• 제목/요약/키워드: acute renal injury

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비만 환자에서 리라글루티드 증량 과정에서 발생한 급성 신손상 (Acute Kidney Injury after Dose-Titration of Liraglutide in an Obese Patient)

  • 이희진;박혜순
    • 비만대사연구학술지
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    • 제1권2호
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    • pp.78-82
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    • 2022
  • Liraglutide (SaxendaR) is prescribed to induce and sustain weight loss in obese patients. The starting dose of liraglutide is 0.6 mg/day for 1 week, which is increased by 0.6 mg/day every week until the full maintenance dose of 3 mg/day is achieved. Such dose titration is needed to prevent side effects, which primarily include gastrointestinal problems such as nausea, diarrhea, constipation, vomiting, dyspepsia, and abdominal pain. A 35-year-old, reportedly healthy obese man receiving liraglutide treatment for obesity visited the emergency room complaining of generalized weakness and dizziness accompanied by repeated diarrhea and vomiting. He reported over 20 episodes of diarrhea starting the day after liraglutide dose escalation from 1.2 mg/day to 1.8 mg/day. Laboratory findings suggested pre-renal acute kidney injury, including serum creatinine 4.77 mg/dl, blood urea nitrogen (BUN) 37 mg/dl, estimated glomerular filtration rate (eGFR) 15 ml/min/1.73 m2, and Fractional excretion of sodium 0.08. After volume repletion therapy, his renal function recovered to a normal range with laboratory values of creatinine 1.08 mg/dl, BUN 14 mg/dl, and eGFR 88 ml/min/1.73 m2. This case emphasizes the need for caution when prescribing glucagon-like peptide-1 receptor agonists, including liraglutide, given the risk of serious renal impairments induced by volume depletion and dehydration through severe-grade diarrhea and vomiting.

신생아와 영아의 지속적 신대체 요법 (Continuous Renal Replacement Therapy in Infants and Neonates)

  • 김성헌;신재일
    • Childhood Kidney Diseases
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    • 제18권1호
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    • pp.13-17
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    • 2014
  • 지속적 신 대체 요법(CRRT)은 급성 신손상이 있는 중증 소아의 치료로 점차 사용이 늘어나고 있으며 CRRT의 기술과 실제 사용법이 발달하면서 작은 영아나 신생아에서도 그 사용이 조금씩 늘어나고 있다. 고암모니아혈증이나 체외막산소화 장치(ECMO) 치료 중에 발생한 급성 신손상 등의 경우 CRRT가 안전하고 효과적인 치료가 될 수 있으나, 혈관 접근이나 출혈 그리고 신생아 전용 CRRT device의 부재로 인한 여러 가지 제한점이 있다. 이 종설에서는 기본적인 CRRT의 원리를 알아보고 신생아와 영아에서 특별히 고려해야 할 사항들에 대해 알아보고자 한다.

Bioactive Compounds for the Treatment of Renal Disease

  • Cho, Kang Su;Ko, In Kap;Yoo, James J.
    • Yonsei Medical Journal
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    • 제59권9호
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    • pp.1015-1025
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    • 2018
  • Kidney diseases including acute kidney injury and chronic kidney disease are among the largest health issues worldwide. Dialysis and kidney transplantation can replace a significant portion of renal function, however these treatments still have limitations. To overcome these shortcomings, a variety of innovative efforts have been introduced, including cell-based therapies. During the past decades, advances have been made in the stem cell and developmental biology, and tissue engineering. As part of such efforts, studies on renal cell therapy and artificial kidney developments have been conducted, and multiple therapeutic interventions have shown promise in the pre-clinical and clinical settings. More recently, therapeutic cell-secreting secretomes have emerged as a potential alternative to cell-based approaches. This approach involves the use of renotropic factors, such as growth factors and cytokines, that are produced by cells and these factors have shown effectiveness in facilitating kidney function recovery. This review focuses on the renotropic functions of bioactive compounds that provide protective and regenerative effects for kidney tissue repair, based on the available data in the literature.

횡문근융해증에 의한 급성 신 손상이 동반된 렙토스피라증 1예 (Rhabdomyolysis Induced Acute Kidney Injury in a Patient with Leptospirosis)

  • 최윤정;박정민;정요한;남종호;정현희;김태우;조규향;도준영;윤경우;박종원
    • Journal of Yeungnam Medical Science
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    • 제28권1호
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    • pp.54-59
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    • 2011
  • Leptospirosis is a spirochetal infectious disease caused by $Leptospira$ $interrogans$, and may vary in degree from an asymptomatic infection to a severe and fatal illness. The kidney is one of the principal target organs of $Leptospira$. Renal disorders caused by $Leptospira$ infection vary from an abnonnality in urinalysis to acute kidney injury (AKI). Incidence of AKI in severe leptospirosis varies from 40% to 60%. AKI reflects the severity of leptospirosis and is generally accompanied by cholestatic jaundice. The pathophysiology of AKI in leptospirosis consists of hypovolemia, direct tubular toxicity, and rhabdomyolysis. Most patients with acute leptospirosis experience severe myalgias, and show laboratory evidence of mild rhabdomyolysis. However, occurrence of severe rhabdomyolysis is rare. We report here on a patient with leoptospirosis, who had severe rhabdomyolysis and acute kidney injury without jaundice.

