Acute kidney injury (AKI) is classified into three types according to its pathophysiology: prerenal, intrinsic renal, and post-renal AKI. Experimental models of AKI can be divided into two categories: in vivo and in vitro. Models can be further subdivided according to how AKI is simulated. The pathophysiology of intrinsic renal and post-renal AKI has been investigated using animal models. Most studies have been conducted in murine models using male mice or rats, while large mammals like sheep, pigs, and monkeys have been used in a limited number of studies. The intrinsic renal AKI model is divided into septic vs. aseptic AKI. Aseptic AKI is subdivided into ischemic vs. nephrotoxic AKI. Lipopolysaccharides (LPS) injection or cecal ligation and puncture (CLP) have been used to simulate the septic AKI model in rodents. Ischemic AKI is the most extensively investigated field to date because ischemic AKI is the most common and serious cause of AKI in both native kidneys and renal allografts. Ischemia-reperfusion injury (IRI) surgery has been used to induce ischemic AKI. There are two different methods of IRI surgery: laparotomy vs. flank approach. Warm temperature and male sex are critical to induction of sufficient grade of renal injury in this model. Many nephrotoxicants pertinent to human disease have been used to reproduce nephrotoxic AKI in rodent models. Cisplatin, a common chemotherapeutic agent, has many pathophysiologic features that overlap with IRI. Other nephrotoxicants such as gentamicin or glycerol were studied in the past, whereas much more attention has recently been devoted to environmental nephrotoxicants such as cadmium. However, variant susceptibility to different doses of nephrotoxicants is a big hurdle to set up a reproducible and consistent model of nephrotoxic AKI. Post-renal AKI is simulated with ureteral obstruction surgery, whereas the unilateral ureteral obstruction (UUO) model has frequently been used. Although some novel findings have been reported through numerous studies using murine AKI models, AKI still remains a challenging condition that lacks specific diagnostic or therapeutic tools because of species barriers or experimental settings. Animal AKI models using mammals genetically closer to human like monkeys would be valuable to simulate human AKI more appropriately.
Acute Kidney Injury* ; Allografts ; Animals* ; Cadmium ; Cisplatin ; Gentamicins ; Glycerol ; Haplorhini ; Humans ; In Vitro Techniques ; Kidney ; Laparotomy ; Ligation ; Lipopolysaccharides ; Male ; Mammals ; Mice ; Models, Animal* ; Models, Theoretical ; Punctures ; Rats ; Reperfusion Injury ; Rodentia ; Sheep ; Swine ; Ureteral Obstruction

Megalocytic interstitial nephritis is a rare form of kidney disease caused by chronic inflammation. We report a case of megalocytic interstitial nephritis occurring in a 45-yrold woman who presented with oliguric acute kidney injury and acute pyelonephritis accompanied by Escherichia coli bacteremia. Her renal function was not recovered despite adequate duration of susceptible antibiotic treatment, accompanied by negative conversion of bacteremia and bacteriuria. Kidney biopsy revealed an infiltration of numerous histiocytes without Michaelis-Gutmann bodies. The patient's renal function was markedly improved after short-term treatment with high-dose steroid.
Acute Disease ; Acute Kidney Injury/complications/*drug therapy/pathology ; Anti-Bacterial Agents/therapeutic use ; Azithromycin/therapeutic use ; Bacteremia/*drug therapy/microbiology/pathology ; Cefotaxime/therapeutic use ; Creatinine/blood ; Escherichia coli ; Escherichia coli Infections/*drug therapy/microbiology/pathology ; Female ; Humans ; Kidney/pathology ; Methylprednisolone/therapeutic use ; Middle Aged ; Nephritis, Interstitial/*drug therapy/immunology/pathology ; Pyelonephritis/complications/*drug therapy/pathology ; Renal Dialysis ; Shock, Septic/drug therapy/microbiology

