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

BACKGROUND: Although emerging evidence suggests that intra-abdominal hypertension (IAH) is a predictor of the development of acute kidney injury (AKI), it remains unclear whether the presence of IAH is a predictor of prognosis in patients with AKI. The purpose of this study was to assess whether the presence of IAH could predict prognosis in critically ill patients with AKI. The prognostic value of urinary biomarkers was also determined. METHODS: In this prospective observational study, we enrolled 57 patients with established AKI, who were admitted to the intensive care unit between February 2012 and June 2014. IAH was defined as a sustained elevation in intra-abdominal pressure of > or =12 mmHg, in three consecutive measurements performed daily on the first 3 days. Urinary neutrophil gelatinase-associated lipocalin (NGAL), liver-type fatty acid-binding protein, and simplified acute physiology score II score at the time of admission were also examined. RESULTS: IAH was observed in 78.9% of patients. The in-hospital mortality was 21.1%, and renal recovery during hospitalization was achieved in 40.4% of patients. Although high urinary NGAL [odds ratio (OR), 1.015] and liver-type fatty acid-binding protein (OR, 1.003) were found to be independent predictors of renal recovery, IAH was not. High urinary NGAL (OR, 1.003) and a high simplified acute physiology score II score (OR, 1.102) were independent predictors of in-hospital mortality, while IAH or urinary liver-type fatty acid-binding protein was not. CONCLUSION: Although IAH is prevalent in critically ill patients with AKI, it did not predict AKI prognosis. However, urinary NGAL was found to be a useful predictor of both renal recovery and in-hospital mortality.
Acute Kidney Injury* ; Biomarkers ; Critical Illness* ; Hospital Mortality* ; Hospitalization ; Humans ; Intensive Care Units ; Intra-Abdominal Hypertension* ; Lipocalins ; Neutrophils ; Observational Study ; Physiology ; Prognosis ; Prospective Studies

We present a case of a 65-year-old man with psoriasis who developed autoimmune hepatitis (AIH) without receiving immunosuppressive therapy with either anti-tumor necrosis factor-α or methotrexate. The AIH had completely resolved at 2 months after prednisolone and azathioprine therapy. This case confirms the need to consider AIH in psoriasis patients who experience new elevations in liver enzymes. To our knowledge, this is first description of the development of AIH in an immunosuppressant-naïve patient with psoriasis.
Aged ; Azathioprine ; Hepatitis, Autoimmune* ; Humans ; Liver ; Methotrexate ; Necrosis ; Prednisolone ; Psoriasis*

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*

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

Effective clearance of inflammatory cells is required for resolution of inflammation. Here, we show in vivo evidence that apoptosis and reverse transendothelial migration (rTEM) are important mechanisms in eliminating neutrophils and facilitating recovery following ischemia/reperfusion injury (IRI) of the kidney. The clearance of neutrophils was delayed in the Bax knockout (KO)BM → wild-type (WT) chimera in which bone marrow derived cells are partially resistant to apoptosis, compared to WTBM → WT mice. These mice also showed delayed functional, histological recovery, increased tissue cytokines, and accelerated fibrosis. The circulating intercellular adhesion molecule-1 (ICAM-1)+ Gr-1+ neutrophils displaying rTEM phenotype increased during the recovery phase and blockade of junctional adhesion molecule-C (JAM-C), a negative regulator of rTEM, resulted in an increase in circulating ICAM-1+ neutrophils, faster resolution of inflammation and recovery. The presence of Tamm-Horsfall protein (THP) in circulating ICAM-1+ neutrophils could suggest that they are derived from injured kidneys. In conclusion, we suggest that apoptosis and rTEM are critically involved in the clearance mechanisms of neutrophils during the recovery phase of IRI.
Acute Kidney Injury* ; Animals ; Apoptosis ; Bone Marrow ; Chimera ; Cytokines ; Fibrosis ; Inflammation ; Intercellular Adhesion Molecule-1 ; Kidney ; Mice ; Neutrophils* ; Phenotype ; Transendothelial and Transepithelial Migration ; Uromodulin

