1.Dihydroartemisinin attenuates ischemia/reperfusion-induced renal tubular senescence by activating autophagy.
Huiling LIU ; Zhou HUANG ; Hong JIANG ; Ke SU ; Zilin SI ; Wenhui WU ; Hanyu WANG ; Dongxue LI ; Ninghua TAN ; Zhihao ZHANG
Chinese Journal of Natural Medicines (English Ed.) 2023;21(9):682-693
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
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Kidney
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Acute Kidney Injury/chemically induced*
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Ischemia
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Reperfusion Injury/drug therapy*
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Autophagy
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Reperfusion
3.Acute amiodarone syndrome after a single intravenous amiodarone bolus.
Xin Rong NG ; Liang Yi WEE ; Veerendra CHADACHAN
Singapore medical journal 2012;53(11):e225-7
Acute amiodarone toxicity after a single dose of intravenous amiodarone is very rarely seen. We report the case of a 64-year-old Chinese man who presented with atrial fibrillation and fluid overload due to congestive cardiac failure. He was treated with a single bolus dose of intravenous amiodarone, after which he developed elevated serum transaminases, coagulopathy, thrombocytopenia and acute renal failure. His parameters returned to normal after 25 days and his recovery was uneventful.
Acute Kidney Injury
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chemically induced
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Amiodarone
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adverse effects
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Anti-Arrhythmia Agents
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adverse effects
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Atrial Fibrillation
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drug therapy
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Blood Coagulation Disorders
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chemically induced
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Heart Failure
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complications
;
drug therapy
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Humans
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Male
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Middle Aged
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Thrombocytopenia
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chemically induced
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Transaminases
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blood
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Treatment Outcome
4.Acute Kidney Injury due to Sodium Bromate Intoxication: A Report of Two Cases.
Dong Hwan RYU ; Kyung Ae JANG ; Seok Min KIM ; Jong Won PARK ; Jun Young DO ; Kyung Woo YOON
The Korean Journal of Internal Medicine 2011;26(4):463-465
Sodium bromate is a strong oxidant used as a neutralizing solution in hair permanents, as well as an auxiliary agent in printing and dyeing. Accidental or deliberate ingestion of bromate solution has rarely been reported in Korea. The clinical manifestations of bromate intoxication are vomiting, diarrhea, central nervous system symptoms, oliguric or non-oliguric acute kidney injury, hemolytic anemia, and deafness; most of these manifestations are reversible, with the exception of renal failure and deafness. Here, we report on two patients who demonstrated distinct clinical progressions. In the first case, a 16-year-old woman was successfully treated with hemodialysis and recovered renal function without hearing loss. However, in the second case, delayed hemodialysis resulted in persistent renal failure and hearing loss in a 77-year-old woman. This suggests that emergency therapeutic measures, including hemodialysis, should be taken as soon as possible, as the rapid removal of bromate may be essential to preventing severe intoxication and its sequelae.
Acute Kidney Injury/*chemically induced/therapy
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Adolescent
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Aged
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Bromates/*toxicity
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Fatal Outcome
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Female
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Hearing Loss
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Humans
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Kidney Failure, Chronic/*therapy
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Renal Dialysis
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Sodium Compounds/*toxicity
6.Contrast-Induced Acute Kidney Injury after Coil Embolization for Aneurysmal Subarachnoid Hemorrhage
Hyun Goo LEE ; Won Ki KIM ; Je Young YEON ; Jong Soo KIM ; Keon Ha KIM ; Pyoung JEON ; Seung Chyul HONG
Yonsei Medical Journal 2018;59(1):107-112
PURPOSE: Contrast-induced acute kidney injury (CI-AKI) is associated with poor outcomes after percutaneous coronary intervention. However, CI-AKI has rarely been evaluated within the neurovascular field. The aim of this study was to investigate the incidence and clinical implication of CI-AKI after coil embolization in patients with an aneurysmal subarachnoid hemorrhage (aSAH). MATERIALS AND METHODS: Between January 2005 and March 2016, 192 patients who underwent coil embolization were enrolled in this study. CI-AKI was defined as an increase from baseline serum creatinine concentration of >25% or >0.5 mg/dL within 72 hours after coil embolization. A poor clinical outcome was defined as a score of ≥3 on the modified Rankin Scale at one-year post-treatment. RESULTS: A total of 16 patients (8.3%) died as a result of medical problems within one year. CI-AKI was identified in 14 patients (7.3%). Prominent risk factors for one-year mortality included CI-AKI [odds ratio (OR): 16.856; 95% confidence interval (CI): 3.437–82.664] and an initial Glasgow Coma Scale (GCS) score ≤8 (OR: 5.565; 95% CI: 1.703–18.184). A poor clinical outcome was associated with old age (≥65 years) (OR: 7.921; 95% CI: 2.977–21.076), CI-AKI (OR: 11.281; 95% CI: 2.138–59.525), an initial GCS score ≤8 (OR 31.02; 95% CI, 10.669–90.187), and a ruptured aneurysm (p=0.016, OR: 4.278) in posterior circulation. CONCLUSION: CI-AKI seems to be an independent predictor of the overall outcomes of aSAH after endovascular treatment.
