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  1. Tan CH, Tan NH, Sim SM, Fung SY, Jayalakshmi P, Gnanathasan CA
    Toxicon, 2012 Dec 1;60(7):1259-62.
    PMID: 22975088 DOI: 10.1016/j.toxicon.2012.08.012
    Mice experimentally envenomed with Hypnale hypnale venom (1× and 1.5×LD₅₀) developed acute kidney injury (AKI) principally characterized by raised blood urea and creatinine. Prolonged blood clotting time and hemorrhage in lungs implied bleeding tendency. Pallor noted in most renal cortices was suggestive of renal ischemia secondary to consumptive coagulopathy. Intravenous infusion of Hemato polyvalent antivenom following experimental envenoming effectively prevented death and AKI in all mice, supporting its potential therapeutic use in envenoming cases.
    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  2. Zainal D, Loo CS
    Singapore Med J, 1996 Feb;37(1):44-7.
    PMID: 8783912
    Acute renal failure (ARF) has undergone many changes with advances both in diagnosis and therapy. A retrospective study covering three and a half years from June 1986 to December 1989 of adults admitted to Hospital of the University of Science Malaysia examined the various aspects of presentation of the syndrome, management and areas where improvement can be made. A total of 164 patients were included in the study. 61.6% were male and 38.4% were female. The mean age was 49.8 +/- 17.2 years with 70% of patients being more than 40 years old. The aetiologies of acute renal failure were analysed and discussed. The majority of the patients (80%) had non-oliguric acute renal failure. Oliguric acute renal failure patients have higher mortality and more frequently need dialysis. Early recognition of acute renal failure and discerning use of nephrotoxic drugs could result in decrease in incidence and severity of renal failure.
    Matched MeSH terms: Acute Kidney Injury/prevention & control
  3. Yunos NM, Bellomo R, Taylor DM, Judkins S, Kerr F, Sutcliffe H, et al.
    Emerg Med Australas, 2017 Dec;29(6):643-649.
    PMID: 28597505 DOI: 10.1111/1742-6723.12821
    OBJECTIVE: Patients commonly receive i.v. fluids in the ED. It is still unclear whether the choice of i.v. fluids in this setting influences renal or patient outcomes. We aimed to assess the effects of restricting i.v. chloride administration in the ED on the incidence of acute kidney injury (AKI).

    METHODS: We conducted a before-and-after trial with 5008 consecutive ED-treated hospital admissions in the control period and 5146 consecutive admissions in the intervention period. During the control period (18 February 2008 to 17 August 2008), patients received standard i.v. fluids. During the intervention period (18 February 2009 to 17 August 2009), we restricted all chloride-rich fluids. We used the Kidney Disease: Improving Global Outcomes (KDIGO) staging to define AKI.

    RESULTS: Stage 3 of KDIGO-defined AKI decreased from 54 (1.1%; 95% confidence interval [CI] 0.8-1.4) to 30 (0.6%; 95% CI 0.4-0.8) (P = 0.006). The rate of renal replacement therapy did not change, from 13 (0.3%; 95% CI 0.2-0.4) to 8 (0.2%; 95% CI 0.1-0.3) (P = 0.25). After adjustment for relevant covariates, liberal chloride therapy remained associated with a greater risk of KDIGO stage 3 (hazard ratio 1.82; 95% CI 1.13-2.95; P = 0.01). On sensitivity assessment after removing repeat admissions, KDIGO stage 3 remained significantly lower in the intervention period compared with the control period (P = 0.01).

    CONCLUSION: In a before-and-after trial, a chloride-restrictive strategy in an ED was associated with a significant decrease in the incidence of stage 3 of KDIGO-defined AKI.

