今日の臨床サポート

多尿

著者: 前川道隆 藤田医科大学ばんたね病院 腎臓内科

監修: 山中克郎 福島県立医科大学会津医療センター総合内科

著者校正/監修レビュー済:2021/06/23
患者向け説明資料

概要・推奨   

  1. 多尿の鑑別診断では、尿量と尿浸透圧を測定し、浸透圧利尿と水利尿を区別することが最初のステップである。
  1. 高血糖は外来で遭遇する浸透圧利尿の原因として最も多いため、患者が口喝・尿量増加を訴える場合には、まず血糖値の測定を行う。入院中の患者では過剰な輸液による塩類利尿多いため、多尿をみたときは体液量や輸液の必要性を評価すべきである
  1. 糖尿病では著明な高血糖により尿細管での再吸収能を超えるブドウ糖が糸球体で濾過されるとブドウ糖による浸透圧利尿が生じ多飲・多尿を生じる。SGLT2sodium glucose co-transporter 2阻害薬は、尿細管におけるブドウ糖の再吸収を阻害し尿糖排泄を促すため、投与初期には1日500mL程度の尿量増加がみられる。
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
前川道隆 : 未申告[2021年]
監修:山中克郎 : 未申告[2021年]

改訂のポイント:
  1. 糖尿病、SGLT2阻害薬による尿量増加について追記した。
  1. 急性腎障害回復期、尿閉解除後の多尿について、より慎重に輸液の必要性を判断するよう記載を変更した。

病態・疫学・診察

疫学情報・病態・注意事項  
  1. 成人において多尿とは、尿量が1日3,000mLを超す状態を指し[1]頻尿や夜間尿とは区別される。
  1. 病態から、自由水の排泄が亢進する水利尿、何らかの浸透圧物質により自由水・塩類がともに喪失する溶質利尿(浸透圧利尿)に分けられる。水利尿では尿崩症と多飲多尿の鑑別を行い、溶質利尿では浸透圧利尿を生じている原因物質を特定することで鑑別を行う。
 
多尿診断のアルゴリズム

多尿の診断は実際の尿量を測定することから始まる。3L/日を超える多尿が確認された場合には、自由水の排泄が亢進する水利尿と、尿中の浸透圧物質が多いことによる溶質利尿を区別するために蓄尿を行って尿浸透圧を評価する。
浸透圧利尿の場合、高血糖や浸透圧利尿薬の使用があれば原因と考え、尿中浸透圧物質の多くを電解質が占める場合には輸液過剰や腎から塩類を喪失する病態を考える。

 
  1. 外来診療では糖尿病の頻度が多いが、尿崩症、電解質異常、薬剤など多尿の原因は多岐にわたる。
  1. 病態ごとの治療が行われるが、体液欠乏や電解質異常を生じることが多く、輸液による体液管理が必要になることも多い。
問診・診察のポイント  
  1. 多尿からの体液喪失による血圧低下、頻脈、起立性低血圧、体重減少、脱力、意識障害に注意する。

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文献 

著者: J R Oster, I Singer, L Thatte, I Grant-Taylor, J M Diego
雑誌名: Arch Intern Med. 1997 Apr 14;157(7):721-9.
Abstract/Text Polyuria is an important symptom or sign because of its potential severity, diverse causes, and interesting pathophysiology. Whereas polyuria induced by water diuresis is reasonably well understood and easily recognized by clinicians, that produced by solute diuresis is more likely to cause confusion. In this article, we focus on solute diuresis as a cause of polyuria, review the classification and pathophysiology of polyuria, and describe the clinical and laboratory studies useful for the evaluation of the polyuric patient. A stepwise, logical approach is provided (1) to determine whether a patient has a water diuresis, a solute diuresis, or both (concurrently), and (2) if a solute diuresis is present, to determine if it is caused by electrolytes (eg, sodium chloride sodium bicarbonate), by nonelectrolytes (eg, glucose, urea), or by both. How to assess these possibilities and to determine the specific cause of the diuresis is discussed in detail. Three representative case examples are provided. Selected causes of a solute diuresis also are reviewed.

