Electrolyte and Blood Pressure最新文献

{"title":"Metabolic Acidosis in Chronic Kidney Disease: Pathogenesis, Clinical Consequences, and Treatment.","authors":"Hyo Jin Kim","doi":"10.5049/EBP.2021.19.2.29","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.2.29","url":null,"abstract":"<p><p>The kidneys play an important role in regulating the acid-base balance. Metabolic acidosis is common in chronic kidney disease (CKD) patients and can lead to poor outcomes, such as bone demineralization, muscle mass loss, and worsening of renal function. Metabolic acidosis is usually approached with evaluating the serum bicarbonate levels but should be assessed by counting blood pH. Current guidelines recommend oral bicarbonate supplementation to maintain the serum bicarbonate levels within the normal range. However, a slow decline in the glomerular filtration rate might occur, even though the serum bicarbonate levels were in the normal range. Because the serum bicarbonate levels decrease when metabolic acidosis advances, other biomarkers are necessary to indicate acid retention for early diagnosis of metabolic acidosis. For this, urine citrate and ammonium excretion may be used to follow the course of CKD patients. Metabolic acidosis can be treated with an increased fruit and vegetable intake and oral alkali supplementation. Previous studies have suggested that administration of oral sodium bicarbonate may preserve kidney function without significant increases in blood pressure and body weight. Veverimer, a non-absorbed, counterion-free, polymeric drug, is emerging to treat metabolic acidosis, but further researches are awaited. Further studies are also needed to clarify the target therapeutic range of serum bicarbonate and the drugs used for metabolic acidosis.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 2","pages":"29-37"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b7/23/ebp-19-29.PMC8715222.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39913672","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":"Venetoclax with Azacitidine Induced Tumor Lysis Syndrome in an Elderly Patient with Acute Myeloid Leukemia: A Case Report.","authors":"Mihee Kim,&nbsp;Hyun-Jin Bang,&nbsp;Ga-Young Song,&nbsp;Seo-Yeon Ahn,&nbsp;Sung-Hoon Jung,&nbsp;Yong-Su Song,&nbsp;Jae-Sook Ahn","doi":"10.5049/EBP.2021.19.2.46","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.2.46","url":null,"abstract":"<p><p>Combination treatment with hypomethylating agents (HMAs) and venetoclax is being used increasingly in elderly patients with acute myeloid leukemia (AML). Venetoclax with HMAs has been reported to be associated with tumor lysis syndrome (TLS) in AML patients with high leukemic burden. We present a case of an elderly AML patient with low leukemic burden who developed TLS while receiving venetoclax and azacitidine (AZA). A 74-year-old man with newly diagnosed AML with NPM1 mutation received combination therapy with venetoclax and AZA in an outpatient clinic. Within 12 hours after starting venetoclax and AZA, the patient was admitted to the emergency room with fever, general weakness, and laboratory findings consistent with TLS. Based on our results, we recommend monitoring at the start of the treatment with venetoclax and HMAs to prevent and control TLS regardless of the leukemic burden and favorable genetic risk.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 2","pages":"46-50"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ad/0e/ebp-19-46.PMC8715223.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39800582","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":"Urate Transporters in the Kidney: What Clinicians Need to Know.","authors":"Sungjin Chung,&nbsp;Gheun-Ho Kim","doi":"10.5049/EBP.2021.19.1.1","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.1.1","url":null,"abstract":"<p><p>Urate is produced in the liver by the degradation of purines from the diet and nucleotide turnover and excreted by the kidney and gut. The kidney is the major route of urate removal and has a pivotal role in the regulation of urate homeostasis. Approximately 10% of the glomerular filtered urate is excreted in the urine, and the remainder is reabsorbed by the proximal tubule. However, the transport of urate in the proximal tubule is bidirectional: reabsorption and secretion. Thus, an increase in reabsorption or a decrease in secretion may induce hyperuricemia. In contrast, a decrease in reabsorption or an increase in secretion may result in hyperuricosuria. In the proximal tubule, urate reabsorption is mainly mediated by apical URAT1 (<i>SLC22A12</i>) and basolateral GLUT9 (<i>SLC2A9</i>) transporter. OAT4 (<i>SLC22A11</i>) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia. Renal hypouricemia is caused by <i>SLC22A12</i> or <i>SLC2A9</i> loss-of-function mutations, and it may be complicated by exercise-induced acute kidney