    Matched MeSH terms: Acute Kidney Injury/prevention & control
  4. Tan YC, Abdul Sattar M, Ahmeda AF, Abdul Karim Khan N, Murugaiyah V, Ahmad A, et al.
    PLoS One, 2020;15(4):e0231472.
    PMID: 32298299 DOI: 10.1371/journal.pone.0231472
    Oxidative stress is involved in the pathogenesis of a number of diseases including hypertension and renal failure. There is enhanced expression of nicotinamide adenine dinucleotide (NADPH oxidase) and therefore production of hydrogen peroxide (H2O2) during renal disease progression. This study investigated the effect of apocynin, an NADPH oxidase inhibitor and catalase, an H2O2 scavenger on Cyclosporine A (CsA) nephrotoxicity in Wistar-Kyoto rats. Rats received CsA (25mg/kg/day via gavage) and were assigned to vehicle, apocynin (2.5mmol/L p.o.), catalase (10,000U/kg/day i.p.) or apocynin plus catalase for 14 days. Renal functional and hemodynamic parameters were measured every week, and kidneys were harvested at the end of the study for histological and NADPH oxidase 4 (NOX4) assessment. Oxidative stress markers and blood urea nitrogen (BUN) were measured. CsA rats had higher plasma malondialdehyde (by 340%) and BUN (by 125%), but lower superoxide dismutase and total antioxidant capacity (by 40%, all P<0.05) compared to control. CsA increased blood pressure (by 46mmHg) and decreased creatinine clearance (by 49%, all P<0.05). Treatment of CsA rats with apocynin, catalase, and their combination decreased blood pressure to near control values (all P<0.05). NOX4 mRNA activity was higher in the renal tissue of CsA rats by approximately 63% (P<0.05) compared to controls but was reduced in apocynin (by 64%), catalase (by 33%) and combined treatment with apocynin and catalase (by 84%) compared to untreated CsA rats. Treatment of CsA rats with apocynin, catalase, and their combination prevented hypertension and restored renal functional parameters and tissue Nox4 expression in this model. NADPH inhibition and H2O2 scavenging is an important therapeutic strategy during CsA nephrotoxicity and hypertension.
    Matched MeSH terms: Acute Kidney Injury/prevention & control
  5. Abdul Hamid Z, Budin SB, Wen Jie N, Hamid A, Husain K, Mohamed J
    J Zhejiang Univ Sci B, 2012 Mar;13(3):176-85.
    PMID: 22374609 DOI: 10.1631/jzus.B1100133
    Paracetamol (PCM) overdose can cause nephrotoxicity with oxidative stress as one of the possible mechanisms mediating the event. In this study, the effects of ethyl acetate extract of Zingiber zerumbet rhizome [200 mg per kg of body weight (mg/kg) and 400 mg/kg] on PCM-induced nephrotoxicity were examined. Rats were divided into five groups containing 10 rats each. The control group received distilled water while other groups were treated with extract alone (400 mg/kg), PCM alone (750 mg/kg), 750 mg/kg PCM+200 mg/kg extract (PCM+200-extract), and 750 mg/kg PCM+400 mg/kg extract (PCM+400-extract), respectively, for seven consecutive days. The Z. zerumbet extract was given intraperitoneally concurrent with oral administration of PCM. Treatment with Z. zerumbet extract at doses of 200 and 400 mg/kg prevented the PCM-induced nephrotoxicity and oxidative impairments of the kidney, as evidenced by a significantly reduced (P<0.05) level of plasma creatinine, plasma and renal malondialdehyde (MDA), plasma protein carbonyl, and renal advanced oxidation protein product (AOPP). Furthermore, both doses were also able to induce a significant increment (P<0.05) of plasma and renal levels of glutathione (GSH) and plasma superoxide dismutase (SOD) activity. The nephroprotective effects of Z. zerumbet extract were confirmed by a reduced intensity of renal cellular damage, as evidenced by histological findings. Moreover, Z. zerumbet extract administered at 400 mg/kg was found to show greater protective effects than that at 200 mg/kg. In conclusion, ethyl acetate extract of Z. zerumbet rhizome has a protective role against PCM-induced nephrotoxicity and the process is probably mediated through its antioxidant properties.
    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  6. Alharazy SM, Kong N, Saidin R, Gafor AH, Maskon O, Mohd M, et al.
    Angiology, 2014 Mar;65(3):225-6.
    PMID: 23564021 DOI: 10.1177/0003319713483544
    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  7. Pariyani R, Ismail IS, Azam A, Khatib A, Abas F, Shaari K, et al.
    J Pharm Biomed Anal, 2017 Feb 20;135:20-30.
    PMID: 27987392 DOI: 10.1016/j.jpba.2016.12.010
    Orthosiphon stamineus (OS) is a popular medicinal herb used in traditional Chinese medicine as a diuretic agent and for renal system disorders. This study employed 1H NMR based metabolomics approach to investigate the possible protective activity of OS in cisplatin induced nephrotoxicity owing to its diuretic and antioxidant activities. Aqueous (OSAE) and 50% aqueous ethanolic (OSFE) extracts of OS leaves were orally administered at 400mg/kg BW doses to rats which were then intraperitoneally injected with cisplatin at 5mg/kg BW dose. The 1H NMR profile of the urine samples collected on day 5 after cisplatin administration were analyzed by multivariate pattern recognition techniques, whereby 19 marker metabolites suggestive in the involvement of TCA cycle, disturbed energy metabolism, altered gut microflora and BCAA metabolism pathways were identified. It was observed that OSFE caused significant changes (p<0.05) in the levels of 8 markers namely leucine, acetate, hippurate, lysine, valine, 2-oxoglutarate, 3-HBT and acetoacetate resulting in a moderate ameliorative effect, however, it did not completely protect from nephrotoxicity. OSAE did not demonstrate significant down regulatory effects on any markers, albeit, it potentiated the cisplatin nephrotoxicity by inducing significant increase in glucose, glycine, creatinine, citrate, TMAO, acetate and creatine levels. A Principal Component Analysis (PCA) of the 1H NMR spectra of OS extracts identified that OSFE had higher concentrations of the secondary metabolites such as caffeic acid, chlorogenic acid, protocatechuic acid and orthosiphol, among others. Whereas, OSAE was characterized by higher concentrations of acetate, lactate, succinic acid, valine and phosphatidylcholine. This research denotes the first comprehensive analysis to identify the effects of OS extracts on cisplatin nephrotoxicity.
    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  8. Karnad DR, Nor MBM, Richards GA, Baker T, Amin P, Council of the World Federation of Societies of Intensive and Critical Care Medicine
    J Crit Care, 2018 Feb;43:356-360.
    PMID: 29132978 DOI: 10.1016/j.jcrc.2017.11.007
    Severe malaria is common in tropical countries in Africa, Asia, Oceania and South and Central America. It may also occur in travelers returning from endemic areas. Plasmodium falciparum accounts for most cases, although P vivax is increasingly found to cause severe malaria in Asia. Cerebral malaria is common in children in Africa, manifests as coma and seizures, and has a high morbidity and mortality. In other regions, adults may also develop cerebral malaria but neurological sequelae in survivors are rare. Acute kidney injury, liver dysfunction, thrombocytopenia, disseminated intravascular coagulopathy (DIC) and acute respiratory distress syndrome (ARDS) are also common in severe malaria. Metabolic abnormalities include hypoglycemia, hyponatremia and lactic acidosis. Bacterial infection may coexist in patients presenting with shock or ARDS and this along with a high parasite load has a high mortality. Intravenous artesunate has replaced quinine as the antimalarial agent of choice. Critical care management as per severe sepsis is also applicable to severe malaria. Aggressive fluid boluses may not be appropriate in children. Blood transfusions may be required and treatment of seizures and raised intracranial pressure is important in cerebral malaria in children. Mortality in severe disease ranges from 8 to 30% despite treatment.
    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  9. Poh WY, Omar MS, Tan HP
    Ann Saudi Med, 2018 8 6;38(4):269-276.
    PMID: 30078025 DOI: 10.5144/0256-4947.2018.269
    BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) is rec.ognized as a common complication of radiographic contrast-enhanced procedures. N-acetylcysteine (NAC) is commonly prescribed, but CI-AKI can still develop despite NAC administration as prophylaxis.