PMID 9125003  Arch Intern Med. 1997 Apr 14;157(7):721-9.
著者: Gregor Lindner, Christoph Schwarz, Georg-Christian Funk
雑誌名: Nephrol Dial Transplant. 2012 Mar;27(3):962-7. doi: 10.1093/ndt/gfr428. Epub 2011 Aug 2.
Abstract/Text BACKGROUND: Hypernatraemia is common in critically ill patients and has been shown to be an independent predictor of mortality. Osmotic urea diuresis can cause hypernatraemia due to significant water losses but is often not diagnosed. Free water clearance (FWC) and electrolyte free water clearance (EFWC) were proposed to quantify renal water handling. We aimed to (i) identify patients with hypernatraemia due to osmotic urea diuresis and (ii) investigate whether FWC and EFWC are helpful in identifying renal loss of free water.
METHODS: In this retrospective study, we screened a registry for patients, who experienced intensive care unit (ICU)-acquired hypernatraemia. Among them, patients with hypernatraemia due to osmotic urea diuresis were detected by a case-by-case review. Total fluid and electrolyte balances together with FWC and EFWC were calculated for days of rising serum sodium and stable serum sodium.
RESULTS: We identified seven patients (10% of patients with ICU-acquired hypernatraemia) with osmotic diuresis due to urea. All patients were intubated during development of hypernatraemia and received enteral nutrition. The median highest serum sodium level of 153 mmol (Q1: 151-Q3: 155 mmol/L) was reached after a 5-day period of rise in serum sodium. During this period, FWC was -904 mL/day (Q1: -1574-Q3: -572), indicating renal water retention, while EFWC was 1419 mL/day (Q1: 1052-Q3: 1923), showing renal water loss. While FWC did not differ between time of stable serum sodium and development of hypernatraemia, EFWC was significantly higher during rise in serum sodium.
CONCLUSION: Osmotic urea diuresis is a common cause of hypernatraemia in the ICU. EFWC was useful in the differential diagnosis of polyuria during rising serum sodium levels, while FWC was misleading.

PMID 21810766  Nephrol Dial Transplant. 2012 Mar;27(3):962-7. doi: 10.・・・
著者: Bhavna Bhasin, Juan Carlos Q Velez
雑誌名: Am J Kidney Dis. 2016 Mar;67(3):507-11. doi: 10.1053/j.ajkd.2015.10.021. Epub 2015 Dec 11.
Abstract/Text Polyuria, defined as daily urine output in excess of 3.0 to 3.5L/d, can occur due to solute or water diuresis. Solute-induced polyuria can be seen in hospitalized patients after a high solute load from exogenous protein administration or following relief of urinary obstruction. Similar clinical scenarios are rarely encountered in the outpatient setting. We describe a case of polyuria due to high solute ingestion and excessive water intake leading to a mixed picture of solute and water diuresis. Restriction of the daily solute load and water intake resulted in complete resolution of polyuria. Determination of the daily excreted urinary osmoles may yield important clues to the cause of polyuria and should be included in the routine workup of polyuria.

Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
PMID 26687922  Am J Kidney Dis. 2016 Mar;67(3):507-11. doi: 10.1053/j.・・・
著者: Nicole Nigro, Mathis Grossmann, Cherie Chiang, Warrick J Inder
雑誌名: Intern Med J. 2018 Mar;48(3):244-253. doi: 10.1111/imj.13627.
Abstract/Text The main determinants for the maintenance of water homeostasis are the hormone arginine vasopressin (AVP) and thirst. Disturbances in these regulatory mechanisms can lead to polyuria-polydipsia syndrome, which comprises of three different conditions: central diabetes insipidus (DI) due to insufficient secretion of AVP, nephrogenic DI caused by renal insensitivity to AVP action and primary polydipsia due to excessive fluid intake and consequent physiological suppression of AVP. It is crucial to determine the exact diagnosis because treatment strategies vary substantially. To differentiate between the causes of the polyuria-polydipsia syndrome, a water deprivation test combined with desmopressin administration is the diagnostic 'gold standard'. Thereby, AVP activity is indirectly evaluated through the measurement of urine osmolality after prolonged dehydration. However, this test has several limitations and may fail to distinguish precisely between patients with primary polydipsia and mild forms of central and nephrogenic DI. The direct measurement of AVP during the water deprivation test, which was reported in the 1980s, has not been widely adopted due to availability, assay issues and diagnostic performance. Recently, copeptin, the c-terminal portion of the larger precursor peptide of AVP, has been evaluated in the setting of polyuria-polydipsia syndrome and appears to be a useful candidate biomarker for the differential diagnosis. A standardised method for the water deprivation test is presented as part of a joint initiative of the Endocrine Society of Australia, the Australasian Association of Clinical Biochemists and the Royal College of Pathologists of Australasia to harmonise dynamic endocrine tests across Australia.

© 2017 Royal Australasian College of Physicians.
PMID 28967192  Intern Med J. 2018 Mar;48(3):244-253. doi: 10.1111/imj.・・・
著者: Atsutaka Yasui, Ganghyuck Lee, Tetsuaki Hirase, Tatsuroh Kaneko, Stefan Kaspers, Maximilian von Eynatten, Tomoo Okamura
雑誌名: Diabetes Ther. 2018 Apr;9(2):863-871. doi: 10.1007/s13300-018-0385-5. Epub 2018 Feb 27.
Abstract/Text INTRODUCTION: Empagliflozin, a sodium glucose co-transporter 2 (SGLT2) inhibitor, ameliorates hyperglycemia in patients with type 2 diabetes (T2D) by inducing sustained glucosuria. Empagliflozin treatment was previously associated with a transient increase in 24-h urine volume in Caucasian patients with T2D, however comparable evidence in Japanese T2D individuals is scarce. We therefore assessed acute and chronic changes in 24-h urine volume and fluid intake with empagliflozin in Japanese patients with T2D.
METHODS: In this randomized, double-blind, placebo-controlled, parallel-group, multiple-dose, 4-week trial, 100 Japanese patients with T2D were randomized to receive either 1, 5, 10, or 25 mg empagliflozin or placebo once-daily. Changes from baseline in 24-h urine volume and fluid intake were assessed at days 1, 27, and 28 after the initiation of empagliflozin.
RESULTS: The 24-h urine volume and fluid intake were comparable across all treatment groups at baseline. Patients treated with either 10 or 25 mg empagliflozin (i.e., the licensed doses in Japan) showed a significant increase in 24-h urine volume compared to placebo at day 1 (mean change from baseline: + 0.83, + 1.08, and + 0.29 L/day in the empagliflozin 10 and 25 mg groups and the placebo group, respectively; both p < 0.001 vs. placebo). However, 24-h urine volume levels in the empagliflozin groups were comparable to placebo at day 27 and 28 (differences vs placebo < 0.1 L/day; p > 0.05). The 24-h fluid intake was comparable across all study groups throughout the entire study period. No events consistent with dehydration were reported during empagliflozin treatment.
CONCLUSION: Treatment initiation with empagliflozin in Japanese patients with T2D was associated with transient diuresis; however, overall urine volume returned towards baseline levels within 4 weeks of treatment. These findings are consistent with a physiological, adaptive mechanism of the kidney to maintain overall body fluid balance in response to treatment initiation with a SGLT2 inhibitor.
TRIAL REGISTRATION NUMBER: NCT00885118.
FUNDING: Nippon Boehringer Ingelheim Co., Ltd.

