added conditions. We also prepared streptozotocin-induced diabetic renal tissues. Results We found that p130Cas stainings were located in peripheral cytoplasm of r-GECs and m-GECs as dots in linear alignment, partially colocalized with actin-binding proteins such as synaptopodin and alpha-actinin, and locally connected to the ends of actin filaments. In diabetic conditions, the intensities of p130Cas stainings were diminished in more pathological HG plus AGE-added condition of r-GECs and m-GECs and in chronic diabetic renal tissues. p130Cas protein was decreased significantly by HG, AGE and HG plus AGE in both cells compared with normal glucose or osmotic control conditions. p130Cas mRNA expression levels were also suppressed similarly in diabetic conditions. Conclusion We suggest that diabetic conditions modulate the quantitative and distributional changes of podocyte p130Cas and therefore affect the filtration function of podocytes.

Vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P- and E-selectin play a pivotal role for initiation of atherosclerosis. Ginsenoside, a class of steroid glycosides, is abundant in Panax ginseng root, which has been used for prevention of illness in Korea. In this study, we investigated the mechanism(s) by which ginsenoside Rg2 may inhibit VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-κB) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1 expression. PD98059, inhibitor of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) did not affect VCAM-1 and ICAM-1 expression stimulated with LPS. SP600125, inhibitor of c-Jun N-terminal kinase (JNK), reduced LPS-mediated ICAM-1 but not VCAM-1 expression. LPS reduced IkappaBα (IκBα) expression, in a time-dependent manner within 1 hr. Ginsenoside Rg2 prevented the decrease of IκBα expression stimulated with LPS. Moreover, ginsenoside Rg2 reduced LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner. These data provide a novel mechanism where the ginsenoside Rg2 may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease.

Invasive aspergillosis (IA) is most commonly seen in patients with risk factors, such as cytotoxic chemotherapy, prolonged neutropenia, corticosteroids, transplantation and acquired immune deficiency syndrome. IA commonly occurs in the respiratory tract. Extra-pulmonary aspergillosis is usually a part of a disseminated infection, and primary invasive intestinal aspergillosis is very rare. Herein, we report a case of an immunocompetent 53-year-old male who suffered recurrent septic shock in the intensive care unit (ICU) and was finally diagnosed as invasive intestinal aspergillosis without dissemination. IA is rarely considered for patients who do not have an immune disorder. Thus, when such cases do occur, the diagnosis is delayed and the clinical outcome is often poor. However, there is a growing literature reporting IA cases in patients without an immune disorder, mostly among ICU patients. Primary intestinal aspergillosis should be considered for critically ill patients, especially with severe disrupted gastrointestinal mucosal barrier.

We read with great interest the contribution by Bazso et al. [1]. They reported the case of a 12-year-old girl with juvenile idiopathic arthritis (JIA) who developed systemic lupus erythematosus (SLE) after 10 years and speculated a few hypotheses of “shared autoimmunity,” the complete dysregulation of the immune system, and the side eVect of the anti-TNF therapy. However, we would like to suggest a diVerent and possible pathomechanism of the overlapping JIA and SLE case. The patient presented Escherichia coli (E. coli) septicemia at the age of 22 and subsequently developed clinical, immunological, and pathological manifestations fulWlling the diagnostic criteria of SLE within the following 8 weeks. SigniWcantly, Uthman et al. [2] also reported a case of SLE following E. coli sepsis in a 72-year-old woman, postulating three plausible pathomechanisms. Firstly, Robertson and Pisetsky [3] reported that Wve of the eight patients with E. coli bacteremia demonstrated increased levels of antibodies to single-stranded (ss) DNA from E. coli. Secondly, Gilkeson et al. [4] showed that normal mice immunized with ssDNA derived from E. coli developed an immune-mediated proliferative glomerulonephritis secondary to renal deposition of anti-DNA antibodies as in SLE. Thirdly, E. coli is known to produce heat shock protein (HSP), and Schultz et al. [5] suggested a role of HSP in the pathogenesis of rheumatic diseases like SLE. The host initially reacts to microbial infections with an enhanced cellular and humoral response to the microbial HSP, and cross-reactivity may occur with the HSP of the stressed host because of structural similarities to the microbial HSP [5]. Therefore, there is a possibility that E. coli septicemia might play a critical role as an inducer in the development of SLE in the Bazso et al.’s patient. However, further studies are necessary to elucidate the exact relationship and molecular pathogenic pathway between the JIA and SLE overlap in the future.

Vascular NADPH oxidase plays a pivotal role in producing superoxide in endothelial cells and thus acts in the initiation and development of inflammatory cardiovascular diseases such as atherosclerosis. Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has multiple beneficial effects for treating cardiovascular disease but the effect of EGCG on the expression of vascular NADPH oxidase remains unknown. In this study, we investigated the mechanism(s) by which EGCG might inhibit the expression of subunits of NADPH oxidase, namely p47(phox), p67(phox) and p22(phox), induced by angiotensin II (Ang II) in human umbilical vein endothelial cells. Ang II increased the expression levels of p47(phox), p67(phox), and p22(phox), but EGCG counteracted this effect on p47(phox). Moreover, EGCG did not affect the production of reactive oxygen species induced by Ang II. These data suggest a novel mechanism whereby EGCG might provide direct vascular benefits for treating inflammatory cardiovascular diseases.