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미니돼지의 신허혈-재관류에 의한 급성신손상 모델에서의 유용한 바이오마커 (Effective Biomarkers for Miniature Pig in Acute Kidney Injury Using Renal Ischemia-Reperfusion Model)

  • 김세은;심경미;최석화;강성수
    • 한국임상수의학회지
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    • 제29권5호
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    • pp.372-376
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    • 2012
  • 급성신손상은 높은 이환율과 치사율을 나타내는 심각한 질환이며, 허혈-재관류에 의한 신손상은 급성신손상의 중요한 원인이 된다. 본 연구는 미니돼지에서 급성신손상을 진단하는데 임상적으로 유용한 바이오마커를 찾아내기 위해 실시되었다. 세 마리의 미니돼지에서 60분간 신동맥을 결찰하여 양측성 신허혈을 유도하였다. 각 미니돼지에서 결찰 전, 결찰 후 0, 1, 3, 5일에 혈액 및 뇨 검체를 채취하였다. 혈청 및 뇨 검체에서 BUN, creatinine, 나트륨 및 요산을 측정한 후 나트륨 및 요산의 분획배설율($FE_{Na}$, $FE_{UA}$)을 산출하였다. 또한 IL-6, IL-18, L-FABA 및 GST를 Western immunoblotting을 실시하여 측정하였다. 결과에서 세 마리 미니돼지 모두 혈청 BUN과 creatinine 농도는 결찰 후 1일째에 유의적으로 증가하였다. 그러나 $FE_{Na}$$FE_{UA}$는 현저한 개체차를 보였다. 수술 전과 후를 비교했을 때 허혈 이후의 뇨 검체에서는 IL-6, IL-18, L-FABP 및 GST의 농도가 유의적으로 증가하였다. 결론적으로, $FE_{Na}$$FE_{UA}$에 대해서는 추가적인 연구가 필요하다고 생각되며, 혈청 BUN, creatinine과 뇨 IL-6, IL-18, L-FABP 및 GST는 돼지의 허혈-재관류 모델에서 다른 바이오마커와 함께 급성신손상을 진단하는 민감한 바이오마커가 될 수 있을 것이라 생각된다.

Effectiveness of inactivated hantavirus vaccine on the disease severity of hemorrhagic fever with renal syndrome

  • Yi, Yongjin;Park, Hayne;Jung, Jaehun
    • Kidney Research and Clinical Practice
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    • 제37권4호
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    • pp.366-372
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    • 2018
  • Background: An inactivated Hantaan virus vaccine (iHV) has been broadly used as a preventive strategy for hemorrhagic fever with renal syndrome (HFRS) by the South Korean Army. After the vaccination program was initiated, the overall incidence of HFRS cases was reduced in the military population. While there are about 400 HFRS cases annually, few studies have demonstrated the efficacy of the iHV in field settings. Therefore, this study aimed to evaluate the iHV efficacy on HFRS severity. Methods: From 2009 to 2017, HFRS cases were collected in South Korean Army hospitals along with patients' vaccination history. HFRS patients were classified retrospectively into two groups according to vaccination records: no history of iHV vaccination and valid vaccination. Vaccine efficacy on the severity of acute kidney injury (AKI) stage and dialysis events were investigated. Results: The effects of the iHV on renal injury severity in between 18 valid vaccinated and 110 non-vaccinated patients were respectively evaluated. In the valid vaccination group, six of the 18 HFRS patients (33.3%) had stage 3 AKI, compared to 60 of the 110 (54.5%) patients in the non-vaccination group. The iHV efficacy against disease progression ($VE_p$) was 58.1% (95% confidence interval, 31.3% to 88.0%). Conclusion: The iHV efficacy against the progression of HFRS failed to demonstrate statistically significant protection. However, different severity profiles were observed between the iHV and non-vaccination groups. Additional studies with larger populations are needed to demonstrate the effectiveness of the iHV in patients with HFRS.

급성신부전이 발생한 중증 외상 환자에서 저분자량헤파린 투여 후 발생한 심각한 출혈 합병증 (Serious Bleeding Complication Due to the Use of Low-molecular-weight heparin to treat a Traumatic Patient with Acute Renal Failure)

  • 경규혁;김운원;박성진;김기훈;김진수;박종권
    • Journal of Trauma and Injury
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    • 제24권2호
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    • pp.164-167
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    • 2011
  • Trauma is an important risk factor for a pulmonary thromboembolism, and anticoagulation is essential to prevent deep vein thrombosis (DVT) in patients with trauma. Low-molecular-weight heparin (LMWH) is excreted in the kidney; therefore, using LMWH in patients with renal insufficiency may increase the risk of bleeding complication. The following case describes a 55-year-old traffic accident victim who had massive bleeding and underwent a laparotomy for bleeding control. The patient had acute renal failure, and enoxaparin was administered for the prophylaxis of DVT. Although the patient suffered from serious complications such as pericardial hematoma, the patient recovered without sequellae and was discharged at day 84.

