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김근호 ( Gheun Ho Kim ) 대한간학회 2011 Clinical and Molecular Hepatology(대한간학회지) Vol.17 No.2(S)
Both sodium and water excretion is impaired in liver failure, producing hypervolemic (edematous) dilutional hyponatremia. Portal hypertension, the pathophysiologic hallmark of cirrhosis, causes splanchnic vasodilation to induce arterial underfilling. This triggers the baroreceptor-mediated activation of anti-natriuretic hormones and non-osmotic release of arginine vasopressin to restore circulatory integrity. Recent studies using vasopressin-2 receptor antagonists showed the short-term effects of relieving hyponatremia. Hypernatremia infrequently occurs in cirrhotic patients when hypotonic diarrheal fluid loss is complicated with the use of lactulose. Patients with liver disease usually have normokalemia because decreased distal sodium delivery counteracts the stimulatory effect of aldosterone on potassium secretion. Hyperkalemia is usually caused by drugs such as potassium-sparing diuretics, angiotensin converting enzyme inhibitors, and angiotensin receptor antagonists. Inadequate intake or increased loss of potassium may produce hypokalemia, and hepatic encephalopathy may be precipitated because renal ammoniagenesis is enhanced by hypokalemia. Respiratory alkalosis is the most common acid-base derangement in cirrhotic patients as a result of hyperventilation. Renal failure is defined by a decrease in glomerular filtration rate (GFR) and indicated by the presence of azotemia. Serum creatinine is still useful to diagnose renal failure although it has limitations to evaluate GFR in cirrhotic patients. Diagnosis of acute kidney injury (AKI) is made in patients in whom serum creatinine rises abruptly by 0.3 mg/dL or more or increases by 150% or more from baseline. Before diagnosing the patients to have hepatorenal syndrome, reversible causes of AKI such as volume deletion, acute tubular necrosis, and post-renal failure should be sought and treated.
김근호(Gheun Ho Kim),진호준(Ho Joon Jin),정우경(Woo Kyung Chung),안규리(Cu Rie Ahn),김성권(Suhng Gwon Kim),이정상(Jung Sang Lee) 대한내과학회 1995 대한내과학회지 Vol.49 No.1
Objectives: Past researches on the biochemical properties and pathogenicity of hantavirus have been mainly from rodent isolates, and we performed this study to obtain human isolates from patients with hemorrhagic fever with renal syndrome (HFRS) and to analyze the rate and source of viral isolation. Methods: Blood and urine specimens were collected from 48 patients with HFRS and inoculated onto subconfluent monolayers of Vero-E 6 cells, and human isolates of hantavirus were identified by direct and indirect immunofluorescent techniques, immunoblot analysis, and reverse transcriptase-directed polymerase chain reaction(RT-PCR). Results: Nineteen viral isolates(31 samples) were recovered from the blood and urine of 48 patients(90 samples) during days 3-11 following the onset of illness. Isolation rates of the virus from whole blood, serum, plasma, urine, and peripheral blood monuclear cells were 75%, 30%, 25%, 25%, and 18%, respectively. Viruses were more frequently isolated during days 3-9 of the illness(37%) than after day 9 (17%). Specific hantavirus antigens of isolates were identified by both indirect and direct immunofluorescent techniques and immunoblot analysis. The hantairus genomic sequences were detected in some of the isolates by RT-PCR. Conclusion: Nineteen hatavirus isolates were successfully recovered from 48 HFRS patients, mainly in the whole blood. Further investigations will be required to elucidate the differences in the pathogenicity of these human isolates using serologic and molecular biologic methods.
김근호(Gheun Ho Kim),조종태(Jong Tae Cho),양원석(Won Suk Yang),김윤구(Yoon Goo Kim),한진석(Jin Suk Han),김성권(Suhng Gwon Kim),이정상(Jung Sang Lee) 대한내과학회 1991 대한내과학회지 Vol.40 No.1
In order to observe the sequential changes of the urine electrolytes and urine anion gap (UAG) during the course of Korean hemorrhagic fever (KHF), we measured spot urine electrolytes and urine osmolality in 16 patients with KHF, and calculated UAG from them as an index of the renal tubular dysfunction. Also, we observed the relationships between the initial value of spot urine anion gap and the clinical findings and severity in each patient. Spot urine sodium and potassium concentrations were higher in the early phases (oliguric to early diuretic phase) than in the late phases. Spot UAG values were highest in the oliguric phase and decreased sequentially. Urine osmolality decreased sequentially from the oliguric to the convalescent phase. The initial spot UAC values of each patient were related with the clinical severity in the early phases and with the degrees of hyponatremia, azotemia and metabolic acidosis as well. Spot UAG was elevated when spot urine sodium or potassium concentration was higher, and was lowered when urine osmolality was decreased or polyuria occurred. From the above results, we concluded that the changes of spot UAG through the phases might be related with the renal tubular damage in KHF.
