• Title/Summary/Keyword: Nephrology

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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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    • v.42 no.12
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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.

Disseminated adenovirus infection in a 10-year-old renal allograft recipient

  • Lee, Bora;Park, Eujin;Ha, Jongwon;Ha, Il Soo;Cheong, Hae Il;Kang, Hee Gyung
    • Kidney Research and Clinical Practice
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    • v.37 no.4
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    • pp.414-417
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    • 2018
  • Disseminated adenovirus infection can result in high mortality and morbidity in immunocompromised patients. Here, we report the case of a 10-year-old renal allograft recipient who presented with hematuria and dysuria. Adenovirus was isolated from his urine. His urinary symptoms decreased after intravenous hydration and reduction of immunosuppressants. However, 2 weeks later he presented with general weakness and laboratory tests indicated renal failure necessitating emergency hemodialysis. Adenovirus was detected in his sputum; therefore, intravenous ganciclovir and immunoglobulin therapy were initiated. Renal biopsy revealed diffuse necrotizing granulomatous tubulointerstitial nephritis compatible with renal involvement of the viral infection. Adenovirus was detected in his serum. Despite cidofovir administration for 2 weeks, adenovirus was also detected in the cerebrospinal fluid, resulting in generalized tonic-clonic seizure. The patient died 7 weeks after the onset of urinary symptoms. Adenovirus should be considered in screening tests for post-renal transplantation patients who present with hemorrhagic cystitis.

Acute aortoiliac thrombosis in minimal change disease

  • Soyoung Lee;Hwarim Kang;Jongho Shin;Kyeong Min Kim
    • Journal of Medicine and Life Science
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    • v.19 no.3
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    • pp.125-129
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    • 2022
  • Patients with nephrotic syndrome (NS) are generally known to be at greater risk for thrombosis, with arterial thrombosis-related complications being relatively rare compared to venous thrombosis-related complications. This report describes a 46-year-old male with historically proven minimal change disease (MCD) complicated by acute aortoiliac thrombosis. He had been diagnosed with MCD 8 months previously and was treated successfully with steroids. He was prescribed a second course of high-dose steroids (prednisolone 1 mg/kg/day) due to a relapse of MCD at the outpatient clinic 8 days before the emergency department visit. The patient presented with severe pain in both lower limbs and was diagnosed with aortoiliac thrombosis that developed during high-dose steroid treatment. He subsequently underwent surgical thromboembolectomy. Hypoalbuminemia has the strongest association with the risk of thromboembolism. According to international clinical practice guidelines, anticoagulant therapy is recommended when serum albumin is ≤2-2.5 g/dL. However, as serum albumin levels may be relatively high in the early phase of NS, as in this case report, an individualized anticoagulation strategy for each patient should be considered, regardless of serum albumin levels.

Recovery of Delayed Graft Function after Calcineurin Inhibitor Sparing Regimen in a Renal Transplant Patient with Calcineurin Inhibitor Toxicity: A Case Report

  • Kang, Seok Hui;Yun, Woo Sung;Cho, Kyu Hyang;Do, Jun Young;Yoon, Kyung Woo;Park, Jong Won
    • Korean Journal of Transplantation
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    • v.28 no.3
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    • pp.165-168
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    • 2014
  • The recipient candidate was a 51-year-old male with end-stage renal disease owing to diabetes mellitus. The initial immunosuppressive regimen included basiliximab for induction and tacrolimus, mycophenolate mofetil, and steroids. Urine output was 413 mL/day on the operative day and 100 mL/day on the postoperative day (POD) 1. There was no definite stenosis of the ureter or vessels. He had anuria on POD 2~4 and he had undergone hemodialysis. His serum creatinine level did not decrease. Therefore, a graft biopsy was performed on POD 4. The pathologic finding was consistent with acute calcineurin inhibitor (CNI) toxicity. There was no evidence of rejection or acute tubular necrosis. Anuria continued on POD 6; therefore, we started sirolimus instead of a CNI based regimen. Graft function was gradually recovered 1 day after reduction of CNI dose and hemodialysis was stopped. The serum creatinine level was normalized on POD 10. He was discharged on POD 21.