injury. URAT1 and GLUT9 are also drug targets for uricosuric agents. Sodium-glucose cotransporter inhibitors may induce hyperuricosuria by inhibiting GLUT9b located in the apical plasma membrane. Urate secretion is mediated by basolateral OAT1 (<i>SLC22A6</i>) and OAT3 (<i>SLC22A8</i>) and apical ATP-binding cassette super-family G member 2 (<i>ABCG2</i>), NPT1 (<i>SLC17A1</i>), and NPT4 (<i>SLC17A3</i>) transporter in the proximal tubule. NPT1 and NPT4 may be key players in renal urate secretion in humans, and deletion of <i>SLC22A6</i> and <i>SLC22A8</i> in mice leads to decreased urate excretion. Dysfunctional variants of <i>ABCG2</i> inhibit urate secretion from the gut and kidney and may cause gout. In summary, the net result of urate transport in the proximal tubule is determined by the dominance of transporters between reabsorption (URAT1, OAT4, and GLUT9) and secretion (ABCG2, NPT1, NPT4, OAT1, and OAT3).</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/04/9f/ebp-19-1.PMC8267069.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39208371","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":"Confirming Genetic Abnormalities of Hypokalemic Periodic Paralysis Using Next-Generation Sequencing: A Case Report and Literature Review.","authors":"Hae Ri Kim,&nbsp;Jae Wan Jeon,&nbsp;Eu Jin Lee,&nbsp;Young Rok Ham,&nbsp;Ki Ryang Na,&nbsp;Kang Wook Lee,&nbsp;Kee Hong Park,&nbsp;Seon Young Kim,&nbsp;Dae Eun Choi","doi":"10.5049/EBP.2021.19.1.10","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.1.10","url":null,"abstract":"<p><p>Hypokalemic periodic paralysis (hypoPP) is a disorder characterized by episodic, short-lived, and hypo-reflexive skeletal muscle weakness. HypoPP is a rare disease caused by genetic mutations related to expression of sodium or calcium ion channels. Most mutations are associated with autosomal dominant inheritance, but some are found in patients with no relevant family history. A 28-year-old man who visited the emergency room for paralytic attack was assessed in this study. He exhibited motor weakness in four limbs. There was no previous medical history or family history. The initial electrocardiogram showed a flat T wave and QT prolongation. His blood test was delayed, and sudden hypotension and bradycardia were observed. The blood test showed severe hypokalemia. After correcting hypokalemia, his muscle paralysis recovered without any neurological deficits. The patient's thyroid function and long exercise test results were normal. However, because of the history of high carbohydrate diet and exercise, hypoPP was suspected. Hence, next-generation sequencing (NGS) was performed, and a mutation of Arg669His was noted in the <i>SCN4A</i> gene. Although hypoPP is a rare disease, it can be suspected in patients with hypokalemic paralysis, and iden tification of this condition is important for preventing further attacks and improving patient outcomes. Diagnosing hypoPP through targeted NGS is a cost-effective and useful method.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 1","pages":"10-14"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/49/b7/ebp-19-10.PMC8267070.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39208372","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":"Osmotic Demyelination Syndrome Associated with Hypernatremia Caused by Lactulose Enema in a Patient with Chronic Alcoholism.","authors":"Jeong Ho Lee,&nbsp;Chang Seong Kim,&nbsp;Eun Hui Bae,&nbsp;Soo Wan Kim,&nbsp;Seong Kwon Ma","doi":"10.5049/EBP.2021.19.1.15","DOIUrl":"https://doi.org/10.5049/EBP.2021.19.1.15","url":null,"abstract":"<p><p>A 44-year-old man with chronic alcoholism presented with seizure and loss of consciousness. He was diagnosed with alcoholic hepatic encephalopathy, and his neurologic symptoms recovered after lactulose enema treatment. His initial serum sodium level was 141mEq/L. However, his mental state became confused after treatment with lactulose enema for five days, and his serum sodium level increased to 178mEq/L. After five days of gradual correction of serum sodium level from 178mEq/L to 140mEq/L, the patient's mental state recovered, but motor weakness in both limbs remained. Therefore, magnetic resonance imaging of the brain was performed. T2-weighted brain images showed bilateral symmetrical hyperintensities in the central pons, basal ganglia, thalami, hippocampi and unci, which were consistent with central pontine and extrapontine myelinolysis. We report a rare case of osmotic demyelination syndrome that occurred as a result of a rapid increase from a normal sodium level to hypernatremia caused by lactulose enema administered to treat alcoholic hepatic encephalopathy.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"19 1","pages":"15-18"},"PeriodicalIF":0.0,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ee/65/ebp-19-15.PMC8267071.