Augmenter of Liver Regeneration Alleviates Renal Hypoxia-Reoxygenation Injury by Regulating Mitochondrial Dynamics in Renal Tubular Epithelial Cells

  • Long, Rui-ting;Peng, Jun-bo;Huang, Li-li;Jiang, Gui-ping;Liao, Yue-juan;Sun, Hang;Hu, Yu-dong;Liao, Xiao-hui
    • Molecules and Cells
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    • 제42권12호
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    • pp.893-905
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    • 2019
  • Mitochondria are highly dynamic organelles that constantly undergo fission and fusion processes that closely related to their function. Disruption of mitochondrial dynamics has been demonstrated in acute kidney injury (AKI), which could eventually result in cell injury and death. Previously, we reported that augmenter of liver regeneration (ALR) alleviates renal tubular epithelial cell injury. Here, we gained further insights into whether the renoprotective roles of ALR are associated with mitochondrial dynamics. Changes in mitochondrial dynamics were examined in experimental models of renal ischemia-reperfusion (IR). In a model of hypoxia-reoxygenation (HR) injury in vitro, dynamin-related protein 1 (Drp1) and mitochondrial fission process protein 1 (MTFP1), two key proteins of mitochondrial fission, were downregulated in the Lv-ALR + HR group. ALR overexpression additionally had an impact on phosphorylation of Drp1 Ser637 during AKI. The inner membrane fusion protein, Optic Atrophy 1 (OPA1), was significantly increased whereas levels of outer membrane fusion proteins Mitofusin-1 and -2 (Mfn1, Mfn2) were not affected in the Lv-ALR + HR group, compared with the control group. Furthermore, the mTOR/4E-BP1 signaling pathway was highly activated in the Lv-ALR + HR group. ALR overexpression led to suppression of HR-induced apoptosis. Our collective findings indicate that ALR gene transfection alleviates mitochondrial injury, possibly through inhibiting fission and promoting fusion of the mitochondrial inner membrane, both of which contribute to reduction of HK-2 cell apoptosis. Additionally, fission processes are potentially mediated by promoting tubular cell survival through activating the mTOR/4E-BP1 signaling pathway.

Endotoxin-induced renal tolerance against ischemia and reperfusion injury is removed by iNOS, but not eNOS, gene-deletion

  • Kim, Jee-In;Jang, Hee-Seong;Park, Kwon-Moo
    • BMB Reports
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    • 제43권9호
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    • pp.629-634
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    • 2010
  • Endotoxin including lipopolysaccharide (LPS) confers organ tolerance against subsequent challenge by ischemia and reperfusion (I/R) insult. The mechanisms underlying this powerful adaptive defense remain to be defined. Therefore, in this study we attempted to determine whether nitric oxide (NO) and its associated enzymes, inducible NOS (iNOS) and endothelial NOS (eNOS, a constitutive NOS), are associated with LPS-induced renal tolerance against I/R injury, using iNOS (iNOS knock-out) or eNOS (eNOS knock-out) gene-deleted mice. A systemic low dose of LPS pretreatment protected kidney against I/R injury. LPS treatment increased the activity and expression of iNOS, but not eNOS, in kidney tissue. LPS pretreatment in iNOS, but not eNOS, knock-out mice did not protect kidney against I/R injury. In conclusion, the kidney tolerance to I/R injury conferred by pretreatment with LPS is mediated by increased expression and activation of iNOS.

Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress

  • Uddin, Md Jamal;Pak, Eun Seon;Ha, Hunjoo
    • The Korean Journal of Physiology and Pharmacology
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    • 제22권5호
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    • pp.567-575
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    • 2018
  • Acute kidney injury (AKI), which is defined as a rapid decline of renal function, becomes common and recently recognized to be closely intertwined with chronic kidney diseases. Current treatment for AKI is largely supportive, and endoplasmic reticulum (ER) stress has emerged as a novel mediator of AKI. Since carbon monoxide attenuates ER stress, the objective of the present study aimed to determine the protective effect of carbon monoxide releasing molecule-2 (CORM2) on AKI associated with ER stress. Kidney injury was induced after LPS (15 mg/kg) treatment at 12 to 24 h in C57BL/6J mice. Pretreatment of CORM2 (30 mg/kg) effectively prevented LPS-induced oxidative stress and inflammation during AKI in mice. CORM2 treatment also effectively inhibited LPS-induced ER stress in AKI mice. In order to confirm effect of CO on the pathophysiological role of tubular epithelial cells in AKI, we used mProx24 cells. Pretreatment of CORM2 attenuated LPS-induced ER stress, oxidative stress, and inflammation in mProx24 cells. These data suggest that CO therapy may prevent ER stress-mediated AKI.