김세중 교수
Sejoong Kim
서울대학교 · 의학
연구실 소개
김세중 교수의 연구실은 마이크로유체 기반의 '신장 온 어 칩'(Kidney-on-a-Chip) 기술을 핵심으로 하여 인간 신장 생리와 약물 유도 신손상(신독성)을 보다 정확하게 재현하고자 합니다. 기존 동물 모델의 한계를 보완해 인간의 약물 대사 및 신장 기능을 보다 유사한 조건에서 분석할 수 있는 생물학적 모델 개발에 주력하고 있으며, 특히 항생제 등 약물의 투여 방식이 신장 독성에 미치는 영향을 정량적으로 평가하는 데에 초점을 맞추고 있습니다. 또한, 신질환의 유전적 요인과 관련된 생물학적 메커니즘 규명에도 기여하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15Nephrotoxicity is often underestimated because renal clearance in animals is higher compared to in humans. This paper aims to illustrate the potential to fill in such pharmacokinetic gaps between animals and humans using a microfluidic kidney model. As an initial demonstration, we compare nephrotoxicity of a drug, administered at the same total dosage, but using different pharmacokinetic regimens. Kidney epithelial cell, cultured under physiological shear stress conditions, are exposed to gentam
Our study suggests that LF may better preserve RRF over the 12-month treatment period in incident CAPD patients.
ClinicalTrials.org Identifier: NCT02887469.
Traditional approaches to pathophysiology are advancing but still have many limitations that arise from real biologic systems and their associated physiological phenomena being too complicated. Microfluidics is a novel technology in the field of engineering, which provides new options that may overcome these hurdles. Microfluidics handles small volumes of fluids and may apply to various applications such as DNA analysis chips, other lab-on-a-chip analyses, micropropulsion, and microthermal techn
The findings of this study suggest that PLA2R SNPs might be associated with the risk of developing MN.
Using kidney-on-a-chip, researchers can create experimental environments resembling the physiological environments in human organs and obtain experimental results that better reflect human physiology. Kidney-ona- chip can be used to overcome the drawbacks of traditional animal models and to more effectively identify drug effects, interactions, and drug-induced nephrotoxicity.
TNF superfamily member 13 (TNFSF13) has been identified as a susceptibility gene for IgA nephropathy in recent genetic studies. However, the role of TNFSF13 in the progression of IgA nephropathy remains unresolved. We evaluated two genetic polymorphisms (rs11552708 and rs3803800) and plasma levels of TNFSF13 in 637 patients with IgA nephropathy, and determined the risk of ESRD according to theses variable. Neither of the examined genetic polymorphisms associated with a clinical outcome of IgA ne
We developed and externally validated a continuous AKI prediction model using RNN algorithms. Our model could provide real-time assessment of future AKI occurrences and individualized risk factors for AKI in general inpatient cohorts; thus, we suggest approaches to support clinical decisions based on prediction models for in-hospital AKI.
HA is associated with the development of AKI and high mortality in hospitalized patients. Replacement of albumin after the development of AKI may contribute to renal recovery. Further clinical trials are warranted.
Inhibition of renal prostaglandin synthesis by non-steroidal anti-inflammatory drugs (NSAIDs) causes various electrolyte and acid-base disturbances including sodium retention (edema, hypertension), hyponatremia, hyperkalemia, and decreased renal function. Decreased sodium excretion can result in weight gain, peripheral edema, attenuation of the effects of antihypertensive agents, and rarely aggravation of congestive heart failure. Although rare, NSAIDs can cause hyponatremia by reducing renal fr
Patients with poor nutritional status and extensive lung involvement tend to experience deterioration of nodular bronchiectatic MAC lung disease.
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