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39206882","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":"Hypertension and Electrolyte Disorders in Patients with COVID-19.","authors":"Jeong-Hoon Lim,&nbsp;Hee-Yeon Jung,&nbsp;Ji-Young Choi,&nbsp;Sun-Hee Park,&nbsp;Chan-Duck Kim,&nbsp;Yong-Lim Kim,&nbsp;Jang-Hee Cho","doi":"10.5049/EBP.2020.18.2.23","DOIUrl":"https://doi.org/10.5049/EBP.2020.18.2.23","url":null,"abstract":"<p><p>The worldwide coronavirus disease 2019 (COVID-19) pandemic is still in progress, but much remains unknown about the disease. In this article, we review the association of hypertension or the renin-angiotensin system (RAS) with COVID-19 and the correlation between electrolyte disorders and disease severity. Underlying hypertension is likely to be associated with severe or critical COVID-19, but the relationship is not clear owing to confounding factors. Angiotensin-converting enzyme 2 (ACE2) plays an important role in the non-classical RAS pathway and binds to a receptor binding domain of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The RAS blockade is known to increase ACE2 levels, but controversy remains regarding the effect of RAS blockade therapy in the course of COVID-19. Some reports have indicated a protective effect of RAS blockade on COVID-19, whereas others have reported an association of RAS blockade therapy with the occurrence of severe complications such as acute kidney injury and admission to the intensive care unit. Electrolyte disorders are not uncommon in patients with COVID-19, and severe COVID-19 has frequently shown hypokalemia, hyponatremia, and hypocalcemia. Electrolyte imbalances are caused by alteration of RAS, gastrointestinal loss, effects of proinflammatory cytokines, and renal tubular dysfunction by the invasion of SARS-CoV-2.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"18 2","pages":"23-30"},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5c/ed/ebp-18-23.PMC7781764.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38790774","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":"Cisplatin-induced Atrioventricular Block Requiring a Pacemaker: Two Case Reports and a Literature Review.","authors":"Hyun-Jin Bang,&nbsp;Ho Young Lee,&nbsp;Hyeon-Jong Kim,&nbsp;Namsik Yoon,&nbsp;Ik-Joo Chung,&nbsp;Woo Kyun Bae","doi":"10.5049/EBP.2020.18.2.49","DOIUrl":"https://doi.org/10.5049/EBP.2020.18.2.49","url":null,"abstract":"<p><p>Chemotherapeutic drugs can cause cardiac toxicities such as cardiomyopathy, arrhythmia, and cardiovascular disease. The well-known side effects of cisplatin are nephrotoxicity, nausea, vomiting, and electrolyte imbalance. Cardiotoxicity induced by cisplatin is rare, and its pathophysiology is unknown. Here, we present two cases of complete and high-degree atrioventricular (AV) block that occurred during cisplatin-based chemotherapy and required pacemaker placement. A 64-year-old woman and a 75-year-old man, who had no underlying heart disease, developed dyspnea without chest pain and bradycardia during cisplatin-based chemotherapy. However, there were no significant differences in their serum electrolyte levels, cardiac enzyme levels, and echocardiography results before and after drug administration. The ECGs were confirmed with complete AV block and high-degree AV block, which requiring pacemaker placement. We assume that cisplatin directly caused the complete, high-degree AV block, which required a pacemaker placement in our cases. In such cases, a cumulative dose of cisplatin over 240 mg/m2 is a risk factor for early symptoms of AV block. If patients complain of dyspnea without chest pain during cisplatin-based chemotherapy, arrhythmic complications should be considered. This information may be helpful for clinicians treating patients with cisplatin chemotherapy.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"18 2","pages":"49-52"},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a5/06/ebp-18-49.PMC7781763.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39125545","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":"Hyponatremia Associated with Pulmonary Arterial Hypertension: Syndrome of Inappropriate Antidiuresis Versus Right Heart Failure.","authors":"Juyeon Kang,&nbsp;Dae Hyun Lim,&nbsp;Gheun-Ho Kim","doi":"10.5049/EBP.2020.18.2.40","DOIUrl":"https://doi.org/10.5049/EBP.2020.18.2.40","url":null,"abstract":"<p><p>Because it is associated with mortality, hyponatremia is an important feature of pulmonary arterial hypertension. Its mechanisms remain unclear, although right heart failure resulting from pulmonary arterial hypertension may lead to systemic congestion and arterial underfilling. However, most patients with pulmonary arterial hypertension are clinically euvolemic and have no peripheral edema. Unlike patients with underlying heart disease, neurohumoral activation is not demonstrated in hyponatremic patients with pulmonary arterial hypertension, who show features of congestive heart failure only at later stages in their disease. Here, a case vignette is introduced, and the pathophysiology of hyponatremia in pulmonary arterial hypertension will be discussed. Syndrome of inappropriate antidiuresis (SIAD) appears to underlie hyponatremia in the initial phase of pulmonary arterial hypertension. The mechanisms by which various lung diseases can lead to SIAD remain an enigma.