Acute Kidney Injury/chemically induced
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Acute Kidney Injury/diagnostic imaging
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Acute Kidney Injury/etiology
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Acute Kidney Injury/mortality
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Adult
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Aged
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Aged, 80 and over
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Aneurysm/complications
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Aneurysm/diagnostic imaging
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Aneurysm/therapy
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Angiography
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Contrast Media/adverse effects
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Embolization, Therapeutic/adverse effects
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Female
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Humans
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Incidence
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Male
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Middle Aged
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Subarachnoid Hemorrhage/complications
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Subarachnoid Hemorrhage/diagnostic imaging
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Subarachnoid Hemorrhage/therapy
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Treatment Outcome
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Young Adult
7.Clinical features, laboratory findings and imaging appearances of venous diethylene glycol poisoning in patients with liver disease.
Ming-yue LUO ; Bing-liang LIN ; Zhi-liang GAO
Chinese Medical Journal 2009;122(19):2315-2320
BACKGROUNDThere was a hospital outbreak of venous diethylene glycol poisoning in Guangzhou, China. It is the only massive episode of venous diethylene glycol poisoning in history. Here we report its clinical features, laboratory findings, and imaging appearances.
METHODSThe clinical features of 15 venous diethylene glycol poisoning patients with liver disease were analyzed and summarized. Their laboratory findings and imaging appearances were comparatively analyzed before and after poisoning.
RESULTSAll poisoned patients presented with oliguric acute renal failure with anuria after a mean of 6 days. Carbon dioxide combination power of 13 patients dropped after a mean of 9 days with valley value on the 10th day, when metabolic acidosis developed. Gastroenteric symptoms or aggravation of gastroenteric symptoms were displayed in 11 patients after a mean of 9 days. Neurological system impairment was observed in 10 patients after a mean of 14 days. Seven patients had low fever after a mean of 6 days. Causes of death of 14 patients included multiple organ dysfunction syndrome, severe lung infection and massive haemorrhage of digestive tract. Blood creatinine and urea nitrogen were abnormal after a mean of 5 days with peak value on the 11th and 14th days, respectively. Serum calcium had no obvious change, and phosphorus was distinctively increased. Liver functions did not change significantly. Poisoned patients had higher white blood cell counts, but lower red blood cell counts and hemoglobin value. Of the 7 patients who exhibited mild, moderate or severe patchy consolidation shadowing in the lung, 2 manifested mild or severe gaseous distention and dilation of gastroenteric tract.
CONCLUSIONSMain features of venous diethylene glycol poisoning in patients with liver disease include oliguric acute renal failure, metabolic acidosis, gastroenteric symptoms or aggravation of gastroenteric symptoms, neurological system impairment and low fever, with a mortality rate of 93.33% in poisoned patients. There is also higher white blood cell counts and anemia, patchy consolidation shadowing in the lung, gaseous distention and dilation of gastroenteric tract, which occurs later than mild patchy consolidation shadowing and earlier than moderate patchy consolidation shadowing in the lung.
Acute Kidney Injury ; chemically induced ; Adolescent ; Adult ; Aged ; Benzopyrans ; poisoning ; Child ; Child, Preschool ; Drug Contamination ; Ethylene Glycols ; poisoning ; Female ; Humans ; Liver Diseases ; drug therapy ; Male ; Middle Aged
8.Pretreatment with dexmedetomidine ameliorates renal inflammation and oxidative stress in rats with lipopolysaccharide-induced sepsis and acute kidney injury.
Yu-Jie CHEN ; Chu-Lian GONG ; Fang TAN ; Shao-Li ZHOU
Journal of Southern Medical University 2015;35(10):1472-1475
OBJECTIVETo investigate the effects of dexmedetomidine on inflammatory reaction, oxidative stress, and renal pathologies in a rat model of lipopolysaccharide (LPS)-induced sepsis.