김근호 ( Gheun Ho Kim ),김용수 ( Yong Soo Kim ) 대한신장학회 2008 Kidney Research and Clinical Practice Vol.27 No.1
1. 신석증의 가장 흔한 원인은 칼슘옥살산염 결석이다. 2. 칼슘옥살산염 결석이 재발하는 경우는 고칼슘뇨증, 고요산뇨증, 고옥살산뇨증 및 저구연산뇨증의 대사 요인에 대한 검토를 위하여 혈청 및 24시간요화학검사와 및 결석분석을 시행한다. 고칼슘혈증 환자에서는 부갑상선호르몬과 비타민 D 농도를 반드시 측정하고, 24시간요화학검사에서는 칼슘과 요산 뿐 아니라 옥살산염과 구연산염도 포함시킨다. 3. 고옥살산뇨증은 24시간요 옥살산염 배설이 45 mg 혹은 0.5 mmoL을 초과하는 경우로 정의되고, 요 중 옥살산염 배설이 증가할수록 칼슘옥살산염 결석 위험이 높아진다. 4. 고옥살산뇨증에는 유전 소인과 식이습관이 관여하며, 옥살산염 섭취에 따른 영향보다는 칼슘 섭취가 부족하여 장에서 옥살산염 흡수가 증가하는 요인이 중요하다. 5. 칼슘옥살산염 재발을 방지하기 위해서는 요량이 1일 2L 정도 유지되도록 수분을 충분히 섭취하고, 칼슘섭취를 제한하지 않는 것이 중요하다. 또한 염분과 육류는 제한하고, 야채와 과일을 충분히 섭취하지만 옥살산염이 많이 포함된 시금치, 견과류, 초콜릿 등을 가급적 피한다.
요 삼투질농도차를 이용한 요 암모늄 배설의 평가 : 요 음이온차와 비교
김근호(Gheun Ho Kim),전은실(Eun Sil Jun),허우성(Woo Sung Huh),김연수(Yon Su Kim),안규리(Cu Rie Ahn),한진석(Jin Suk Han),김성권(Suhng Gwon Kim),이정상(Jung Sang Lee) 대한내과학회 1995 대한내과학회지 Vol.48 No.5
Objectives: Urine osmolal gap(UOG) and urine anion gap(UAG) have been suggested for the indirect measures of urine NH4+ excretion. The clinical usefulness of UOG in the patients with urine acidification defect is much less known in comparison with that of UAG. Methods: We measured UOG[=urine osmolality-{2(Na++K+)+urea}] and compared with urine NH4+ and UAG(=Na+ +K+ -Cl- ) in 5 patients with distal renal tubular acidosis patients(RTA) and 8 healthy adults with acid loading(NC), whose arterial blood bicarbonate concentrations were 19.5±1.6mM (mean+SEM) and 19.6±0.6mM, respectively. Results: Urine NH4+ excretory rate of RTA(26.8±4.9mmol/day) was lower(p<0.01)than that of NC (52.6±3.7mmol/day), UOG of RTA(129.7±17.0mM) was lower(p<0.05) than that of NC(319.7±58.4mM), and UAG of RTA(52.2±9.4mM) was higher(p<0.01)than that of NC(-16.2±5.5mM). Urine osmolality had good correlations with the sum of major urinary solutes calculated by 2(Na+ + K+ +NH4+)+urea in spot urine(r=0.90, p<0.01) and 24- hour urine collection(r=0.95, p<0.01). UOG had positive correlations with spot urine NH4+ concentration(r=0.97, p<0.01) and 24 hour urine NH4+ excretion(r=0.69, p=0.01). UAG had inverse correlations with spot urine NH4+ concentration(r=-0.78, p<0.01) and 24-hour urine NH4+ excretion(r=-0.75, p<0.01). The lower urine NH4+ in RTA was reflected by the lower UOG(<150mM) and the higher UAG(>5mM). Conclusion: Urine osmolal gap as well as urine anion gap was a useful clinical index reflecting urine ammonium in the patients with distal renal tubular acidosis, and urine osmolal gap below 150mM and urine anion gap above 5mM would suggest the impaired urine ammonium excretion.