No abstract available.
Acute Kidney Injury* ; Heat Stroke* ; Hot Temperature*

No abstract available.

BACKGROUND: Renal infarction (RI) is an uncommon disease that is difficult to diagnose. As little is known about clinical characteristics of this disease, we investigated its underlying risk factors and outcomes. METHODS: We performed a retrospective single-center study of 89 patients newly diagnosed with acute RI between January 2002 and March 2015 using imaging modalities. Clinical features, possible etiologies, and long-term renal outcome data were reviewed. RESULTS: The patients' mean age was 63.5 ± 15.42 years; 23.6% had diabetes and 56.2% had hypertension. Unilateral and bilateral involvements were shown in 80.9% and 19.1% of patients, respectively; proteinuria and hematuria were reported in 40.4% and 41.6%, respectively. Cardiovascular disease was the most common underlying disease, followed by renal vascular injury and hypercoagulability disorder. Fourteen patients had no specific underlying disease. At the time of diagnosis, acute kidney injury (AKI) was found in 34.8% of patients. Univariate analysis revealed diabetes mellitus (DM), leukocytosis, and high C-reactive protein (CRP) as significant risk factors for the development of AKI. On multivariate analysis, DM and high CRP levels were independent predictors for AKI. During follow-up, chronic kidney disease developed in 27.4% of patients. Univariate and multivariate Cox regression analyses showed old age to be an independent risk factor for this disease, whereas AKI history was a negative risk factor. CONCLUSION: DM patients or those with high CRP levels should be observed for renal function deterioration. Clinicians should also monitor for RI in elderly patients.
Acute Kidney Injury ; Aged ; C-Reactive Protein ; Cardiovascular Diseases ; Diabetes Mellitus ; Diagnosis ; Follow-Up Studies ; Hematuria ; Humans ; Hypertension ; Infarction* ; Leukocytosis ; Multivariate Analysis ; Proteinuria ; Renal Artery ; Renal Insufficiency, Chronic ; Retrospective Studies ; Risk Factors* ; Thrombophilia ; Vascular System Injuries

The nonstructural protein 4 (NSP4) of rotavirus encoded by gene 10, plays an important role in rotavirus pathogenicity. In this study, NSP4 gene sequences of human rotaviruses circulating in Seoul, Korea between March 2004 and April 2005 were determined. The nucleotide sequence data indicated that the NSP4 genes of human rotavirus Korean isolates were 750 or 751 bases in length and encoded one open reading frame of 175 amino acids with two glycosylation sites. The NSP4 of Korean isolates exhibited amino acid sequence homologies between 59.4% and 98.9%. The NSP4 of CAU4 and CAU15 showed a high degree of amino acid sequence homologies with NSP4 genotype A viruses, but the NSP4 of CAU5, CAU6, CAU11, CAU14, CAU16 and CAU22 exhibited a high degree of amino acid sequence homologies with NSP4 genotype B viruses. Interestingly, CAU3 and CAU7 showed low degree of amino acid sequence homology with those of currently described NSP4 genotypes A to D and belonged a distinct lineage on the phylogenetic tree. These findings suggests that distinct NSP4 type was circulating among human rotavirus strains in the local community of Seoul and raising intriguing questions regarding possible explanations for new genotype.
Amino Acid Sequence ; Amino Acids ; Base Sequence ; Genetic Variation* ; Genotype ; Glycosylation ; Herpesvirus 1, Cercopithecine ; Humans* ; Korea ; Open Reading Frames ; Rotavirus* ; Seoul* ; Sequence Homology, Amino Acid ; Virulence

PURPOSE: In this study, the etiology and the change of clinical characteristics of hyponatremia, in relation to the increased used of thiazide diuretics, have been assessed. METHODS: To perform a retrospective cohort study, a total sum of 322 patients who have been admitted in a single tertiary referral hospital between 2004 and 2009, were included. RESULTS: The most common cause of hyponatremia was due to thiazide diuretics (37.6%). Among the 121 patients who suffered from thiazide induced hyponatremia, 60 (48.0%) patients took combination thiazide. The incidence of hyponatremia has shown a tendency to increase from 2004 to 2009 (trend test, p<0.001). The incidence of hyponatremia due to the use of combination types has also increased (trend test, p<0.001). Thiazide induced hyponatremia showed no difference when compared to hyponatremia due the other causes, except the fact that the portion of female patients was higher (73.6% vs 64.6%, p<0.001), mean age was older (74.7 vs 69.9 years-old, p<0.001), and incidence of cerebrovascular accident was also higher (19.8% vs 6.5%, p<0.001). CONCLUSION: The use of thiazide is increasing and hence thiazide-induced hyponatremia is also increasing. This is thought to be particularly related to the increase of thiazide-combined drugs. Thiazideinduced hyponatremia shows a higher incidence in old age, female sex and those who have a history of a cerebrovascular event. Hence more caution is needed when using thiazide diuretics as antihypertensives, and plasma sodium levels should be monitored carefully.
Antihypertensive Agents ; Cohort Studies ; Diuretics ; Female ; Humans ; Hyponatremia ; Incidence ; Plasma ; Retrospective Studies ; Sodium ; Sodium Chloride Symporter Inhibitors ; Stroke ; Tertiary Care Centers

