• 대한수의학회지
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• 제57권1호
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• pp.55-57
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• 2017

A 5-year-old, 2.7 kg, spayed female Scottish Fold cat presented with hematemesis after administration of oral zaltoprofen, a non-steroidal anti-inflammatory drug, by the owner. Diagnostic imaging and blood analyses indicated development of acute kidney injury (AKI) resulting from zaltoprofen ingestion. To correct dehydration and anemic conditions, the cat received intravenous fluid therapy with whole blood transfusion and peroral N-acetylcysteine. Clinical signs resolved, but persistent azotemia was unresolved indicating that AKI could progress to chronic kidney disease. This case suggests that although zaltoprofen may have low adverse effects on humans, administration of zaltoprofen in cats can have serious adverse effects.

• Childhood Kidney Diseases
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• 제17권2호
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• pp.117-121
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• 2013

결석으로 인한 요관 폐쇄는 신후성 신부전의 주요한 원인으로 즉각적인 치료가 필요하다. 폐색 후 이뇨는 폐쇄성 요로 질환의 막힘 제거될 때 흔히 나타날 수 있는 증상으로 특별한 치료 없이 회복되는 경우가 많으나 저혈압이나 전해질 이상 등의 소견이 나타날 경우에는 수액 요법을 통한 치료가 필요하다. 단일신 환아에서 4 mm 크기의 작은 결석으로 인한 신후성 신부전이 발생하였으며 결석이 배출되고 발생한 폐쇄 후 이뇨는 보존적 치료로 회복되었다. 대부분의 4 mm 미만의 작은 결석은 저절로 배출 된다고 알려져 있으나 저자들은 4 mm 크기의 결석으로 생긴 신후성 신부전 및 폐쇄 후 이뇨가 발생한 예를 경험하였기에 보고하는 바이다.

• Journal of Veterinary Science
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• 제23권5호
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• pp.72.1-72.14
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• 2022

Background: The treatment of acute kidney injury (AKI), a common disease in dogs, is limited. Therefore, an effective method to prevent AKI in veterinary clinics is particularly crucial. Objectives: Hydrogen sulfide (H₂S) is the third gaseous signal molecule involved in various physiological functions of the body. The present study investigated the effect of H₂S on cisplatin-induced AKI and the involved mechanisms in dogs. Methods: Cisplatin-injected dogs developed AKI symptoms as indicated by renal dysfunction and pathological changes. In the H₂S-treated group, 50 mM sodium hydrosulfide (NaHS) solution was injected at 1 mg/kg/h for 30 min before cisplatin injection. After 72 h, tissue and blood samples were collected immediately. We performed biochemical tests, optical microscopy studies, analysis with test kits, quantitative reverse-transcription polymerase chain reaction, and western blot analysis. Results: The study results demonstrated that cisplatin injection increased necroptosis and regulated the corresponding protein expression of receptor interacting protein kinase (RIPK) 1, RIPK3, and poly ADP-ribose polymerase 1; furthermore, it activated the expressions of inflammatory factors, including tumor necrosis factor-alpha, nuclear factor kappa B, and interleukin-1β, in canine kidney tissues. Moreover, cisplatin triggered oxidative stress and affected energy metabolism. Conversely, an injection of NaHS solution considerably reduced the aforementioned changes. Conclusions: In conclusion, H₂S protects the kidney from cisplatin-induced AKI through the mitigation of necroptosis and inflammation. These findings provide new and valuable clues for the treatment of canine AKI and are of great significance for AKI prevention in veterinary clinics.

• 한국해양바이오학회지
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• 제13권2호
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• pp.86-93
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• 2021

A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.