Intramural duodenal hematoma is a rare finding in the adult, especially when related to iatrogenic complications of ulcer treatment, it can lead to biliary obstruction and pancreatitis, which can be fatal in severe case. We report one case of intramural duodenal hematoma complicated with pancreatitis after endoscopic hemostasis in a chronic renal failure patient with maintenance hemodialysis. He had a duodenal ulcer bleeding treated with endoscopic epinephrine injection and electro-coagulation therapy, but on the second day, he complained of persistent abdominal pain, nausea and vomiting. Abdominal ultrasound showed acute, edematous pancreatitis and a mass with low echodensity in the wall of the 2nd portion of the duodenum. Symptom and laboratory findings were persistent under conservative therapy, 7 days later, gastric resection, hematoma evacuation was carried out, subsequently the patient recovered from the pancreatitis but the patient died of septic shock and multiple organ dysfunction.
Abdominal Pain ; Adult ; Duodenal Ulcer ; Duodenum ; Epinephrine ; Hematoma* ; Hemorrhage ; Hemostasis, Endoscopic* ; Humans ; Kidney Failure, Chronic* ; Nausea ; Pancreatitis* ; Renal Dialysis* ; Shock, Septic ; Ulcer ; Ultrasonography ; Vomiting

BACKGROUND/AIMS: The potential physiologic roles of Klotho in acute kidney injury (AKI) have recently been demonstrated in animal models. However, to date, there have been no human studies investigating the expression of renal Klotho in AKI. METHODS: We retrospectively collected biopsy specimens and clinical data of AKI patients between January 2001 and December 2012. Klotho expression was determined by immunohistochemical staining, and the clinical-pathological correlation was examined. RESULTS: Among the 34 patients diagnosed with acute tubular necrosis or acute tubulointerstitial nephritis, 21 patients without chronic histological lesions were included. The mean age was 37.3 +/- 18.5 years and the mean peak creatinine level was 8.2 +/- 5.5 mg/dL. In total, 10 patients (47.6%) received temporary renal replacement therapy (RRT); however, 17 patients (81%) showed functional recovery with creatinine levels of < 1.3 mg/dL after 1 month. The intensity of Klotho expression was scored as a percentage of Klotho-positive area. The renal Klotho score showed a significant negative correlation with the initial or peak creatinine level. When the patients were divided into three groups according to the Klotho score (low, middle, high), the low group had a significantly higher peak creatinine level and a more frequent requirement for RRT. However, the Klotho score was not a significant predictor of renal recovery. CONCLUSIONS: The results demonstrated that renal Klotho expression in humans decreased significantly according to the severity of AKI, regardless of the etiology, and that low expression was associated with a poor short-term outcome.
Acute Kidney Injury/diagnosis/etiology/*metabolism/physiopathology/therapy ; Adolescent ; Adult ; Biomarkers/analysis ; Biopsy ; Down-Regulation ; Female ; Glucuronidase/*analysis ; Humans ; Immunohistochemistry ; Kidney/*chemistry/pathology/physiopathology ; Kidney Tubular Necrosis, Acute/diagnosis/etiology/*metabolism/physiopathology/therapy ; Male ; Middle Aged ; Necrosis ; Predictive Value of Tests ; Recovery of Function ; Renal Replacement Therapy ; Retrospective Studies ; Risk Factors ; Severity of Illness Index ; Time Factors ; Treatment Outcome ; Young Adult