Autoimmune pancreatitis is a recently established clinicopathologic entity often associated with various types of other autoimmune diseases. We report a case of postrenal acute kidney injury (AKI) due to retroperitoneal fibrosis associated with autoimmune pancreatitis. The seventy one year old male patient was admitted because of oliguria and lower extremity edema. He had been diagnosed to have autoimmune pancreatitis and retroperitoneal fibrosis by increased serum IgG and IgG4 level with the presence of rim like attenuation around pancreas and the retroperitoneal fibrosing mass in abdominal CT scan 1 year ago but was lost to follow up. Magnetic resonance cholangiopancretogram and follow up abdominal CT scan showed progressed retroperitoneal fibrosis with newly developed bilateral hydronephrosis and atrophied left kidney despite partial improvement in pancreatitis. Because of progressively rising serum creatinine and oliguria, percutaneous nephrostomy in right kidney was performed. Steroid treatment was initiated with insertion of double J catheter at right ureter and renal function gradually returned. We report here a rare case of postrenal AKI developed in unilateral functioning kidney complicated by combined retroperitoneal fibrosis and autoimmune pancreatitis.
Acute Kidney Injury ; Autoimmune Diseases ; Catheters ; Creatinine ; Edema ; Follow-Up Studies ; Humans ; Hydronephrosis ; Immunoglobulin G ; Kidney ; Lost to Follow-Up ; Lower Extremity ; Magnetic Resonance Spectroscopy ; Male ; Nephrostomy, Percutaneous ; Oliguria ; Pancreas ; Pancreatitis ; Retroperitoneal Fibrosis ; Ureter

BACKGROUND/AIMS: It has been suggested that chronic kidney disease (CKD) is a risk factor for Clostridium difficile infection (CDI) and is associated with increased mortality among patients infected with C. difficile. However, recent studies of the clinical impact of CKD on CDI in Asians are still insufficient. We sought to determine the relationship between CKD and CDI in a Korean population. METHODS: This was a single-center, retrospective case-control study. In total, 171 patients with CDI were included as cases and 342 age- and gender-matched patients without CDI were used as controls. We compared the prevalence of CKD in the study sample and identified independent risk factors that could predict the development or prognosis of CDI. RESULTS: Independent risk factors for CDI included stage IV to V CKD not requiring dialysis (odds ratio [OR], 2.90) and end-stage renal disease requiring dialysis (OR, 3.34). Patients with more advanced CKD (estimated glomerular filtration rate < 30) and CDI showed higher in-hospital mortality and poorer responses to the initial metronidazole therapy. CONCLUSIONS: More advanced CKD is an independent risk factor for CDI and is associated with higher in-hospital mortality and poor treatment responses in CDI patients. Thus, in CKD patients, careful attention should be paid to the occurrence of CDI and its management to improve the outcome of CDI.
Aged ; Anti-Infective Agents/therapeutic use ; Chi-Square Distribution ; Clostridium difficile/*pathogenicity ; Enterocolitis, Pseudomembranous/diagnosis/drug therapy/*microbiology/mortality ; Female ; Hospital Mortality ; Humans ; Kidney Failure, Chronic/*complications/diagnosis/therapy ; Logistic Models ; Male ; Metronidazole/therapeutic use ; Middle Aged ; Multivariate Analysis ; Odds Ratio ; Prevalence ; Renal Dialysis ; Renal Insufficiency, Chronic/*complications/diagnosis/mortality/therapy ; Republic of Korea/epidemiology ; Retrospective Studies ; Risk Factors ; Treatment Outcome

Secondary hyperparathyroidism is a common complication of chronic kidney disease and known to be associated with soft tissue calcification affecting patients' morbidity and mortality. However few cases of intestinal calcification related to secondary hyperparathyroidism have been reported. Herein we report a case of peritonitis complicating small intestinal perforation in a patient who had undergone peritoneal dialysis and had sustained hyperparathyroidism. Diffuse calcifications and perforations in small intestine were identified in abdomino-pelvic CT scan as well as in resected small intestine. Because of relapsing microperforation and resultant intra-abdominal abscess, the patient has been in fasting status depending on total parenteral nutrition for over 8 months after surgery.
Abdominal Abscess ; Fasting ; Humans ; Hyperparathyroidism ; Hyperparathyroidism, Secondary ; Intestinal Perforation ; Intestine, Small ; Parenteral Nutrition, Total ; Peritoneal Dialysis ; Peritonitis ; Renal Insufficiency, Chronic