    OBJECTIVE: Identify the predictive factors for development of CI-AKI in patients prescribed NAC.

    DESIGN: Prospective, cross-sectional.

    SETTING: A tertiary hospital in Malaysia.

    PATIENTS AND METHODS: All adult patients who were prescribed NAC for prevention of CI-AKI were identified through an NAC drug us.age monitoring card maintained by the inpatient pharmacy. The study was conducted from March to July 2017.

    MAIN OUTCOME MEASURES: Statistically significant predictive fac.tors for development of CI-AKI despite NAC administration.

    SAMPLE SIZE: 152 RESULTS: The most commonly recognized risk factors for CI-AKI present in the study population were renal impairment (n=131, 86.2%), anemia (n=107, 70.4%), and diabetes mellitus (n=90, 59.2%). Hydration therapy was initiated in 128 patients (84.2%) prior to the contrast-enhanced procedure. Sixty-one (40.1%) were treated with nephrotoxic medications concomitantly with NAC. Fifteen (9.9%) patients developed AKI. Hypotension (OR: 6.02; 95% CI 1.25-28.97) and use of high contrast volume (OR: 6.56; 95% CI: 1.41-30.64) significantly increased the odds for AKI. Prior hydration therapy (OR: 0.13; 95% CI 0.03-0.59) showed protective effects.

    CONCLUSION: The risk predictors identified for CI-AKI were hypotension, high contrast volume and prior hydration therapy.

    LIMITATION: May not have identified other confounding factors for development of CI-AKI.

    CONFLICT OF INTEREST: None.