Ischemic acute kidney injury (AKI) is a common medical problem with significant mortality and morbidity, affecting a large number of patients globally. Ischemic AKI is associated with intrarenal inflammation as well as systemic inflammation; thus, the innate and adaptive immune systems are implicated in the pathogenesis of ischemic AKI. Among various intrarenal immune cells, T cells play major roles in the injury process and in the repair mechanism affecting AKI to chronic kidney disease transition. Importantly, T cells also participate in distant organ crosstalk during AKI, which affects the overall outcomes. Therefore, targeting T cell-mediated pathways and T cell-based therapies have therapeutic promise for ischemic AKI. Here, we review the major populations of kidney T cells and their roles in ischemic AKI.

Progressive ptosis and headache developed in a 50-year-old woman with non-small cell lung cancer. Although brain magnetic resonance imaging showed improved cerebellar metastasis after prior radiotherapy without any other abnormality, the follow-up examination taken 6 months later revealed metastasis to the cavernous sinus. The diagnosis of metastasis to the cavernous sinus is often difficult because it is a very rare manifestation of lung cancer, and symptoms can occur prior to developing a radiologically detectable lesion. Therefore, when a strong clinical suspicion of cavernous sinus metastasis exists, thorough neurologic examination and serial brain imaging should be followed up to avoid overlooking the lesion.
Brain ; Carcinoma, Non-Small-Cell Lung ; Cavernous Sinus ; Caves ; Female ; Follow-Up Studies ; Headache ; Humans ; Lung Neoplasms ; Magnetic Resonance Imaging ; Middle Aged ; Neoplasm Metastasis ; Neuroimaging ; Neurologic Examination

Splenic artery pseudoaneurysm is a rare, but potentially lethal, vascular lesion. The mortality rate may be 75-90%, if the aneurysm ruptures. The risk for rupture of an untreated splenic artery pseudoaneurysm is about 37%. Hence, early diagnosis and prompt surgical intervention are vital to improve survival. However, vague symptoms make early diagnosis difficult. We report here a case of a giant splenic artery pseudoaneurysm presenting with acute kidney injury. The patient had been treated previously for infective endocarditis, and after 4 months, acute kidney injury developed. Imaging studies revealed a giant splenic artery pseudoaneurysm. Splenectomy and distal pancreatectomy were performed. After surgery, renal function was improved.
Acute Kidney Injury ; Aneurysm ; Aneurysm, False ; Early Diagnosis ; Endocarditis ; Humans ; Pancreatectomy ; Rupture ; Splenectomy ; Splenic Artery

Idiopathic membranous nephropathy is a common cause of nephrotic syndrome, and has been reported as a cause of idiopathic primary glomerulonephropathy in up to 90% of patients. However, the treatment options remain controversial. We report two cases of idiopathic membranous nephropathy that were treated with rituximab. A 54-year-old man and a 64-year old man were admitted for rituximab therapy. They had previously been treated with combinations of immunosuppressive agents including cyclophosphamide, cyclosporine, mycophenolate, and steroids. However, the patients' heavy proteinuria was not resolved. Both patients received rituximab therapy, 2 weeks apart. After several months of follow-up and a second round of rituximab treatment for each patient, their proteinuria decreased and partial remission of disease was achieved in both patients.
Antibodies, Monoclonal, Murine-Derived ; Cyclophosphamide ; Cyclosporine ; Follow-Up Studies ; Glomerulonephritis, Membranous* ; Humans ; Immunosuppressive Agents ; Middle Aged ; Nephrotic Syndrome ; Proteinuria ; Steroids ; Rituximab