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"18 2","pages":"40-43"},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/89/2a/ebp-18-40.PMC7781766.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39125543","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":"Liver Infarction and Venous Thromboembolism after Tamoxifen Use in an ADPKD Patient with Encapsulating Peritoneal Sclerosis: A Case Report.","authors":"Kyoung Min Kwak,&nbsp;Gwang Ho Choi,&nbsp;Kwang Eon Shim,&nbsp;Ho Yong Jin,&nbsp;Seok Hyung Kim,&nbsp;Jong Woo Yoon,&nbsp;Hyunsuk Kim","doi":"10.5049/EBP.2020.18.2.44","DOIUrl":"https://doi.org/10.5049/EBP.2020.18.2.44","url":null,"abstract":"<p><p>Encapsulating peritoneal sclerosis (EPS) is a potentially fatal complication after long-term peritoneal dialysis, and tamoxifen can be used for its prevention and treatment. However, tamoxifen is known to increase the risk of venous thromboembolism. A 49-year-old woman was admitted with sudden abdominal pain. The patient had received peritoneal dialysis for 20 years and switched to hemodialysis after the diagnosis of EPS. Tamoxifen (10mg) and prednisolone (20mg) had been administered for 8 months. On computed tomography, the left hepatic lobe was hardly illuminated, leading to a diagnosis of liver infarction. A month later, she was re-admitted due to abdominal pain and extensive deep vein thrombosis of the leg. The administration of tamoxifen was stopped and prednisolone was reduced to 10mg. As her malnutrition progressed, she succumbed to death of gram negative sepsis. The patient was concluded to have liver infarction and extensive venous thrombosis as a side effect of tamoxifen.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"18 2","pages":"44-48"},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c5/fd/ebp-18-44.PMC7781765.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39125544","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":"Association of Proteinuria with Urinary Concentration Defect in Puromycin Aminonucleoside Nephrosis.","authors":"Chor Ho Jo,&nbsp;Sua Kim,&nbsp;Gheun-Ho Kim","doi":"10.5049/EBP.2020.18.2.31","DOIUrl":"https://doi.org/10.5049/EBP.2020.18.2.31","url":null,"abstract":"<p><strong>Background: </strong>Puromycin aminonucleoside (PA) can induce nephrotic syndrome in rats, and proteinuria is an important mediator of tubulointerstitial injury in glomerulopathy. We assumed that glomerular proteinuria may affect tubular function, such as urinary concentration, and investigated whether a urinary concentration defect is associated with proteinuria in puromycin aminonucleoside nephrosis (PAN). We also investigated the defect response to enalapril.</p><p><strong>Methods: </strong>Glomerular proteinuria was induced by a single intraperitoneal injection of PA (150mg/kg BW) in male Sprague-Dawley rats. In a half of these rats, enalapril (35mg/kg BW) was administered daily in a food mixture for two weeks. After the animal experiment, kidneys were harvested for immunoblot analysis and histopathologic examination.</p><p><strong>Results: </strong>Compared with the control group, PA-treated rats had severe proteinuria, polyuria, and a lower urine osmolality. PA treatment induced remarkable tubulointerstitial injury and significant reductions in protein abundances of aquaporin-1 and Na-K-2Cl co-transporter type 2 (NKCC2). Proteinuria significantly correlated with osteopontin expression in the kidney and inversely correlated with renal expression of aquaporin-1, aquaporin-2, and NKCC2. The degree of tubulointerstitial injury significantly correlated with proteinuria, urine output, and osteopontin expression and inversely correlated with urine osmolality and renal expression of aquaporin-1, aquaporin-2, and NKCC2. No significant differences in parameters were found between PA-treated rats with and without enalapril.</p><p><strong>Conclusion: </strong>In PAN, glomerular proteinuria was associated with tubulointerstitial injury and water diuresis. Downregulation of aquaporin-1 and NKCC2 can impair countercurrent multiplication and cause a urinary concentration defect in PAN.</p>","PeriodicalId":35352,"journal":{"name":"Electrolyte and Blood Pressure","volume":"18 2","pages":"31-39"},"PeriodicalIF":0.0,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1a/fe/ebp-18-31.PMC7781767.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38790775","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}