    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  10. Cooper DJ, Plewes K, Grigg MJ, Rajahram GS, Piera KA, William T, et al.
    Trials, 2018 Apr 24;19(1):250.
    PMID: 29690924 DOI: 10.1186/s13063-018-2600-0
    BACKGROUND: Plasmodium knowlesi is the most common cause of human malaria in Malaysia. Acute kidney injury (AKI) is a frequent complication. AKI of any cause can have long-term consequences, including increased risk of chronic kidney disease, adverse cardiovascular events and increased mortality. Additional management strategies are therefore needed to reduce the frequency and severity of AKI in malaria. In falciparum malaria, cell-free haemoglobin (CFHb)-mediated oxidative damage contributes to AKI. The inexpensive and widely available drug paracetamol inhibits CFHb-induced lipid peroxidation via reduction of ferryl haem to the less toxic Fe3+ state, and has been shown to reduce oxidative damage and improve renal function in patients with sepsis complicated by haemolysis as well as in falciparum malaria. This study aims to assess the ability of regularly dosed paracetamol to reduce the incidence and severity of AKI in knowlesi malaria by attenuating haemolysis-induced oxidative damage.

    METHODS: PACKNOW is a two-arm, open-label randomised controlled trial of adjunctive paracetamol versus no paracetamol in patients aged ≥ 5 years with knowlesi malaria, conducted over a 2-year period at four hospital sites in Sabah, Malaysia. The primary endpoint of change in creatinine from enrolment to 72 h will be evaluated by analysis of covariance (ANCOVA) using enrolment creatinine as a covariate. Secondary endpoints include longitudinal changes in markers of oxidative stress (plasma F2-isoprostanes and isofurans) and markers of endothelial activation/Weibel-Palade body release (angiopoietin-2, von Willebrand Factor, P-selectin, osteoprotegerin) over 72 h, as well as blood and urine biomarkers of AKI. This study will be powered to detect a difference between the two treatment arms in a clinically relevant population including adults and children with knowlesi malaria of any severity.

    DISCUSSION: Paracetamol is widely available and has an excellent safety profile; if a renoprotective effect is demonstrated, this trial will support the administration of regularly dosed paracetamol to all patients with knowlesi malaria. The secondary outcomes in this study will provide further insights into the pathophysiology of haemolysis-induced oxidative damage and acute kidney injury in knowlesi malaria and other haemolytic diseases.

    TRIAL REGISTRATION: Clinicaltrials.gov, NCT03056391 . Registered on 12 October 2016.

    Matched MeSH terms: Acute Kidney Injury/prevention & control*
  11. Garcia S, Bhatt DL, Gallagher M, Jneid H, Kaufman J, Palevsky PM, et al.
    JACC Cardiovasc Interv, 2018 11 26;11(22):2254-2261.
    PMID: 30466822 DOI: 10.1016/j.jcin.2018.07.044
    OBJECTIVES: The aim of this study was to compare intravenous (IV) sodium bicarbonate with IV sodium chloride and oral acetylcysteine with placebo for the prevention of contrast-associated acute kidney injury (CAAKI) and intermediate-term adverse outcomes.

    BACKGROUND: Data are conflicting on the optimal strategy to reduce CAAKI and related complications after percutaneous coronary intervention (PCI).

    METHODS: The PRESERVE (Prevention of Serious Adverse Events Following Angiography) trial used a 2 × 2 factorial design to randomize 5,177 patients with stage III or IV chronic kidney disease undergoing angiography to IV 1.26% sodium bicarbonate or IV 0.9% sodium chloride and 5 days of oral acetylcysteine or placebo. A subgroup analysis was conducted of the efficacy of these interventions in patients who underwent PCI during the study angiographic examination. The primary endpoint was a composite of death, need for dialysis, or persistent kidney impairment at 90 days; CAAKI was a secondary endpoint.

    RESULTS: A total of 1,161 PRESERVE patients (mean age 69 ± 8 years) underwent PCI. The median estimated glomerular filtration rate was 50.7 ml/min/1.73 m2 (interquartile range: 41.7 to 60.1 ml/min/1.73 m2), and 952 patients (82%) had diabetes mellitus. The primary endpoint occurred in 15 of 568 patients (2.6%) in the IV sodium bicarbonate group and 24 of 593 patients (4.0%) in the IV sodium chloride group (odds ratio: 0.64; 95% confidence interval: 0.33 to 1.24; p for interaction = 0.41) and in 23 of 598 patients (3.8%) in the acetylcysteine group and 16 of 563 patients (2.8%) in the placebo group (odds ratio: 1.37; 95% confidence interval: 0.71 to 2.62; p for interaction = 0.29). There were no significant between-group differences in the rates of CAAKI.

    CONCLUSIONS: Among patients with CKD undergoing PCI, there was no benefit of IV sodium bicarbonate over IV sodium chloride or of acetylcysteine over placebo for the prevention of CAAKI or intermediate-term adverse outcomes.

    Matched MeSH terms: Acute Kidney Injury/prevention & control*
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