90 research outputs found

    Dietary salt intake and hypertension

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    Over the past century, salt has been the subject of intense scientific research related to blood pressure elevation and cardiovascular mortalities. Moderate reduction of dietary salt intake is generally an effective measure to reduce blood pressure. However, recently some in the academic society and lay media dispute the benefits of salt restriction, pointing to inconsistent outcomes noted in some observational studies. A reduction in dietary salt from the current intake of 9-12 g/day to the recommended level of less than 5-6 g/day will have major beneficial effects on cardiovascular health along with major healthcare cost savings around the world. The World Health Organization (WHO) strongly recommended to reduce dietary salt intake as one of the top priority actions to tackle the global non-communicable disease crisis and has urged member nations to take action to reduce population wide dietary salt intake to decrease the number of deaths from hypertension, cardiovascular disease and stroke. However, some scientists still advocate the possibility of increased risk of CVD morbidity and mortality at extremes of low salt intake. Future research may inform the optimal sodium reduction strategies and intake targets for general populations. Until then, we have to continue to build consensus around the greatest benefits of salt reduction for CVD prevention, and dietary salt intake reduction strategies must remain at the top of the public health agenda.ope

    Uric Acid Puzzle: Dual Role as Anti-oxidantand Pro-oxidant

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    Hyperuricemia is known to be associated with the presence of cardiovascular and metabolic syndrome and with the development of incipient kidney disease and an accelerated renal progression. However, an elevated uric acid level was not generally regarded as a true etiology or mediator, but an indicator of these diseases. Uric acid has recently regained the clinical interest and popularity based on emerging data suggesting the causative role of hyperuricemia in cardiovascular and renal disease. Experimental data demonstrates oxidative stress is one of the earliest phenomena observed in vascular, renal, liver cells and adipocytes exposed to uric acid. Since uric acid is one of the major antioxidants of plasma acting as a free radical scavenger and a chelator of transitional metal ion, uric acid-induced oxidative stress seems paradoxical. Data regarding the clinical implication of hyperuricemia is even more confusing, which defines hyperuricemia as a useless parameter to be eliminated from routine follow-up or a major risk factor to be therapeutic target. With a review of experimental and epidemiologic data, the presence of molecular switch to regulate the role of uric acid as anti- or pro-oxidant in different compartment of our body is suggested, which may shed light on understanding the paradoxical role of uric acid and solving the "uric acid debate".ope

    ACE insertion/deletion polymorphism and diabetic nephropathy: clinical implications of genetic information

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    Approximately 20-40% of diabetic patients develop nephropathy which is the leading cause of ESRD in developed countries. The ACE I/D polymorphism is thought to be a marker for functional polymorphism which regulates circulating and tissue ACE activity. While the initial study found a protective effect of the II genotype on the development of nephropathy in IDDM patients, subsequent studies have addressed the role of ACE I/D polymorphism in the development and progression of diabetic nephropathy. RAAS blockers are the first line drugs for the treatment hypertension associated with diabetes and have been widely used in everyday clinical practice for the purpose of reducing proteinuria in patients with various renal diseases. However, the antiproteinuric effect of RAAS blockers is variable and the percentage of reducing proteinuria is in the range of 20-80%. The antiproteinuric effect of RAAS blockers may be related to a number of factors: the type or the dose of RAAS blockers, the duration of therapy, the level of sodium intake, and the type of patient's ACE I/D genotype. Besides the nongenetic factors, drug responses, can be influenced by ACE gene polymorphism. In this review, we discuss the relationship between ACE I/D polymorphism and diabetic nephropathy and therapeutic response of RAAS blockers.ope