METHODSThirty-two SD rats were randomly divided into 4 groups, including a sham-operated group, LPS group with LPS (5 mg/kg) injection via the caudal vein 30 min before the operation, dexmedetomidine (Dex) +LPS group with additional Dex (10 µg/kg) injection via the caudal vein 10 min before LPS injection, and yohimbine+DEX+LPS group with intraperitoneal yohimbine (1 mg/kg) injection 40 min before and Dex injection 10 min before LPS injection. The levels of IL-1β, SOD and MDA in the plasma and renal tissues were determined, and the renal pathologies were examined.
RESULTSCompared with the sham-operated rats, the rats in LPS group showed significantly increased IL-1β and MDA levels and lowered SOD activity in the plasma and renal tissues (P<0.05) with obvious renal pathologies. Dex pretreatment obviously lowered IL-1β and MDA levels and enhanced SOD activity in the plasma and renal tissues in LPS-challenged rats (P<0.05), and significantly lessened LPS-induced renal pathologies.
CONCLUSIONDex can protect the rats against LPS-induced renal injury by alleviating the inflammatory reactions and cytokine oxidative stress, and this effect is mediated possibly by α2 receptors.
Acute Kidney Injury ; drug therapy ; Animals ; Dexmedetomidine ; pharmacology ; Inflammation ; drug therapy ; Interleukin-1beta ; metabolism ; Kidney ; drug effects ; physiopathology ; Lipopolysaccharides ; Malondialdehyde ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Sepsis ; chemically induced ; drug therapy ; Superoxide Dismutase ; metabolism
9.Prevention and Management of Adverse Reactions Induced by Iodinated Contrast Media.
Yi Wei WU ; Kheng Song LEOW ; Yujin ZHU ; Cher Heng TAN
Annals of the Academy of Medicine, Singapore 2016;45(4):157-164
Iodinated radiocontrast media (IRCM) is widely used in current clinical practice. Although IRCM is generally safe, serious adverse drug reactions (ADRs) may still occur. IRCM-induced ADRs may be subdivided into chemotoxic and hypersensitivity reactions. Several factors have been shown to be associated with an increased risk of ADRs, including previous contrast media reactions, history of asthma and allergic disease, etc. Contrast media with lower osmolality is generally recommended for at-risk patients to prevent ADRs. Current premedication prophylaxis in at-risk patients may reduce the risk of ADRs. However, there is still a lack of consensus on the prophylactic role of premedication. Contrast-induced nephropathy (CIN) is another component of IRCM-related ADRs. Hydration remains the mainstay of CIN prophylaxis in at-risk patients. Despite several preventive measures, ADRs may still occur. Treatment strategies for potential contrast reactions are also summarised in this article. This article summarises the pathophysiology, epidemiology and risk factors of ADRs with emphasis on prevention and treatment strategies. This will allow readers to understand the rationale behind appropriate patient preparation for diagnostic imaging involving IRCM.
Acute Kidney Injury
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chemically induced
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prevention & control
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therapy
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Contrast Media
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adverse effects
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Drug Hypersensitivity
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etiology
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prevention & control
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therapy
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Drug-Related Side Effects and Adverse Reactions
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etiology
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prevention & control
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therapy
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Fluid Therapy
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Humans
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Iodine Radioisotopes
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adverse effects
10.Acute renal failure following the use of rosiglitazone in a chronic kidney disease patient.
R Abdul GHANI ; S ZAINUDIN ; N A KAMARUDDIN ; N C T KONG
Singapore medical journal 2009;50(1):e32-4
Drug-induced acute interstitial nephritis is a well-recognised and important reversible cause of acute renal failure. Peroxisome-proliferator activated receptor-gamma agonists, such as rosiglitazone, have been proven to be safe in chronic kidney disease patients. We describe a 65-year-old man with long-standing diabetes mellitus and hypertension, presenting with a five-day history of fluid overload and uraemic symptoms. There was no ingestion of analgesics, alternative medicine and other nephrotoxic drugs, the only new prescription being rosiglitazone, which was commenced during his last clinic follow-up two weeks prior to presentation. He required haemodialysis with minimal improvement in renal profile, despite cessation of the offending drug. Renal biopsy revealed findings consistent with acute interstitial nephritis. An episode of upper gastrointestinal bleeding with bleeding duodenal ulcer limited the use of steroids. He was treated with a course of mycophenolate mofetil which showed good gradual response and he remained stable with residual renal impairment.
Acute Kidney Injury
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chemically induced
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drug therapy
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Aged
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Humans
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Hypoglycemic Agents
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adverse effects
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Immunosuppressive Agents
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therapeutic use
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Kidney Failure, Chronic
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complications
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Male
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Mycophenolic Acid
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analogs & derivatives
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therapeutic use
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Renal Dialysis
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Thiazolidinediones
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adverse effects