PMID 29488164  Diabetes Ther. 2018 Apr;9(2):863-871. doi: 10.1007/s133・・・
著者: Solomon Bitew, Louis Imbriano, Nobuyuki Miyawaki, Steven Fishbane, John K Maesaka
雑誌名: Clin J Am Soc Nephrol. 2009 Feb;4(2):309-15. doi: 10.2215/CJN.02740608.
Abstract/Text BACKGROUND AND OBJECTIVES: The existence and prevalence of cerebral salt wasting (CSW) or the preferred term, renal salt wasting (RSW), and its differentiation from syndrome of inappropriate antidiuretic hormone (SIADH) have been controversial. This controversy stems from overlapping clinical and laboratory findings and an inability to assess the volume status of these patients. The authors report another case of RSW without clinical cerebral disease and contrast it to SIADH.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Three patients with hyponatremia, hypouricemia, increased fractional excretion (FE) of urate, urine sodium >20 mmol/L, and concentrated urines were infused with isotonic saline after collection of baseline data.
RESULTS: One patient with RSW had pneumonia without cerebral disease and showed increased plasma aldosterone and FEphosphate, and two patients with SIADH had increased blood volume, low plasma renin and aldosterone, and normal FEphosphate. The patient with RSW responded to isotonic saline by excretion of dilute urines, prompt correction of hyponatremia, and normal water loading test after volume repletion. Hypouricemia and increased FEurate persisted after correction of hyponatremia. Two patients with SIADH failed to dilute their urines and remained hyponatremic during 48 and 110 h of saline infusion.
CONCLUSIONS: The authors demonstrate appropriate stimulation of ADH in RSW. Differences in plasma renin and aldosterone levels and FEphosphate can differentiate RSW from SIADH, as will persistent hypouricemia and increased FEurate after correction of hyponatremia in RSW. FEphosphate was the only contrasting variable at baseline. The authors suggest an approach to treat the hyponatremic patient meeting criteria for SIADH and RSW and changing CSW to the more appropriate term, RSW

PMID 19201917  Clin J Am Soc Nephrol. 2009 Feb;4(2):309-15. doi: 10.22・・・
著者: Richard H Sterns, Stephen M Silver
雑誌名: J Am Soc Nephrol. 2008 Feb;19(2):194-6. doi: 10.1681/ASN.2007101118. Epub 2008 Jan 23.
Abstract/Text The term cerebral salt wasting (CSW) was introduced before the syndrome of inappropriate antidiuretic hormone secretion was described in 1957. Subsequently, CSW virtually vanished, only to reappear a quarter century later in the neurosurgical literature. A valid diagnosis of CSW requires evidence of inappropriate urinary salt losses and reduced "effective arterial blood volume." With no gold standard, the reported measures of volume depletion do not stand scrutiny. We cannot tell the difference between CSW and the syndrome of inappropriate antidiuretic hormone secretion. Furthermore, the distinction does not make a difference; regardless of volume status, hyponatremia complicating intracranial disease should be treated with hypertonic saline.

PMID 18216309  J Am Soc Nephrol. 2008 Feb;19(2):194-6. doi: 10.1681/AS・・・
著者: M C Bishop
雑誌名: Br J Urol. 1985 Feb;57(1):1-5.
Abstract/Text Fifty-five patients with chronic urinary retention and incipient or actual renal failure were studied. In the majority of patients renal function improved after bladder decompression, irrespective of whether or not a diuresis occurred. Excessive loss of salt and water was rarely a matter of concern and most patients did not require intravenous fluid replacement. Several lost weight and experienced a fall in blood pressure during the period of diuresis without adverse effect upon renal functional recovery. A profound fall in blood pressure occurred in only three patients, all of whom required long-term sodium supplementation. It is concluded that the problem of salt and water loss after bladder decompression in patients with renal failure is exaggerated and difficult to predict. Over-enthusiastic replacement of fluid in strict accordance with output could readily lead to fluid overload and prolongation of the diuretic period. Therefore fluid replacement should be determined by the clinical condition of the patient and measurement of improving renal function with less emphasis on urine output and its electrolyte content.