• Pediatric Infection and Vaccine
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• 제24권2호
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• pp.112-116
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• 2017

가와사키병은 다른 원인이 없는 발열과 함께 피부점막에 특징적인 병변을 보이는, 소아에서는 비교적 흔한 질환으로 일반적으로 급성기에는 혈역학적으로 안정적이다. 저자들은 심한 저혈압과 함께 급성 신손상이 있는 상태에서 내원한 8세 남아가 치료 중에 가와사키병으로 진단된 증례를 경험하였다. 최근에는 가와사키병 초기에 불안정한 혈역학적 상태를 가와사키병 쇼크증후군이라는 개념으로 정의하고 있다. 환아는 면역글로불린 치료 후 임상적으로 회복되었으나 관상동맥 확장 합병증이 확인되어 아스피린을 복용하고 있으며, 가와사키병의 합병증으로서는 비교적 드문 고혈압이 확인되어 베타 차단제를 사용하고 있다. 본 증례를 통해 가와사키병 쇼크증후군의 임상 양상을 알고, 혈관염이라는 가와사키병의 특성을 고려해볼 때 혈압 모니터링의 중요성을 깨닫게 되었다.

• Childhood Kidney Diseases
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• 제17권2호
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• pp.127-131
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• 2013

요낭종이란 신장 및 비뇨기계로부터 누출된 소변이 신장 및 신우 주위에 캡슐상의 낭종을 형성하는 드문 질환으로 자연발생적인 신우의 파열로 인한 누출은 매우 드물며, 대부분 요로와 신우 내강의 압력 증가에 의해 발생한다. 본 증례에서 18세 여자 환아는 내원 7일 전부터 시작된 고열과 핍뇨 및 호흡곤란을 주소로 내원하였다. 환아는 출생시 다운 증후군을 진단받았으며 평소 배뇨는 원활하였다. 입원 후 환아는 패혈증 쇼크 및 급성 신손상, 급성 호흡 곤란 증후군 진단 하에 항생제 및 스테로이드 충격 요법 시행 후 핍뇨, 호흡곤란 및 혈액검사 호전 소견 보였으나 7일 동안 유치된 도뇨관 제거 후 환아는 요 폐색 소견이 관찰되었다. 복부 전산화 단층 촬영상 좌측 신장 주위에 요낭종이 확인되어 좌측 요관에 Double-J catheter가 삽입 되었으며 신우의 파열 부위에 조영제 누출이 확인되었다. 시술 후 요 폐색 소견은 호전되었고, 배뇨성 방광 요도 조영술 상 좌측 신장의 4단계 방광 요관 역류가 관찰되었다. Double-J catheter 제거 3개월 후 좌측 신장 주변의 요낭종은 대부분 소실되었고, 좌측 신장의 방광 요관 역류는 보이지 않았다. 저자들은 급성 신부전 환아에서 유치 도뇨관 제거 후 배뇨곤란 및 요 폐색 소견을 보인 신 주위 요낭종 1례를 경험하였기에 보고하는 바이다.

• Journal of Microbiology and Biotechnology
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• 제32권6호
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• pp.740-748
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• 2022

As circ_UBE2D2 has been confirmed to have targeted binding sites with multiple miRNAs involved in septic acute kidney injury (SAKI), efforts in this study are directed to unveiling the specific role and relevant mechanism of circ_UBE2D2 in SAKI. HK-2 cells were treated with lipopolysaccharide (LPS) to construct SAKI model in vitro. After sh-circ_UBE2D2 was transfected into cells, the transfection efficiency was detected by qRT-PCR, cell viability and apoptosis were determined by MTT assay and flow cytometry, and expressions of Bcl-2, Bax and Cleaved-caspase 3 were quantified by western blot. Target genes associated with circ_UBE2D2 were predicted using bioinformatics analysis. After the establishment of SAKI rat model, HE staining and TUNEL staining were exploited to observe the effect of circ_UBE2D2 on tissue damage and cell apoptosis. The expression of circ_UBE2D2 was overtly elevated in LPS-induced HK-2 cells. Sh-circ_UBE2D2 can offset the inhibition of cell viability and the promotion of cell apoptosis induced by LPS. Circ_UBE2D2 and miR-370-3p as well as miR-370-3p and NR4A3 have targeted binding sites. MiR-370-3p inhibitor reversed the promoting effect of circ_UB2D2 silencing on viability of LPS-treated cells, but shNR4A3 neutralized the above inhibitory effect of miR-370-3p inhibitor. MiR-370-3p inhibitor weakened the down-regulation of NR4A3, Bax and Cleaved caspase-3 and the up-regulation of Bcl-2 induced by circ_UB2D2 silencing, but these trends were reversed by shNR4A3. In addition, sh-circ_UBE2D2 could alleviate the damage of rat kidney tissue. Circ_UBE2D2 mitigates the progression of SAKI in rats by targeting miR-370-3p/NR4A3 axis.