BACKGROUND: Glomerular diseases of diverse origins are characterized by heavy proteinuria and tubulointerstitial changes in pathology. Numerous studies have recently demonstrated that interstitial fibrosis and tubular atrophy are better predictors of renal disease progression compared with glomerular pathology. One of the important mechanisms of these tubulointerstitial injury is tubulointerstitial damage due to increased protein trafficking across the proximal tubular epithelial cells. We tested the hypothesis that tubular cells exposed to high concentration of protein express TGF-beta, which can be related to tubulointerstitial fibrosis, and Fas antigen, which can be associated with tubular cell apoptosis. METHODS: Cultured human proximal tubular cells were incubated with varying concentrations of BSA (1, 10 mg/mL) and nephrotic range proteinuria, due to diabetic nephropathy (1, 10 mg/mL), with or without inactivation of complement. After 24 hr-incubation period, the expressions of TGF-beta and Fas mRNA were examined by RT-PCR. RESULTS: The amount of expression of TGF-beta was increased in BSA 10 mg/mL group (0.78+/-0.12, p=0.016) and in diabetic proteinuria 10 mg/mL group (0.7+/-0.08, p=0.012) compared to control group which was incubated in medium alone (0.48+/-0.02), and the amount of expression of Fas was increased in BSA 10 mg/mL group (0.97+/-0.09, p=0.021) and showed increased tendency in diabetic proteinuria 10 mg/mL group (0.94+/-0.14, p=0.067) also. Furthermore, the anti TGF-beta antibody ameliorated the increased albumin-induced expression of Fas. CONCLUSION: Collectively, our results showed that protein overload increased the expression of TGF-beta & Fas, which can play an important role in tubulointerstitial atrophy by inducing apoptosis of renal tubular cells.
Antigens, CD95 ; Apoptosis ; Atrophy ; Complement System Proteins ; Diabetic Nephropathies ; Disease Progression ; Epithelial Cells ; Fibrosis ; Humans* ; Pathology ; Protein Transport ; Proteinuria* ; RNA, Messenger ; Transforming Growth Factor beta*

BACKGROUND: Glomerular diseases of diverse origins are characterized by heavy proteinuria and tubulointerstitial changes in pathology. Numerous studies have recently demonstrated that interstitial fibrosis and tubular atrophy are better predictors of renal disease progression compared with glomerular pathology. One of the important mechanisms of these tubulointerstitial injury is tubulointerstitial damage due to increased protein trafficking across the proximal tubular epithelial cells. We tested the hypothesis that tubular cells exposed to high concentration of protein express TGF-beta, which can be related to tubulointerstitial fibrosis, and Fas antigen, which can be associated with tubular cell apoptosis. METHODS: Cultured human proximal tubular cells were incubated with varying concentrations of BSA (1, 10 mg/mL) and nephrotic range proteinuria, due to diabetic nephropathy (1, 10 mg/mL), with or without inactivation of complement. After 24 hr-incubation period, the expressions of TGF-beta and Fas mRNA were examined by RT-PCR. RESULTS: The amount of expression of TGF-beta was increased in BSA 10 mg/mL group (0.78+/-0.12, p=0.016) and in diabetic proteinuria 10 mg/mL group (0.7+/-0.08, p=0.012) compared to control group which was incubated in medium alone (0.48+/-0.02), and the amount of expression of Fas was increased in BSA 10 mg/mL group (0.97+/-0.09, p=0.021) and showed increased tendency in diabetic proteinuria 10 mg/mL group (0.94+/-0.14, p=0.067) also. Furthermore, the anti TGF-beta antibody ameliorated the increased albumin-induced expression of Fas. CONCLUSION: Collectively, our results showed that protein overload increased the expression of TGF-beta & Fas, which can play an important role in tubulointerstitial atrophy by inducing apoptosis of renal tubular cells.
Antigens, CD95 ; Apoptosis ; Atrophy ; Complement System Proteins ; Diabetic Nephropathies ; Disease Progression ; Epithelial Cells ; Fibrosis ; Humans* ; Pathology ; Protein Transport ; Proteinuria* ; RNA, Messenger ; Transforming Growth Factor beta*