Aurantio-obtusin exerts an anti-inflammatory effect on acute kidney injury by inhibiting NF-κB pathway

  • Haiyan Xiang;Yun Zhang;Yan Wu;Yaling Xu;Yuanhao Hong
    • The Korean Journal of Physiology and Pharmacology
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    • v.28 no.1
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    • pp.11-19
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    • 2024
  • Acute kidney injury (AKI) is one of the major complications of sepsis. Aurantio-obtusin (AO) is an anthraquinone compound with antioxidant and anti-inflammatory activities. This study was developed to concentrate on the role and mechanism of AO in sepsis-induced AKI. Lipopolysaccharide (LPS)-stimulated human renal proximal tubular epithelial cells (HK-2) and BALB/c mice receiving cecal ligation and puncture (CLP) surgery were used to establish in vitro cell model and in vivo mouse model. HK-2 cell viability was measured using MTT assays. Histological alterations of mouse renal tissues were analyzed via hematoxylin and eosin staining. Renal function of mice was assessed by measuring the levels of serum creatinine (SCr) and blood urea nitrogen (BUN). The concentrations of pro-inflammatory cytokines in HK-2 cells and serum samples of mice were detected using corresponding ELISA kits. Protein levels of factors associated with nuclear factor kappa-B (NF-κB) pathway were measured in HK-2 cells and renal tissues by Western blotting. AO exerted no cytotoxic effect on HK-2 cells and AO dose-dependently rescued LPS-induced decrease in HK-2 cell viability. The concentrations of pro-inflammatory cytokines were increased in response to LPS or CLP treatment, and the alterations were reversed by AO treatment. For in vivo experiments, AO markedly ameliorated renal injury and reduced high levels of SCr and BUN in mice underwent CLP operation. In addition, AO administration inhibited the activation of NF-κB signaling pathway in vitro and in vivo. In conclusion, AO alleviates septic AKI by suppressing inflammatory responses through inhibiting the NF-κB pathway.

Effect of atorvastatin on dendritic cells of tubulointerstitium in diabetic rats

  • Tu, Yafang;Jia, Ruhan;Ding, Guohua;Chen, Ling
    • BMB Reports
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    • v.43 no.3
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    • pp.188-192
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    • 2010
  • Inflammatory reactology has become increasingly important in diabetic kidney disease. In this study, we estabilished STZ-induced diabetic rat model to investigate whether dendritic cells (DCs) mediated tubulointerstitial damages, and whether the effects by DCs were mediated by P-selectin expression and can be inhibited by atorvastatin. The study demonstrated that there was an accumulation of DCs in diabetic rats mediated by P-selectin. It also showed the accumulation of DCs and expression of P-selectin was closely correlated with the degree of renal tubulointerstitial injury. These effects were markedly attenuated by atorvastatin. Thus, DCs play a role in tubulointerstitial damages, atorvasttin can prevent renal tubulointerstitium from damage by inhibiting the P-selectin expression and DCs migration.

Intestinal Paragonimiasis with Colonic Ulcer and Hematochezia in An Elderly Taiwanese Woman

  • Liu, Chung-Te;Chen, Yen-Cheng;Chen, Tso-Hsiao;Barghouth, Ursula;Fan, Chia-Kwung
    • Parasites, Hosts and Diseases
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    • v.50 no.4
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    • pp.349-352
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    • 2012
  • A 94-year-old female with end-stage renal disease presents with fever, fatigue, and hematochezia. She had previously resided in Hunan Province, China, and Myanmar, and she immigrated to Taiwan 30 years ago. Colonoscopy revealed a colonic ulcer. Biopsy of the colonic ulcer showed ulceration of the colonic mucosa, and many Paragonimus westermani-like eggs were noted. Serum IgG antibody levels showed strong reactivity with P. westermani excretory-secretory antigens by ELISA. Intestinal paragonimiasis was thus diagnosed according to the morphology of the eggs and serologic finding. After treatment with praziquantel, hematochezia resolved. The present case illustrates the extreme manifestations encountered in severe intestinal paragonimiasis.

Recurrence of Minimal Change Disease Following a Motor Vehicle Trauma: An Atypical Cause and Review of Literature

  • Depa, Jayaramakrishna;Coritsidis, George
    • Journal of Trauma and Injury
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    • v.32 no.2
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    • pp.111-114
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    • 2019
  • Minimal change disease (MCD) in children has a favorable long-term prognosis, and development of end-stage renal disease is very uncommon; less than 5%. In the first case of its kind, we report a 21-year-old female with a history of MCD at the age of 6, who had late relapse subsequent to a motorcycle accident resulting in a de-gloving skin injury and intensive care unit admission. MCD was confirmed by normal light microscopy, podocyte effacement on electron microscopy and absence of any deposits on immunofluorescence 3 weeks after the incident due to critical illness. It is postulated that the skin injury is what caused the relapse of MCD.