Colchicine is a relatively safe medication that is widely used for both prevention and treatment of gout attack. However, serious adverse events, includingmyoneuropathy and multiorgan failure, have been reported. We report a case of colchicine-induced myoneuropathy in a female kidney transplant recipient who had been taking cyclosporine. She developed gastrointestinal discomfort and paresthesia 5 days after the initiation of colchicine. She showed signs of myoneuropathy, and hepatic and renal injury. Colchicine toxicity was suspected, and colchicine was discontinued. Her symptoms and laboratory findings improved gradually. Literature was reviewed for previous reports of colchicine-induced myoneuropathy in solid organ transplant recipients.
Colchicine ; Cyclosporine ; Female ; Gout ; Humans ; Kidney ; Paresthesia ; Transplants

BACKGROUND: The purpose of this study was to evaluate the incidence of contrast-induced nephropathy (CIN), and the effect of intravenous albumin for prophylaxis of CIN in patients with liver cirrhosis (LC) and chronic kidney disease (CKD). METHODS: We conducted a retrospective study of 81 subjects with LC and CKD (estimated glomerular filtration rate (eGFR)<60mL/min/1.73m2) who underwent contrast-enhanced computed tomography (CT). Patients received either isotonic sodium bicarbonate solution (3mL/kg for 1h before CT and 1mL/kg/h for 6h after CT) or albumin (20% albumin, 25mL for 1h before CT and 75mL for 6h after CT). CIN was defined as an increase of > or =25% or > or =0.5mg/dL in serum creatinine level. RESULTS: Overall, CIN developed in three patients (3.7%). Of the 81 subjects, 43 received sodium bicarbonate solution and 38 received albumin. Both groups were comparable with regard to age, sex, diabetes mellitus, and baseline eGFR. The albumin group showed a significantly poorer liver function profile. CIN incidence did not differ significantly between the groups: it occurred in one (2.3%) of the 43 subjects receiving sodium bicarbonate and two (5.3%) of the 38 subjects receiving albumin (P=0.6). However, the albumin group showed a significantly smaller increase in body weight (P=0.03). CONCLUSION: The incidence of CIN in patients with LC and CKD undergoing contrast-enhanced CT after preventive measures was relatively low. The incidence of CIN was not significantly different between sodium bicarbonate and albumin groups.
Body Weight ; Creatinine ; Diabetes Mellitus ; Glomerular Filtration Rate ; Humans ; Incidence ; Liver ; Liver Cirrhosis ; Renal Insufficiency, Chronic ; Retrospective Studies ; Sodium Bicarbonate

PURPOSE: HBsAg-positive kidney recipients are at increased risk for mortality and graft failure. The aims of this study were to identify the outcomes of HBsAg-positive recipients who received preemptive antiviral agents after successful kidney transplantation and to analyze risk factors for HBV reactivation. METHODS: We retrospectively reviewed the medical records of 944 patients performed kidney transplantation between 1999 and 2010. RESULTS: HBsAg-negative recipients were 902 patients and HBsAg-positive recipients, 42. Among HBsAg-positive recipients, HBV reactivation was detected in 7 patients and well controlled by switch or combination therapy. Graft failure developed in only one patient due to chronic rejection regardless of HBV reactivation but no deaths occurred. All patients were alive at the end of follow-up and none developed end-stage liver disease or hepatocellular carcinoma. There was statistically significant difference in graft survival between HBsAg-positive recipients and HBsAg-negative. Multivariate analysis identified increased HBV DNA levels (>5 x 10(4) IU/mL) in the HBsAg-positive kidney transplant recipients as a risk factor for HBV reactivation (P = 0.007). CONCLUSION: Effective viral suppression with antiviral agents in HBsAg-positive renal transplant recipients improves patient outcome and allograft survival. Antiviral therapy may be especially beneficial in patients with high HBV DNA levels prior to transplantation.
Allografts ; Antiviral Agents ; Carcinoma, Hepatocellular ; DNA ; Follow-Up Studies ; Graft Survival ; Hepatitis B virus ; Humans ; Kidney ; Kidney Transplantation* ; Liver Diseases ; Medical Records ; Mortality ; Multivariate Analysis ; Retrospective Studies ; Risk Factors ; Transplantation ; Transplants