PMID 3971092  Br J Urol. 1985 Feb;57(1):1-5.
著者: Josée Bouchard, Sharon B Soroko, Glenn M Chertow, Jonathan Himmelfarb, T Alp Ikizler, Emil P Paganini, Ravindra L Mehta, Program to Improve Care in Acute Renal Disease (PICARD) Study Group
雑誌名: Kidney Int. 2009 Aug;76(4):422-7. doi: 10.1038/ki.2009.159. Epub 2009 May 13.
Abstract/Text Fluid accumulation is associated with adverse outcomes in critically ill patients. Here, we sought to determine if fluid accumulation is associated with mortality and non-recovery of kidney function in critically ill adults with acute kidney injury. Fluid overload was defined as more than a 10% increase in body weight relative to baseline, measured in 618 patients enrolled in a prospective multicenter observational study. Patients with fluid overload experienced significantly higher mortality within 60 days of enrollment. Among dialyzed patients, survivors had significantly lower fluid accumulation when dialysis was initiated compared to non-survivors after adjustments for dialysis modality and severity score. The adjusted odds ratio for death associated with fluid overload at dialysis initiation was 2.07. In non-dialyzed patients, survivors had significantly less fluid accumulation at the peak of their serum creatinine. Fluid overload at the time of diagnosis of acute kidney injury was not associated with recovery of kidney function. However, patients with fluid overload when their serum creatinine reached its peak were significantly less likely to recover kidney function. Our study shows that in patients with acute kidney injury, fluid overload was independently associated with mortality. Whether the fluid overload was the result of a more severe renal failure or it contributed to its cause will require clinical trials in which the role of fluid administration to such patients is directly tested.

PMID 19436332  Kidney Int. 2009 Aug;76(4):422-7. doi: 10.1038/ki.2009.・・・
著者: John H Boyd, Jason Forbes, Taka-aki Nakada, Keith R Walley, James A Russell
雑誌名: Crit Care Med. 2011 Feb;39(2):259-65. doi: 10.1097/CCM.0b013e3181feeb15.
Abstract/Text OBJECTIVE: To determine whether central venous pressure and fluid balance after resuscitation for septic shock are associated with mortality.
DESIGN: We conducted a retrospective review of the use of intravenous fluids during the first 4 days of care.
SETTING: Multicenter randomized controlled trial.
PATIENTS: The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were receiving a minimum of 5 μg of norepinephrine per minute.
INTERVENTIONS: None.
MEASUREMENTS AND MAIN RESULTS: Based on net fluid balance, we determined whether one's fluid balance quartile was correlated with 28-day mortality. We also analyzed whether fluid balance was predictive of central venous pressure and furthermore whether a guideline-recommended central venous pressure of 8-12 mm Hg yielded a mortality advantage. At enrollment, which occurred on average 12 hrs after presentation, the average fluid balance was +4.2 L. By day 4, the cumulative average fluid balance was +11 L. After correcting for age and Acute Physiology and Chronic Health Evaluation II score, a more positive fluid balance at both at 12 hrs and day 4 correlated significantly with increased mortality. Central venous pressure was correlated with fluid balance at 12 hrs, whereas on days 1-4, there was no significant correlation. At 12 hrs, patients with central venous pressure <8 mm Hg had the lowest mortality rate followed by those with central venous pressure 8-12 mm Hg. The highest mortality rate was observed in those with central venous pressure >12 mm Hg. Contrary to the overall effect, patients whose central venous pressure was <8 mm Hg had improved survival with a more positive fluid balance.
CONCLUSIONS: A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased risk of mortality in septic shock. Central venous pressure may be used to gauge fluid balance ≤ 12 hrs into septic shock but becomes an unreliable marker of fluid balance thereafter. Optimal survival in the VASST study occurred with a positive fluid balance of approximately 3 L at 12 hrs.

