Acute Kidney Injury ; chemically induced ; Humans ; Paraquat ; poisoning ; Rhabdomyolysis ; chemically induced

Acute kidney injury (AKI) is an important factor for the occurrence and development of CKD. The protective effect of dihydroartemisinin on AKI and and reported mechanism have not been reported. In this study, we used two animal models including ischemia-reperfusion and UUO, as well as a high-glucose-stimulated HK-2 cell model, to evaluate the protective effect of dihydroartemisinin on premature senescence of renal tubular epithelial cells in vitro and in vivo. We demonstrated that dihydroartemisinin improved renal aging and renal injury by activating autophagy. In addition, we found that co-treatment with chloroquine, an autophagy inhibitor, abolished the anti-renal aging effect of dihydroartemisinin in vitro. These findings suggested that activation of autophagy/elimination of senescent cell might be a useful strategy to prevent AKI/UUO induced renal tubular senescence and fibrosis.
Animals ; Kidney ; Acute Kidney Injury/chemically induced* ; Ischemia ; Reperfusion Injury/drug therapy* ; Autophagy ; Reperfusion

Acute Kidney Injury ; chemically induced ; Adult ; Antipsychotic Agents ; adverse effects ; Humans ; Male ; Rhabdomyolysis ; chemically induced ; Sulpiride ; adverse effects

Acute Kidney Injury ; chemically induced ; enzymology ; Animals ; Disease Models, Animal ; Gentamicins ; Peptidyl-Dipeptidase A ; metabolism ; Rats

Patients with organophosphate poisoning usually die from respiratory depression and respiratory failure. The incidence of rhabdomyolysis is relatively low, but the mortality rate is extremely high once it occurs. In this paper, the treatment of a patient with acute phoxim poisoning was analyzed. The patient developed severe rhabdomyolysis syndrome on the 3rd day of treatment, the creatine kinase exceeded the normal value by more than 300 times (up to 103510.65 U/L) , and renal failure occurred. Clinical treatment included active detoxification, blood purification, organ support, and internal environment maintenance. The patient's rhabdomyolysis continued, and the condition worsened. Finally, the family gave up the treatment and the patient died. It is suggested that attention should be paid to the occurrence of rhabdomyolysis syndrome during the treatment of organophosphorus poisoning, and timely blood purification technology may be the key to treatment.
Humans ; Rhabdomyolysis/chemically induced* ; Organothiophosphorus Compounds ; Creatine Kinase ; Incidence ; Acute Kidney Injury

Contrast-induced acute kidney injury (CI-AKI) refers to acute kidney injury that occurs after intravascular contrast media is applied. It is the third most common cause for acute renal failure in hospitalized patients and can cause severe renal impairment and adverse cardiovascular outcomes. In severe cases, it can even lead to the death of the patient. Due to its complicated pathogenesis, the pathogenesis of CI-AKI has not yet been elucidated. Therefore, it is of great significance to further study the pathogenesis for the prevention of CI-AKI. Moreover, a good animal model of CI-AKI is an important tool for in-depth research on the pathogenesis of acute kidney injury induced by contrast agents.
Animals ; Acute Kidney Injury/chemically induced* ; Contrast Media/adverse effects* ; Models, Animal

Acute Kidney Injury ; chemically induced ; Anti-Infective Agents ; adverse effects ; Child, Preschool ; Humans ; Male ; Organometallic Compounds ; adverse effects

Acute Kidney Injury ; chemically induced ; Contrast Media ; adverse effects ; Diabetes Mellitus, Type 2 ; physiopathology ; Humans ; Risk Factors

Acute Kidney Injury ; chemically induced ; Child ; Humans ; Male ; Methotrexate ; administration & dosage ; adverse effects ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy

OBJECTIVESTo test the hypothesis that urine N-acetyl-beta-D-glucosaminidase (NAG) is a nearly biomarker for acute kidney injury in patients with acute paraquat poisoning.

METHODSForty-four patients with paraquat intoxication and 40 age and gender-matched healthy control participants were recruited. The urine N-acetyl-beta-D-glucosaminidase was determined by spectrophotometric methods.

RESULTSThe urine N-acetyl-beta-D-glucosaminidase activities in the patients with paraquat poisoning were higher than the corresponding values in the control participants (P<0.01); The prevalence rate of mortality was significantly higher in subjects with N-acetyl-beta-D-glucosaminidase activities ≥25 U/g Cr than in those N-acetyl-beta-D-glucosaminidase activities <25 Ulg Cr (34.4% vs 16.7%, P<0.01).

CONCLUSIONSThe urine N-acetyl-beta-D-glucosaminidase could be used as an early biomarker for acute kidney injury and predictor of mortality inpatients with acute paraquat intoxication.

Acetylglucosaminidase ; urine ; Acute Kidney Injury ; chemically induced ; diagnosis ; Adolescent ; Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Paraquat ; poisoning ; Young Adult