Apoptosis frequently occurs in acute renal injury but molecular mechanisms responsible for this distinct form of cell death are largely unknown. Fas belongs to the TNF/nerve growth factor superfamily and engagement by Fas ligand induces apoptosis in various epithelial cells. To investigate the role of apoptosis and associated molecular mechanisms, we examined the occurrence of apoptosis and Fas expression as well as the therapeutic effect of alpha-MSH, a potent anti-inflammatory cytokine in ischemic ARF rat model as well as its effect on Fas expression. The expression of Fas was studied by western blot analysis and semiquantitative RT-PCR. Apoptosis was assessed by the TUNEL method and the degree of apoptosis and Fas expression, as well as biochemical, histological data were compared between the alpha-MSH and the vehicle treated groups in 40 minute renal artery clamping ischemic ARF rat models. Intraperitoneally administered alpha-MSH significantly reduced renal injury, measured by plasma blood urea nitrogen, creatinine level and the degree of tubular necrosis(106.5+/-13.3/54.7+/-5.45mg/dL for BUN, 1.77+/-0.29/1.03+/-0.06mg/dL for creatinine 24 hours after ischemia)(p=0.003, p=0.01), (5.4+/-1.94/2.6+/-0.7 for injury score 24 hours after ischemia)(p=0.01). Ischemia caused significant upregulation of Fas mRNA and protein and was accompanied by morphological evidence of apoptosis. alpha-MSH significantly reduced the degree of apoptosis, as well as Fas[(mean apoptotic cell : 23.7+/-12.5/11.0+/-5.7 per 200 field at 4 hours after ischemia(p=0.04), 31.6+/-24.7/18.1+/-11.5 per 200 field at 24 hours after ischemia(p=0.25)]. (Fas protein expression : sham : 1409+/-355DI(densitometric index)) 2818.3+/-1100/1306+/-643.4DI at 24 hours and 5541.5+/-1597.5/ 2866.7+/-788.9DI at 72 hours after ischemia)(p=0.07, 0.047). These results suggest that Fas upregulation induced tubular cell apoptosis may contribute to the pathogenesis of ischemic ARF and the beneficial effect of alpha-MSH is partially mediated by these inhibitory effects on Fas system.
Acute Kidney Injury ; alpha-MSH ; Animals ; Apoptosis* ; Blood Urea Nitrogen ; Blotting, Western ; Cell Death ; Constriction ; Creatinine ; Epithelial Cells ; Fas Ligand Protein ; In Situ Nick-End Labeling ; Ischemia ; Models, Animal ; Plasma ; Rats* ; Renal Artery ; RNA, Messenger ; Up-Regulation

BACKGROUND: Tumor necrosis factor a (TNF), potent proinflammatory cytokine, may be related with ischemia/reperfusion injury induced tubular cell inflammation and apoptosis. We examined TNF and its major nuclear transcriptional factor, NFkappaB activation in cultured human tubular cells in hypoxic condition and the effect of alpha-MSH, potent antiinflammatory agent, which have been reported to reduce renal I/R injury in rats. METHODS: Hypoxic culture condition was produced by oxidative pathway inhibitor (Antimycin 2 mM) and glycolytic pathway inhibitor (deoxy-D- glucose 2 mM and 10 mM) for 1 hour and re-oxygenation was performed by placing the cells in normal medium. The expression of TNF mRNA was studied by RT-PCR and NFkappaB DNA binding activity was analysed by Electomobility shift assays (EMSA) and cellular apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP biotin nick-end labelling (TUNEL) method and DNA laddering. These data were compared between the alpha-MSH and the vehicle-treated groups. RESULTS: Measured ATP level was 49% of control by luciferase-based assay kit. I/R injury caused an increase in TNF mRNA and NFkappaB activation and was accompanied by morphological evidence of apoptosis. alpha-MSH significantly reduced the degree of apoptosis, as well as TNF mRNA and NFkappaB activity (TNF/L19 mRNA ratio, vehicle/alpha-MSH: 105.15 +/- 16.5/18.75 +/- 0.85, p<0.05) (NFkappaB activity, vehicle/alpha-MSH: 5624/4803 densitometric index (DI), p<0.05). CONCLUSION: These findings suggest that alpha-MSH can decrease cellular apoptosis in hypoxic tubular cells and this protective effect of alpha-MSH may be related, in partially, with supression of TNF and NFkappaB activity.
Adenosine Triphosphate ; alpha-MSH* ; Animals ; Anoxia ; Apoptosis ; Biotin ; DNA ; Glucose ; Humans* ; Inflammation ; Ischemia* ; Rats ; RNA, Messenger ; Tumor Necrosis Factor-alpha*