    도시계획과 도시정책의 미래 과제와 도전

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    18세기 영국 시인 윌리엄 쿠퍼(William Cowper)는 신은 시골을 만들었고 인간은 도시를 만 들었다고 말했다. 도시는 인간 의지의 산물이자 도시화와 산업화의 상징이다. 한국의 도시는 경제성장의 동력이자 정보교류의 중심으로서 그 중요성이 지속적으로 증가해 왔다. 과거의 경험을 바탕으로 보면 인구증가와 경제성장은 매우 높은 상관관계를 보였다. 산업화가 확대되면서 노동력과 자본이 도시지역으로 유입되고 대규모 시장과 기반시설이 제공됨에 따라 일자리와 혁신역량이 창출되는 긍정적인 효과를 경험하게 되었다. 그러나 한국도시는 이전에는 경험하지 못한 새로운 변화에 직면하고 있다. 1960년대 이후 급격히 성장해온 도시인구는 1990년대에 와서 성장이 둔화되고 인구학적 특징도 크게 변화되었다. 1990년에서 2000년 사이 도시인구의 연간 증가율은 1.8% 감소하여 1960~1990년 사이 30년 동안 매년 도시인구는 11.9% 증가를 보인 것과는 큰 대조를 보인다. 특히 도심부 인구 감소는 거의 모든 대도시에서 관찰되고 있으며 인구의 고령화와 1인가구의 증가도 급속히 진행되고 있다

    Severe Symptomatic Hyponatremia Caused by Low Dose Oral Cyclophosphamide: A Case Report

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    Cyclophosphamide (CY), an alkylating agent, is frequently used in the treatment of various autoimmune disorders and malignancies. Acute hyponatremia is a well-known side effect of moderate to high dose intravenous CY treatment, but is rare in patients treated with low dose intravenous CY. We report the case of a severe symptomatic hyponatremia in a 68-year-old woman with renal impairment who was treated with oral CY (100 mg/day) for anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis (GN). This case demonstrates that even oral CY could be associated with life threatening acute hyponatremia and should be used with caution.ope

    A case of hyperphosphatemia and acute renal failure following the administration of solin? (oral sodium phosphate)

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    Solin(R) (oral sodium phosphate) is a commonly used osmotic laxative solution that has replaced polyethylene glycol in bowel preparation for colonoscopy as it has equal or greater efficacy and patient compliance. However, its use has been associated with several cases of acute renal failure and electrolyte imbalance, especially hyperphosphatemia and hypocalcemia. Those at higher risk of complications are patients who are older and have intestinal obstruction, inflammatory bowel disease, renal failure, or congestive heart failure. We report the case of a 61-year-old woman presenting with paresthesia in both hands after using Solin(R) for bowel preparation for colonoscopy. The patient had hypocalcemia and hyperphosphatemia combined with acute renal failure. She recovered from the renal failure and electrolyte imbalance with intravenous hydration and treatment with phosphate-binding agents.ope

    Effect of Efonidipine on Proteinuria in Patients with Chronic Kidney Disease Receiving RAS Blockade

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    Purpose : Efonidipine, which inhibits both T- and L-type calcium channels, has been shown to be effective in reducing proteinuria and preserve renal function. This study was conducted to compare the effects of efonidipine versus amlodipine on the management of hypertension and proteinuria in patients with chronic kidney disease (CKD) receiving ACE inhibitors or ARB. Methods : This study included 41 CKD patients who were at stages 2-4 and had a urine spot protein/ creatinine ratio of >0.5. Patients were administered amlodipine (5 mg/day) and efonidipine (40 mg/ day) for 3 months in a cross-over design. Blood pressure and spot urine protein/creatinine ratio were compared before and after the cross-over treatment. Results : There were 24 male patients and 17 female patients. The mean age of the patients was 55.9±12.9 years. When the patients’ medication was changed to eponidifine, we obtained the following results. First, there were no significant changes in blood pressure and serum creatinine. Second, the urine spot protein/creatinine ratio was significantly decreased (before the cross-over, 2.9±2.6; after the cross-over, 2.3±1.9 g/g; p=0.02). Finally, the reduction rate of proteinuria was significantly higher in patients with CKD at stages 2-3 than in those with CKD at stage 4 after the cross-over (stage 2, - 26.1%; stage 3, -17%; stage 4, +12.8%; p=0.03). Conclusion : It is concluded that efonidipine may significantly decrease proteinuria compared with amlodipine in CKD patients receiving ACE inhibitors or ARB. Further double-blind clinical trials with a larger sample size are needed to confirm our resultsope