PMID 20975548  Crit Care Med. 2011 Feb;39(2):259-65. doi: 10.1097/CCM.・・・
著者: Ling Zhang, Zhiwen Chen, Yongshu Diao, Yingying Yang, Ping Fu
雑誌名: J Crit Care. 2015 Aug;30(4):860.e7-13. doi: 10.1016/j.jcrc.2015.03.025. Epub 2015 Apr 9.
Abstract/Text PURPOSE: Fluid resuscitation is commonly administered to maintain adequate renal perfusion in critically ill patients to prevent or even treat acute kidney injury (AKI). However, recent studies show that fluid overload is common and might be associated with poor outcomes in patients with AKI. Hence, the objective of this study was to assess the associations of fluid overload with mortality and kidney recovery in patients with AKI.
MATERIALS AND METHODS: We electronically searched original articles published in peer-reviewed journals from their inception to January 2015 in PubMed, EMBASE, the Cochrane Library databases, Google Scholar, and Chinese database (SinoMed). We additionally searched the reference lists of all retrieved articles. We performed a systematic review and meta-analysis of all eligible cohort or case-control studies of fluid overload in patients with AKI. The primary outcomes were mortality and kidney recovery. We pooled adjusted odds ratios (ORs) with 95% confidence intervals (95% CIs) by using Review Manager 5.2 (The Cochrane Collaboration, Oxford, UK).
RESULTS: A total of 5095 patients from 12 cohort studies published from 2008 to 2014 were included. A significant positive association was found between fluid overload and mortality in patients with AKI (OR, 2.23; 95% CI, 1.66-3.01), with similar findings in sepsis (OR, 2.27; 95% CI, 1.69-to 3.03) and nonsepsis subgroups (OR, 3.40; 95% CI, 2.50-4.63). There was also a significant association between mean fluid balance (continuous variables) and mortality (OR, 1.16; 95% CI, 1.07-1.27). Although there was a trend of lower rate of kidney recovery in the fluid overload group, there was no significant association between fluid overload and kidney recovery (OR, 0.66; 95% CI, 0.37-1.15), or dialysis dependence (OR, 0.72; 95% CI, 0.38-1.35).
CONCLUSIONS: Fluid overload is associated with an increased risk of mortality in patients with AKI. The evidence of the relationship between fluid overload and kidney recovery is insufficient.

Copyright © 2015 Elsevier Inc. All rights reserved.
PMID 25979272  J Crit Care. 2015 Aug;30(4):860.e7-13. doi: 10.1016/j.j・・・
著者: M Cerdà-Esteve, E Cuadrado-Godia, J J Chillaron, C Pont-Sunyer, G Cucurella, M Fernández, A Goday, J F Cano-Pérez, A Rodríguez-Campello, J Roquer
雑誌名: Eur J Intern Med. 2008 Jun;19(4):249-54. doi: 10.1016/j.ejim.2007.06.019. Epub 2008 Mar 7.
Abstract/Text Hyponatremia is the most frequent electrolyte disorder in critically neurological patients. Cerebral salt wasting syndrome (CSW) is defined as a renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. The pathogenesis of this disorder is still not completely understood. Sympathetic responses as well as some natriuretic factors play a role in this syndrome. Distinction between SIADH and CSW might be difficult. The essential point is the volemic state. It is necessary to rule out other intermediate causes. Treatment requires volume replacement and maintenance of a positive salt balance. Mineral corticoids may be useful in complicated cases.