• International journal of advanced smart convergence
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• 제12권4호
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• pp.434-442
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• 2023

The relationship between acute kidney injury (AKI) prediction and nephrotoxic drugs, or drugs that adversely affect kidney function, is one that has yet to be explored in the critical care setting. One contributing factor to this gap in research is the limited investigation of drug modalities in the intensive care unit (ICU) context, due to the challenges of processing prescription data into the corresponding drug representations and a lack in the comprehensive understanding of these drug representations. This study addresses this gap by proposing a novel approach that leverages patient prescription data as a modality to improve existing models for AKI prediction. We base our research on Electronic Health Record (EHR) data, extracting the relevant patient prescription information and converting it into the selected drug representation for our research, the extended-connectivity fingerprint (ECFP). Furthermore, we adopt a unique multimodal approach, developing machine learning models and 1D Convolutional Neural Networks (CNN) applied to clinical drug representations, establishing a procedure which has not been used by any previous studies predicting AKI. The findings showcase a notable improvement in AKI prediction through the integration of drug embeddings and other patient cohort features. By using drug features represented as ECFP molecular fingerprints along with common cohort features such as demographics and lab test values, we achieved a considerable improvement in model performance for the AKI prediction task over the baseline model which does not include the drug representations as features, indicating that our distinct approach enhances existing baseline techniques and highlights the relevance of drug data in predicting AKI in the ICU setting.

• Asian Pacific Journal of Cancer Prevention
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• 제16권2호
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• pp.407-410
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• 2015

Background: Acute kidney injury is an important issue in chemotherapy receiving patients an neutrophil gelatinase-associated lipocalin has been proposed as a novel marker. We here aimed to assess the role of urinary levels for assessment after platin exposure. Materials and Methods: Patients who had treated with cisplatin or carboplatin or oxaliplatin containg regimens were included in this study. Baseline and postchemotherapy serum urea, creatinine, urine neutrophil gelatinase-associated lipocalin and urine creatinine levels were determined. To avoid the effects of hydration during chemotherapy infusion the urinary neutrophil gelatinase-associated lipocalin/urine creatinine ratio was used to determine acute kidney injury. Results: Of a total of 42 patients receiving platin compounds,14 (33.3%) received cisplatin containing regimens, 14 (33.3%) received carboplatin and 14 (33.3%) oxaliplatin. The median age was 60 (37-76) years. Nineteen of the patients (45.2%) had lung cancer, 12 (28.6%) colorectal cancer and 11 (26.2%) others. The median pre and post chemotherapy urine neutrophil gelatinase-associated lipocalin/urine creatinin ratio was 15.6 ng/mg and 35.8 ng/mg (p=0.041) in the cisplatin group, 32.5 ng/mg and 86.3 ng/mg (p=0.004) in the carboplatin group and 40.9 ng/mg and 62.3 ng/mg (p=0.243) in the oxaliplatin group. Conclusions: Nephrotoxicity is a serious side effect of chemotherapeutic agentslike cisplatin and carbopaltin, but only to a lower extent oxaliplatin. All platin compounds must be used carefully and urine neutrophil gelatinase-associated lipocalin measurement seems to be promising in detecting acute kidney injury earlier than with creatinine.

• The Korean Journal of Physiology and Pharmacology
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• 제28권1호
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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.