    A case of severe Lactic acidosis induced by metformin overdose

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    Metformin is an oral hypoglycemic agent belonging to the biguanide class that has been used to treat type II diabetes mellitus worldwide. Lactic acidosis is a rare, but serious, adverse effect in metformin-treated patients with renal and hepatic disease, cardiac or respiratory insufficiency, severe infection, and any hypoxic condition. Large overdoses of metformin can also lead to lactic acidosis. Attempted suicide with metformin is rare. Treatment with bicarbonate is generally accepted, although there is no clear evidence that it improves the outcome of lactic acidosis. Bicarbonate hemodialysis and continuous veno-venous hemodiafiltration (CVVHDF) are probably both beneficial in correcting the acidosis, and by actively removing metformin and lactate from the circulation. We report the case of a patient with severe lactic acidosis induced by metformin intoxication who recovered fully after treatment with a combination of bicarbonate hemodialysis and CVVHDFope

    Comparative Analysis of Screening Results from Various ELISA Formats Used for Detection of Anti-Erythropoietin Antibodies in Korean Patients

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    Clinical cases of pure red cell aplasia (PRCA) have been reported during the recombinant human erythropoietin (EPO) therapy for the anemia patients. PRCA is a rare hematological disorder leading to a severe anemia due to an almost complete stop of red blood cell production. Antibody (Ab)-associated PRCA is caused by the EPO-neutralizing Abs that eliminate the biological activity of EPO. In order to detect anti-EPO Abs in human sera, we performed conventional ELISA, directly coated bridging ELISA, and streptavidin coated bridging ELISA, and compared their sensitivity and specificity. Some false positive results were obtained in the conventional ELISA. One positive sample was detected successfully by streptavidin coated bridging ELISA, which was not appeared in the directly coated bridging ELISA. In conclusion, streptavidin coated bridging ELISA was substantially sensitive and specific format and one out of sixty-eight serum samples was proved to be anti-EPO positive.ope

    Salt Sensitivity and Hypertension: A Paradigm Shift from Kidney Malfunction to Vascular Endothelial Dysfunction

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    Hypertension is a complex trait determined by both genetic and environmental factors and is a major public health problem due to its high prevalence and concomitant increase in the risk for cardiovascular disease. With the recent large increase of dietary salt intake in most developed countries, the prevalence of hypertension increases tremendously which is about 30% of the world population. There is substantial evidence that suggests some people can effectively excrete high dietary salt intake without an increase in arterial BP, and another people cannot excrete effectively without an increase in arterial BP. Salt sensitivity of BP refers to the BP responses for changes in dietary salt intake to produce meaningful BP increases or decreases. The underlying mechanisms that promote salt sensitivity are complex and range from genetic to environmental influences. The phenotype of salt sensitivity is therefore heterogeneous with multiple mechanisms that potentially link high salt intake to increases in blood pressure. Moreover, excess salt intake has functional and pathological effects on the vasculature that are independent of blood pressure. Epidemiologic data demonstrate the role of high dietary salt intake in mediating cardiovascular and renal morbidity and mortality. Almost five decades ago, Guyton and Coleman proposed that whenever arterial pressure is elevated, pressure natriuresis enhances the excretion of sodium and water until blood volume is reduced sufficiently to return arterial pressure to control values. According to this hypothesis, hypertension can develop only when something impairs the excretory ability of sodium in the kidney. However, recent studies suggest that nonosmotic salt accumulation in the skin interstitium and the endothelial dysfunction which might be caused by the deterioration of vascular endothelial glycocalyx layer (EGL) and the epithelial sodium channel on the endothelial luminal surface (EnNaC) also play an important role in nonosmotic storage of salt. These new concepts emphasize that sodium homeostasis and salt sensitivity seem to be related not only to the kidney malfunction but also to the endothelial dysfunction. Further investigations will be needed to assess the extent to which changes in the sodium buffering capacity of the skin interstitium and develop the treatment strategy for modulating the endothelial dysfunction.ope
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