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증례 : 광방기에 의해 발생한 Chinese Herb Nephropathy 1예
이재욱 ( Jay Wook Lee ),손민정 ( Min Jung Sohn ),허남주 ( Nam Joo Heo ),주권욱 ( Kwon Wook Joo ),정윤철 ( Yoon Chul Jung ),이정상 ( Jung Sang Lee ),한진석 ( Jin Suk Han ) 대한내과학회 2006 대한내과학회지 Vol.71 No.2
본 증례의 환자는 근위부 신세뇨관 산증, 진행성 만성 신부전증, 세뇨관 위축 및 간질 섬유화 등 CHN에 잘 맞는 임상 증상 및 조직 소견을 보였고, 복용하던 한약재에서 AA가 검출되어 AA에 의한 CHN 또는 AAN으로 진단할 수 있었다. 이러한 환자의 신조직에서 AA-DNA adduct를 추가로 검출할 수 있다면 진단의 정확성을 더욱 높일 수 있을 것으로 보인다. Chinese herb nephropathy (CHN) is characterized by progressive tubulointerstitial nephritis and development of renal failure in a couple of years after diagnosis. Aristolochic acid (AA) is believed to be associated with the development of CHN. The authors report a case of CHN in which AA in the herb regimen was identified by high-performance liquid chromatography (HPLC). A 32-year-old female presented with nausea, vomiting and generalized weakness. She had been taking Chinese herbs for symptomatic care. Clinical and laboratory examinations revealed Fanconi syndrome, renal failure, and severe anemia. Renal biopsy showed severe tubulointerstitial nephritis with moderate tubular atrophy and interstitial fibrosis. She developed end-stage renal failure 4 months after diagnosis. The herb she had been taking was Aristolochia fangchi. HPLC technique was used to identify AA and to measure its concentration in the herb. From the clinical and laboratory data, the patient was diagnosed with CHN caused by aristolochic acid.(Korean J Med 71:224-228, 2006)
만성 대사성 산증에서 요 음이온차를 이용한 요 산성화능의 평가
한진석(Jin Suk Han),주권욱(Kwon Wook Joo),정윤철(Yoon Chul Jung),임춘수(Choon Soo Lim),김연수(Yon Su Kim),안규리(Cu Rie Ahn),김성권(Suhng Gwon Kim),이정상(Jung Sang Lee),김근호(Gheun Ho Kim) 대한내과학회 1993 대한내과학회지 Vol.45 No.4
N/A Objectives : The clinical usefulness of the urine anion gap as an indirect index of theammonium excretion was reported only in patients with hyperchloremic metabolic acidosis. And the significance of the urine anion gap and its relation with other indices of urine acidification are not clearly defined yet. We are aimed to evaluate the clinical usefulness of the urine anion gap and its relations with other indices of urine acidification in normal and high anion gap metabolic acidosis. Methods : We measured the urine acidification indices (ammonium, titratable acid, net acid) and the urine anion gap in 24 patients with chronic renal failure, 7 patients with dista1 renal tubular acidosis, and 8 healthy adults with acid loading (normal controls), whose arterial blood bicarbonate concentrations were 14.0 mmol/ L (7.0 to 20.0 mmol/L)(median;range), 18.1 mmol/L(15.0 to 20.0 mmol/L), 19.5 mmol/L(16.8 to 22.D mmol/L), respectively. Results: The urinary excretion of ammonium in chronic renal failure(4.5 mmol/day; 1.6 to 11.8 mmol/ day) and renal tubular acidosis (19.8 mmol/day; 6.9 to 27.2 mmol/day) were lower than in normal controls (52. 5mmol/day; 37.3 to 69.4mmol/day)(p<0.05). The urinary excretion of titratable acid in chronic renal failure (4.9 mmol/day; 0.1 to 19.7 mmol/day) and renal tubular acidosis (2.8 mmol/day; 0.1 to 20.2 mmol/day) were lower than in normal controls (6.2 mmol/day; 20.6 to 36.9mmol/day)(p<0.05) The urinary excretion of net acid in chronic renal failure(8.8 mmol/day; 0.1 to 28.2 mmol/day) and renal tubular acidosis (12.9 mmol/day; 0. 1 to 33.6 mmol/day) were also lower than in normal controls (77.9mmol/day; 62.7 to 98.9 mmol/day)(p<0. 05). The urine anion gap in chronic renal failure (22.9 mmol/L; 13.0 to 43.2 mmol/L) and renal tubular acidosis (36.0 mmol/L; 7.0 to 82.0 mmol/L) were higher than in normal controls (-14.6 mmol/L; 40.7 to 2.2 mmol/ L) (p<0.05), and had inverse relation with urine ammonium (r=-0.71, p<0.01), titratable acid (r=-0.76, p<0.01), and had inverse relation with urine ammonium (r=-0.83, p <0.01), respectively. The urine anion gap in chronic renal failure and renal tubular acidosis were all above 5.0 mmol/L. Conclusion : We concluded that the urine anion gap in chronic metabolic acidosis would be a good clinical index of the impairment of urine acidification in the distal nephron, and reflect not only urine ammmonium excretion but also urinary excretion of net acid.
