Acute kidney injury (AKI) is a disorder that is manifested by a sudden decrease of renal function within several hours, and AKI remains a significant cause that can lead to increasing morbidity and mortality. Although AKI has been extensively studies in animal models, translating the results from animal studies into clinical use has not been successful due to various factors including basal etiology of kidney deficiency and comorbidities and the complexity of this pathology. As a golden parameter, measuring serum creatinine (SCr) and blood urea nitrogen (BUN) has been conventionally used for determining the renal function, however, these biomarkers has been regarded suboptimal to identify renal injuries in early stages. In this study, we attempted to screen other serum biomarkers in early AKI event using cynomolgus monkeys. Two male monkeys, aged 60 months, were subjected to ischemic injury by unilateral clamping of renal pedicles for forty five minutes and then subsequently reperfused; the unclamped kidney was regarded as non-injured controls. Compared with control kidneys, we have found that the concentration of several inflammatory proteins including MCP1, TGFα, GSTα, were higher in the renal vein of injured kidney compared with control side after 24 and 48 hours of AKI. However, changes of serum level of KIM-1, which is one of the most-widely studied marker in rodent studies, were not different after AKI. Our results provide an useful information while developing a novel marker in AKI.

Retroperitoneal fibrosis (RPF) is a rare disease characterized by the presence of retroperitoneal tissue marked by chronic inflammation and prominent fibrosis. A 67-year-old man presented with general weakness and oliguria. Laboratory findings showed blood urea nitrogen 77.7 mg/dL, serum creatinine 9.24 mg/dL, and an IgG4 level within the normal range. Computed tomography (CT) findings showed bilateral hydronephrosis and distal ureteral obstruction due to fibrotic adhesion to a presacral mass. Laparoscopic biopsy was performed. The authors report a case of acute kidney injury caused by non-IgG4 related focal retroperitoneal fibrosis in the pelvis that was successfully treated using prednisolone and tamoxifen… non-IgG4 related focal retroperitoneal fibrosis caused byacute kidney injury.

Background : Oxidative stress-related iflammatory mechanisms may play an important role in the pathogenesis of cisplatin-induced nephrotoxicity. Safflower (Carthamus tinctorius L.) seed is a crude drug rich in serotonin derivatives to exhibit several biological activities, including antioxidant, anti-inflammation and anti-cancer effects. The purpose of this study was to determine the renoprotective effects of Safflower seed, using cisplatin-induced nephrotoxicity mice. Methods and Results : Safflower seed was orally administered at a dose of 100 and 200 mg/kg body weight for 5 days before the intraperitoneal injection of cisplatin 20 mg/kg body weight, and the effects were compared with those of vehicle-treated cisplatin administered to control and normal mice. In the serum and kidney, renal function parameters reactive oxygen species and expression of protein related to oxidative stress, DNA damage, inflammation and apoptosis were examined. Safflower seed treatment attenuated serum BUN, createinine and renal oxidative stress through reduction of reactive oxygen species and increase in the protein expression level of catalase. Safflower seed reduced renal protein expression of p-p38 and p-JNK (mitogen-activated protein kinase pathway), pro-apoptotic factors (such as Bax and caspase 3) and nuclear factor-kappa B-targeting pro-inflammatory cyclooxygenase-2 and inducible nitric oxide synthase. In addition, Safflower seed treatment led to significantly attenuated histological damage in the kidney. Conclusion : These renoprotective effects of Safflower seed were achieved through attenuation of oxidative stress and its sensitive protein expression associated with inflammation and apoptosis in cisplatin-induced nephrotoxicity mice.

Mannitol is commonly used to reduce intracranial and intraocular pressures and to prevent dialysis-disequilibrium syndrome. However, intravenous mannitol infusion in various cases has the potential to result in acute kidney injury (AKI). We present a case of mannitol-induced AKI that developed after low dose mannitol infusion and resulted in recovery after hemodialysis. A 66-year-old woman was admitted to the hospital with a diagnosis of left middle cerebral artery infarction. On hospital day 5, cerebral edema was observed on a follow-up MRI. D-mannitol 35 g was given intravenously every 8 hours. Four days later, serum creatinine levels were elevated from 1.2 mg/dL to 3.5 mg/dL. The serum osmolal gap was found to be 52.4 mosm/kg H2O and urine output was reduced from 2.78 mL/kg/h to 0.69 mL/kg/h over three days. Hemodialysis over 2 hours was performed and renal function subsequently improved to baseline function. A potential risk of AKI exists even with low dose mannitol infusion in patients with advanced age, underlying renal impairment, and concomitant use of nephrotoxic agents. Mannitol-induced AKI may be rapidly reversed by short-term hemodialysis.