To estimate the prevalence of overactive bladder (OAB) in Korean children, 5-13 years of age, and to assess the associated factors for OAB.A randomly selected cross-section study was conducted in 26 kindergartens and 27 elementary schools nationwide in Korea. A total of 19 240 children were included; a parent was asked to complete the questionnaires, which included items about OAB and voiding and defecating habits. OAB was defined as urgency with or without urge incontinence, usually with increased daytime frequency and nocturia (International Children's Continence Society, 2006). Its prevalence and associated factors were also investigated.The response rate for the questionnaires was 85.84%. The overall prevalence of OAB was 16.59%. The prevalence of OAB decreased with age from 22.99% to 12.16% (P = .0001). The overall incidence of wet and dry OAB was 26.97% and 73.03%, respectively. Compared with normal children, those with OAB had a greater prevalence of nocturnal enuresis, constipation, fecal incontinence, urinary tract infection, delayed bladder control, and poor toilet facilities (P.05). The incidence of increased daytime frequency and urge incontinence was 3.69% and 2.31% (P = .009) and 26.97% and 14.78% (P = .0001) in OAB and non-OAB children, respectively. The corresponding prevalence decreased with age from 5.04% to 3.06% and from 45.74% to 18.50% in OAB children (P = .0001).The overall prevalence of OAB in Korean children, 5-13 years of age, was 16.59% and decreased with age. Nocturnal enuresis, constipation, fecal incontinence, history of urinary tract infection, delayed bladder control, and poor toilet facilities might be factors associated with the development of OAB.

We investigated the efficacy and tolerability of various anticholinergics in Korean children with non-neurogenic overactive bladder (OAB). A total of 326 children (males:females= 157:169) aged under 18 yr (mean age 7.3±2.6 yr) who were diagnosed with OAB from 2008 to 2011 were retrospectively reviewed. The mean duration of OAB symptoms before anticholinergic treatment was 16.9±19.0 months. The mean duration of medication was 5.6±7.3 months. Urgency urinary incontinence episodes per week decreased from 1.9±3.1 to 0.4±1.5 times (P

Neurological complications are rare during the course of Henoch-Schönlein purpura (HSP). We report a 5-year-old girl with HSP who presented with seizures. Sequential magnetic resonance imaging and electroencephalography showed bilateral multifocal cerebral lesions initially, which gradually and completely resolved with clinical improvement. These lesions were compatible with the radiological pattern of the non-hemorrhagic vasculitic involvement of cerebral parenchyma.

To the Editor We read with great interest the contribution by Muscal et al.1 They reported the development of systemic autoimmunity such as systemic lupus erythematosus (SLE) and antiphospholipid antibodies in children with acquired thrombotic thrombocytopenic purpura (TTP). We would like to suggest some potential pathologic mechanisms on the development of concurrent SLE in relation to TTP. Kakishita2 found that TTP after bone marrow transplantation (BMT) could be predicted at an …

목적: VUR는 대부분 요로감염 후에 진단되며, 반복적 요로감염과 역류가 지속되면 신반흔, 신실질의 위축, 고혈압 등 심각한 후유증을 야기할 수 있다. 본 연구에서는 VUR의 임상적 특성과 자연소실율 및 그와 관련된 인자들을 분석하였다. 방법: 1993년 12월부터 2011년 5월까지 충북대학병원 소아청소년과와 비뇨기과에 ...

목적: 단백뇨 질환의 실험모델인 puromycin aminonucleoside (PAN)에서 관찰할 수 있는 족세포의 병리학적 이상에 있어서 P-cadherin의 변화를 생체 외 족세포 배양실험을 통하여 알아보고자 하였다. 방법: PAN에 의한 족세포의 P-cadherin의 변화를 생체 외 배양실험을 통해 알아보고자 백서 사구체 상피세포(GEpC)를 배양하여 다양한 농도의 PAN을 투여하여 confocal 현미경을 통하여 P-cadherin의 분포를 관찰하였고, Western blotting 과 RT-PCR을 사용하여 P-cadherin 발현의 변화를 관찰하였다. 결과: 외곽세포질에 분포하는 P-cadherin은 단일세포 혹은 응집환경에서 PAN의 농도가 올라갈수록 내부로 응집되는 현상를 볼 수 있었다. Western 분석에서, P-cadherin 단백양은 PAN에 농도-의존적으로, 특히, 고농도인 50 mg/mL에서 24시간과 48시간이 노출 조건에서 각각 21.9% (P 【Purpose: To test whether the expression of P-cadherin, a component of slit diaphragms between podocyte foot processes, would be altered by puromycin aminonucleoside (PAN) in a cultured podocyte in vitro. Methods: Rat glomerular epithelial cells (GEpC) were cultured with various concentrations of PAN. The distribution of P-cadherin was examined with a confocal microscope. Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) were used to measure the change in P-cadherin expression. Results: This study found that P-cadherin was concentrated in the inner and peripheral cytoplasm with high concentrations of PAN under immunofluorescence views. Western blotting of GEpC revealed that PAN induced a decrease of P-cadherin in dose- and time-dependent manners. A high dose ( $50{\mu}g/mL$ ) of PAN decreased P-cadherin expression by 21.9% at 24 h (P $50{\mu}g/mL$ ) of PAN also decreased P-cadherin mRNA expression, similar to protein suppression, by 23.5% at 48 h (P】