급성 신장 손상 ; 급성 신손상의 정의와 평가: 임상 진료 지침
김동기 ( Dong Ki Kim ),주권욱 ( Kwon Wook Joo ) 대한내과학회 2015 대한내과학회지 Vol.88 No.4
Acute kidney injury (AKI) is a common clinical syndrome that carries a poor prognosis even in cases with seemingly mild or reversible renal dysfunction. Although this potentially devastating disease is associated with increased mortality, early detection and timely intervention may improve clinical outcomes. In this regard, a standardized definition and classification of AKI, reflecting prognosis on the basis of evidence, may allow early recognition and stage-based management of the disease. Nevertheless, there has been considerable variability and inconsistency in the definition and classification of AKI, resulting in failure to bridge the gap between research and clinical practice. The definition of AKI has evolved, with the introduction of the “Risk, Injury, Failure, Loss, and End-stage renal disease” (RIFLE), and “AKI Network” (AKIN) criteria. The recent “Kidney Disease Improving Global Outcomes” (KDIGO) guidelines proposed a uniform definition of AKI, essentially merging the RIFLE and AKIN criteria. This review will focus on the definition and classification of AKI, as proposed by KDIGO in 2012, and their use in clinical practice for clinicians.
오윤규 ( Yoon Kyu Oh ),나기영 ( Ki Young Na ),이재욱 ( Jay Wook Lee ),장혜련 ( Hye Ryun Chang ),박영선 ( Young Sun Park ),박정환 ( Jung Hwan Park ),주권욱 ( Kwon Wook Joo ),김근호 ( Gheun Ho Kim ),이정상 ( Jung Sang Lee ),한진석 ( 대한신장학회 2003 Kidney Research and Clinical Practice Vol.22 No.2
배경 : 임상에서 흔히 사용하는 이뇨제 furosemide는 비후상행각에서 Na+-K+-2CI- cotranspoter (NKCC2)를 억제하여 NaCl 재흡수를 차단하여 이뇨작용을 나타낸다. Furosemide를 장기간 투여하면 내성과 대사성 알카리증의 부작용이 발생할 수 있는데, 이는 집합관에 도달하는 소디움 증가와 관련 있을 가능성이 있다. 방법 : 저자들은 furosemide의 내성이나 부작용이 집합관 상피 소디움 통로 (ENaC) 단백발현의 변화와 관련이 있는지를 확인하고자, Sprague-Dawley rat에서 farosemide (12 mg/day)을 7일간 지속적 피하 주입한 후 반정량적 immunoblotting과 면역조직화학법을 이용하여 NKCC2, Na +-CL- cotransporter (NCC), ENaC 단백의 발현을 관찰하였다. 실험기간 동안 수분과 전해질 용액 (0.8% NaCl & 0.1% KCl)을 자유롭게 섭취하도록 하여 체액 감소를 방지하였다. 결과 : 부형약 (vehicle)을 투여한 대조군에 비하여, furosemide를 투여한 군에서 각각 요량과 요 소디움 배설이 증가하였으나, 체중, 혈청 알도스테론치 및 크레아티닌 청소율은 차이가 없었다. Furosemid 투여 후 NKCC2 단백은 피질 (151±10 vs. 100±10%, p<0.05)과 외수질 (122±5 vs. 100±3%, p<0.01)에서 증가해 있었다. ENaC 단백은 세 가지 subunit 모두 furosemide 투여 후 대조군에 비하여 피질 (α:187±25 vs. 100±22%, p<0.05; β:155±8 vs. 100±15%, p<0.05; γ:168±16 vs. 100±9%, p<0.05)과 외수질 (α:171±27 vs. 100±17%, p<0.05; β :986±91 vs. 100±33%, p<0.01; γ :242±24 vs. 100±22%, p<0.01)에서 증 가하였다. 면역조직화학법에서도 furosemide를 투여한 군의 집합관 주세포에서 ENaC β-subunit가 더 강하게 염색되었다. 결론 : 이상에서 장기간 furosemide 투여시 집합관 ENaC 발현이 증가하며, 이러한 원위부네프론의 적응 반응이 이뇨제 내성을 유발하는데 기여할 것으로 생각한다. Background : Furosemide inhibit NaCl absorption in the thick ascending limb and produce an increase in distal delivery of Na+. We carried out semiquantitative immunoblotting and immunohistochemistry of rat kidneys to investigate whether chronic furosemide infusion is associated with compensatory increases in the abundance of Na+ transporters in distal nephron. Methods : Osmotic minipumps were implanted into Sprague-Dawley rats to deliver 12 mg/day of furosemide(n=6) with simultaneous administration of 0.8% NaCl and 0.1% KCl in drinking water for 7days. Results : Compared with vehicle infused controls, urine