Jun Young Shin, Sang Min Yoon, Hyuck Jae Choi, Si Nae Lee, Hai Bong Kim, Woo Chul Joo, Joon Ho Song, Moon-Jae Kim, Seoung Woo Lee
{"title":"A Case of Post-radiotherapy Urethral Stricture with Spontaneous Bladder Rupture, Mimicking Obstructive Uropathy due to Cancer Metastasis.","authors":"Jun Young Shin, Sang Min Yoon, Hyuck Jae Choi, Si Nae Lee, Hai Bong Kim, Woo Chul Joo, Joon Ho Song, Moon-Jae Kim, Seoung Woo Lee","doi":"10.5049/EBP.2014.12.1.26","DOIUrl":"https://doi.org/10.5049/EBP.2014.12.1.26","url":null,"abstract":"<p><p>Non-traumatic, spontaneous urinary bladder rupture is a rare complication of urethral stricture. Furthermore, its symptoms are often nonspecific, and misdiagnosis is common. The authors experienced a case of urethral stricture with spontaneous bladder rupture and bilateral hydronephrosis, mimicking obstructive uropathy attributed to cancer metastasis. A 55-year-old woman was admitted with abdominal pain and distension, oliguria, and an elevated serum creatinine level. She had undergone radical hysterectomy for uterine cervical cancer and received post-operative concurrent chemoradiation therapy 13 years previously. Non-contrast enhanced computed tomography showed massive ascites and bilateral hydronephrosis. The initial diagnosis was acute kidney injury due to obstructive uropathy caused by malignant disease. After improvement of her renal function by bilateral percutaneous nephrostomy catheterization, contrast-enhanced computed tomography and a cytologic examination of ascites showed no evidence of malignancy. However, during retrograde pyelography, a severe urethral stricture was found, and subsequent cystography showed leakage of contrast into the peritoneal cavity and cystoscopy revealed a defect of the posterior bladder wall. After urethral dilatation and primary closure of the bladder wall, acute kidney injury and ascites were resolved. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2014.12.1.26","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32534324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andrei Schwartz, Evgeni Brotfain, Leonid Koyfman, Ruslan Kutz, Shaun E Gruenbaum, Moti Klein, Alexander Zlotnik
{"title":"Association between Hypophosphatemia and Cardiac Arrhythmias in the Early Stage of Sepsis: Could Phosphorus Replacement Treatment Reduce the Incidence of Arrhythmias?","authors":"Andrei Schwartz, Evgeni Brotfain, Leonid Koyfman, Ruslan Kutz, Shaun E Gruenbaum, Moti Klein, Alexander Zlotnik","doi":"10.5049/EBP.2014.12.1.19","DOIUrl":"10.5049/EBP.2014.12.1.19","url":null,"abstract":"<p><p>It is well known that new-onset arrhythmias are common in septic patients. It is thought that hypophosphatemia in the early stages of sepsis may contribute to the development of new arrhythmias. In this study, we hypothesized that intravenous (IV) phosphorus replacement may reduce the incidence of arrhythmias in critically ill patients. 34 adult septic patients with hypophosphatemia admitted to the general intensive care unit were treated with IV phosphorus replacement per ICU protocol, and the incidence of new arrhythmias were compared with 16 patients from previously published data. IV phosphorus replacement was associated with a significantly reduced incidence of arrhythmias (38% vs. 63%, p=0.04). There were no differences in observed mortality between subgroups, which may be due to the small sample size. This study demonstrated that IV phosphorus replacement might be effective in reducing the incidence of new arrhythmias in septic patients. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e4/6c/ebp-12-19.PMC4105385.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32532888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dietary salt intake and hypertension.","authors":"Sung Kyu Ha","doi":"10.5049/EBP.2014.12.1.7","DOIUrl":"https://doi.org/10.5049/EBP.2014.12.1.7","url":null,"abstract":"<p><p>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. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2014.12.1.7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32532887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyun Jun Ju, Hong Jin Bae, Dae Eun Choi, Ki Ryang Na, Kang Wook Lee, Young Tai Shin
{"title":"Severe hypernatremia by excessive bamboo salt ingestion in healthy young woman.","authors":"Hyun Jun Ju, Hong Jin Bae, Dae Eun Choi, Ki Ryang Na, Kang Wook Lee, Young Tai Shin","doi":"10.5049/EBP.2013.11.2.53","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.2.53","url":null,"abstract":"<p><p>Severe hypernatremia is an important electrolyte disorder that has serious effects. The patient had no medical history. A. 20-year-old ingested bamboo salt for digestion and weight reduction according to the folk remedies posted on an internet website. She presented with vomiting and diarrhea over ten times per day. Her initial serum sodium concentration was 174mEq/L. Her symptoms improved rapidly with hypotonic saline infusion. She recovered completely without any sequelae in three days. Severe hypernatremia in a normal young adult with clear consciousness and normal renal function has not been reported in Korea yet. So we report a case of severe hypernatremia by excessive bamboo salt ingestion in healthy young woman. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.2.53","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32173912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Obesity associated hypertension: new insights into mechanism.","authors":"Young Sun Kang","doi":"10.5049/EBP.2013.11.2.46","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.2.46","url":null,"abstract":"<p><p>With excess nutrition, the burden of obesity is a growing problem worldwide. The imbalance between energy intake and expenditure leads to variable disorders as all major risk factors for cardiovascular disease. There are many hypothetical mechanisms to explain obesity-associated hypertension. Activation of the RAAS is a key contributing factor in obesity. Particularly, the RAAS in adipose tissue plays a crucial role in adipose tissue dysfunction and obesity-induced inflammation. The phenotypic changes of adipocytes occur into hypertrophy and an inflammatory response in an autocrine and paracrine manner to impair adipocyte function, including insulin signaling pathway. Adipose tissue produce and secretes several molecules such as leptin, resistin, adiponectin, and visfatin, as well as cytokines such as TNF-α, IL-6, MCP-1, and IL-1. These adipokines are stimulated via the intracellular signaling pathways that regulate inflammation of adipose tissue. Inflammation and oxidative stress in adipose tissue are important to interact with the microvascular endothelium in the mechanisms of obesity-associated hypertension. Increased microvascular resistance raises blood pressure. Therefore, a regulatory link between microvascular and perivascular adipose tissue inflammation and adipokine synthesis are provided to explain the mechanism of obesity-associated hypertension. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.2.46","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32173911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent Update of Renin-angiotensin-aldosterone System in the Pathogenesis of Hypertension.","authors":"Ju-Young Moon","doi":"10.5049/EBP.2013.11.2.41","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.2.41","url":null,"abstract":"<p><p>The activation of renin-angiotensin-aldosterine system(RAAS) is one of the main pathogenesis of hypertension. All the components of RAAS are present in the kidneys at higher concentrations compared to plasma levels, and intrarenal formation of angiotensin II (Ang II) is independent of the systemic RAAS. There are some unique features in intrarenal RAAS compared to systemic RAAS. Unlike JG cells where Ang II inhibits renin release via the AngII type 1 (AT1) receptor by negative feedback, in the collecting duct Ang II stimulates renin expression via the AT1 receptor. Upregulated renin produced in the distal nephron may be able to support continued intrarenal Ang II formation leading to amplification or maintenance of the hypertensive state.The recently discovered angiotensin-converting enzyme-related carboxypeptidase 2 (ACE2)-Angiotensin-(1-7) Ang-(1-7)-Mas receptor axis has an opposing function to that of the ACE-Ang II-AT1 receptor axis.The ACE2 deficiency was associated with an increase in blood pressure, and ACE2 knockout mice have highlighted hypertensive response to Ang II infusion associated with exaggerated accumulation of Ang II in the kidney. Recently, several numbers of patients have been evaluated as the activators of ACE2-Ang-(1-7)-Mas receptor axis, which can be divided into two main classes: aimed to increase the activity of ACE2, and directed to stimulate the Ang-(1-7) receptor Mas. In order to investigate new targets for hypertension and kidney disease, further research on the function of the ACE-Ang-(1-7)-Mas receptor axis is required. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.2.41","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32173910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Da-Rae Kim, Joo-Hee Cho, Won-Seok Jang, Jin-Sug Kim, Kyung-Hwan Jeong, Tae-Won Lee, Chun-Gyoo Ihm
{"title":"Severe Hyponatremia Associated with the Use of Angiotensin II Receptor Blocker/thiazide Combinations.","authors":"Da-Rae Kim, Joo-Hee Cho, Won-Seok Jang, Jin-Sug Kim, Kyung-Hwan Jeong, Tae-Won Lee, Chun-Gyoo Ihm","doi":"10.5049/EBP.2013.11.2.56","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.2.56","url":null,"abstract":"<p><p>There are several widely used combinations of angiotensin II receptor blocker (ARB)/thiazide. The complimentary mechanism of action for such anti-hypertensive therapies is that, while ARB inhibits the vasoconstricting and aldosterone-secreting effects of angiotensin II, hydrochlorothiazide affects the renal tubular mechanisms of electrolyte reabsorption and increases excretion of sodium and chloride in the distal tubule, consequently promoting water excretion. In addition, hypokalemia, which may be triggered by a hydrochlorothiazide-induced increase in urinary potassium loss, is resisted by the use of ARB. Hence, the ARB/thiazide combination is safe in terms of potassium imbalance. For these reasons, fixed-dose ARB/thiazide combination anti-hypertensive drugs have been widely used for the treatment of hypertension. However, there have not been many studies done regarding cases where patients under such regimens showed severe hyponatremia, even when the amount of thiazide included was low. Here we report two cases in which severe hyponatremia occurred following treatment with the ARB/thiazide combinations. Upon discontinuation of the regimen, both patients showed recovery from hyponatremia. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.2.56","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32173913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adrenergic genetic mechanisms in hypertension and hypertensive kidney disease.","authors":"Sun Woo Kang","doi":"10.5049/EBP.2013.11.1.24","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.1.24","url":null,"abstract":"<p><p>Catecholamine secretory traits were significantly heritable, as were stress-induced blood pressure changes. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine biosynthesis. In the tyrosine hyroxylase promoter, significant associations were found for urinary catecholamine excretion and for blood pressure response to stress. TH promoter haplotype 2 (TGGG) showed pleiotropy, increasing both norepinephrine excretion and blood pressure during stress. In hypertension, 2 independent case-control studies (1,266 subjects with 53% women and 927 subjects with 24% women) replicated the effect of C-824T in the determination of blood pressure. Chromogranin A (CHGA) plays a fundamental role in the biogenesis of catecholamine secretory granules. Changes in the storage and release of CHGA in clinical and experimental hypertension prompted us to study whether genetic variation at the CHGA locus might contribute to alterations in autonomic function, and hence hypertension and its target organ consequences such as hypertensive kidney disease (nephrosclerosis). Systematic polymorphism discovery across the human CHGA locus revealed such regulatory regions as the proximal promoter and 3'-UTR. In chromaffin cell-transfected CHGA 3'-UTR and promoter/luciferase reporter plasmids, the functional consequences of the regulatory/non-coding allelic variants were documented. Variants in both the proximal promoter and the 3'-UTR displayed statistical associations with hypertension and hypertensive end stage renal disease. Therefore, I would like to review the common genetic variation in TH and CHGA as a cause of inter-individual variation in sympathetic activity, and ultimately blood pressure and hypertensive kidney disease. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.1.24","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31658307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jae-Hyun Choi, Hee Seung Lee, Sun Moon Kim, Hye-Young Kim, Soon Kil Kwon
{"title":"Paranoid Adipsia-induced Severe Hypernatremia and Uremia treated with Hemodialysis.","authors":"Jae-Hyun Choi, Hee Seung Lee, Sun Moon Kim, Hye-Young Kim, Soon Kil Kwon","doi":"10.5049/EBP.2013.11.1.29","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.1.29","url":null,"abstract":"<p><p>We describe a patient with severe hypernatremia and uremia caused by paranoid adipsia who was treated successfully with hydration and hemodialysis. A previously healthy 40-year-old woman developed the paranoid idea that her water was poisoned, so she refused to drink any water. On admission, her blood urea nitrogen was 208mg/dL, creatinine 4.90mg/dL, serum osmolality 452mOsm/L, serum sodium 172mEq/L, urine specific gravity ≥1.030, urine osmolality 698mOsm/L, and urine sodium/potassium/chloride 34/85.6/8mEq/L. We diagnosed her with uremic encephalopathy and started intravenous dextrose, but the sodium correction was incomplete. She underwent two sessions of hemodialysis to treat the uremic encephalopathy and hypernatremia, and recovered fully without neurological sequelae. Although the standard treatment for severe hypernatremia is hydration, hemodialysis can be an additional treatment in cases of combined uremic encephalopathy. </p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.1.29","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31658308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of v2 receptor antagonists in the treatment of hyponatremia.","authors":"Biff F Palmer","doi":"10.5049/EBP.2013.11.1.1","DOIUrl":"https://doi.org/10.5049/EBP.2013.11.1.1","url":null,"abstract":"Under normal circumstances, there is a balance between water intake and water excretion such that plasma osmolality and the serum sodium(Na+) concentration remain relatively constant. The principal mechanism responsible for prevention of hyponatremia and hyposmolality is renal water excretion. In all hyponatremic patients, water intake exceeds renal water excretion. \u0000 \u0000Excretion of water by the kidney is dependent on three factors. First, there must be adequate delivery of filtrate to the tip of the loop of Henle. Second, solute absorption in the ascending limb and the distal nephron must be preserved so that the tubular fluid will be diluted. Lastly, arginine vasopressin (AVP) levels must be low in the plasma. Of these three requirements for water excretion, the one which is most important in the genesis of hyponatremia is the failure to maximally suppress AVP levels. Given the central role of AVP in limiting renal water excretion, AVP receptor antagonists represent a physiologic and rational method to increase renal water excretion.","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5049/EBP.2013.11.1.1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31658304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}