volume and urine sodium amount were increased. However, there were no differences in body weight, serum aldosterone, and creatinine clearance. The abundance of Na+-K+-2CI - cotransporter after furosemide infusion was increased in cortex (151±10 vs. 100±10%, p<0.05) and outer medulla (122±5 vs. 100±3%, p<0.01). In furosemide infusion group, the abundance of all three subunits of epithelial sodium channel (ENaC) was increased both in cortex (α:187±25 vs. 100±17%, p<0.05; β:155±8 vs. 100±15%, p<0.05; γ :168±16 vs. 100±9%, p<0.05) and outer medulla (α:171±27 vs. 100±17%, p<0.05; β :986±91 vs. 100±33%, p<0.01; γ :242±24 vs. 100±22%, p<0.01). Consistent with these results, ENaC β-subunit immunohistochemistry showed a remarkable increase in immunoreactivity in the principal cells of collecting ducts with furosemide treatment. Conclusion : These increases in the abundance of ENaC protein may account for the generation of diuretic tolerance.
손민정 ( Min Jeong Son ),이하정 ( Ha Jeong Lee ),오국환 ( Kook Hwan Oh ),주권욱 ( Kwon Wook Joo ),김성권 ( Sunhn Gwon Kim ) 대한신장학회 2009 Kidney Research and Clinical Practice Vol.28 No.5
Renal vein thrombosis (RVT) is mostly related with other causes. The underlying conditions of RVT were nephrotic syndrome, trauma, cancer, anatomical anomalies, and other hypercoagulable status. Especially hypercoagulable status was rarely caused by obesity. We diagnosed renal vein thrombosis from an obese patient with hypertriglyceridemia. A male patient visited the Seoul National University Hospital for evaluating the reason of his flank pain. The pain started from two weeks ago, He had regarded flank pain as his obesity status (his weight was 84 kg and Body mass index was 29.41 kg/m2). So he had lost his weight by over-sweating one day before. At initial examination, his blood pressure was 128/75 mmHg, pulse rate was 72/min, respiration rate was 20/min and body temperature was 36.2℃. Blood chemistries revealed total cholesterol 218 mg/dL, Blood urea nitrogen/creatinine 12/1.3 mg/dL Urinalysis showed specific gravity 1.015, pH 5.5, protein 2+, blood 2+, RBC/WBC 1-4/<1 HPF on microscopic examination. Twenty-four hour collection of the urine showed protein 329 mg/day, creatinine clearance 90 mL/min. Renal vein thrombosis was visualized on the renal computed tomography and pulmonary embolism on the lung scan. Then, anticoagulant therapy was started after coagulation related tests. However, no abnormality of coagulation tests was detected. The evidence of malignancy was not detected either. After anticoagulation therapy, the pain was subsided. The only underlying cause for his hypercoagulability was considered obese status. Unfortunately we had not checked the triglyceride, initially. So we could not prioritize the reason of renal vein thrombosis into hypertriyglyceridemia. We considered that his obese status and subsequent hypertriyglyceridemia might be one of the causes of renal vein thrombosis.
항에리트로포에틴 (Anti-erythropoietin) 항체에 의한 진성 적혈구계 무형성증 (Pure Red Cell Aplasia) 2예
양재석 ( Jae Seok Yang ),이정은 ( Jung Eun Lee ),박동준 ( Dong Jun Park ),성은영 ( Eun Young Seong ),주권욱 ( Kwon Wook Joo ),안규리 ( Cu Rie Ahn ),한진석 ( Jin Suk Han ),김성권 ( Suhng Gwon Kim ),조한익 ( Han Ik Cho ),이정상 ( Ju 대한신장학회 2004 Kidney Research and Clinical Practice Vol.23 No.5