PMID 18471672  Eur J Intern Med. 2008 Jun;19(4):249-54. doi: 10.1016/j・・・
著者: Lily Kao, Zahraa Al-Lawati, Joli Vavao, Gary K Steinberg, Laurence Katznelson
雑誌名: Pituitary. 2009;12(4):347-51. doi: 10.1007/s11102-009-0188-9. Epub 2009 May 22.
Abstract/Text Hyponatremia is a frequent complication following subarachnoid hemorrhage (SAH), and is commonly attributed either to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting syndrome (CSW). The object of this study is to elucidate the clinical demographics and sequelae of hyponatremia due to CSW in subjects with aneurysmal SAH. Retrospective chart review of patients >18 years with aneurysmal SAH admitted between January 2004 and July 2007 was performed. Subjects with moderate to severe hyponatremia (serum sodium <130 mmol l(-1)) were divided into groups consistent with CSW and SIADH based on urine output, fluid balance, natriuresis, and response to saline infusion. Clinical demographics were compared. Of 316 subjects identified, hyponatremia (serum sodium <135 mmol l(-1)) was detected in 187 (59.2%) subjects and moderate to severe hyponatremia in 48 (15.2%). Of the latter group, 35.4% were categorized with SIADH and 22.9% with CSW. Compared to eunatremic subjects, hyponatremia was associated with significantly longer hospital stay (15.7 +/- 1.9 vs. 9.6 +/- 1.1 days, p < 0.001). Subjects with CSW had similar mortality and duration of hospital stay vs. those with SIADH. Though less common than SIADH, CSW was detected in approximately 23% of patients with history of aneurysmal SAH and was not clearly associated with enhanced morbidity and mortality compared to subjects with SIADH. Further studies regarding the pathogenesis and management, along with the medical consequences, of CSW are important.

PMID 19462244  Pituitary. 2009;12(4):347-51. doi: 10.1007/s11102-009-0・・・
著者: Jasminder Momi, Christopher M Tang, Antoine C Abcar, Dean A Kujubu, John J Sim
雑誌名: Perm J. 2010 Summer;14(2):62-5.
Abstract/Text BACKGROUND: Hyponatremia is a common electrolyte imbalance in hospitalized patients. It is associated with significant morbidity and mortality, especially if the underlying cause is incorrectly diagnosed and not treated appropriately. Often, the hospitalist is faced with a clinical dilemma when a patient presents with hyponatremia of an unclear etiology and with uncertain volume status. Syndrome of inappropriate antidiuretic hormone (SIADH) is frequently diagnosed in this clinical setting, but cerebral salt wasting (CSW) is an important diagnosis to consider.
OBJECTIVE: We wanted to describe the diagnosis, treatment, and history of CSW to provide clinicians with a better understanding of the differential diagnosis for hyponatremia.
CONCLUSION: CSW is a process of extracellular volume depletion due to a tubular defect in sodium transport. Two postulated mechanisms for CSW are the excess secretion of natriuretic peptides and the loss of sympathetic stimulation to the kidney. Making the distinction between CSW and SIADH is important because the treatment for the two conditions is very different.

PMID 20740122  Perm J. 2010 Summer;14(2):62-5.
著者: B F Palmer
雑誌名: Nephrol Dial Transplant. 2000 Feb;15(2):262-8.
Abstract/Text
PMID 10648680  Nephrol Dial Transplant. 2000 Feb;15(2):262-8.
著者: Craig E Taplin, Christopher T Cowell, Martin Silink, Geoffrey R Ambler
雑誌名: Pediatrics. 2006 Dec;118(6):e1904-8. doi: 10.1542/peds.2006-0702. Epub 2006 Nov 13.
Abstract/Text Cerebral salt wasting is an increasingly recognized condition in pediatrics and is characterized by inappropriate natriuresis and volume contraction in the presence of cerebral pathology. Diagnosis can be difficult and therapy challenging. A few single case reports of the successful use of fludrocortisone exist. We report 4 patients with cerebral salt wasting, all of whom presented with hyponatremia in the presence of known intracerebral pathology. All had clinically significant hyponatremia, and 3 had hyponatremic seizures. Two of the patients also satisfied clinical criteria for diabetes insipidus. They all were treated with regimens using increased sodium and fluid administration but experienced ongoing salt wasting. Fludrocortisone was instituted in all 4 patients and in 3 resulted in rapid improvement in net sodium balance, enabling the weaning of hypertonic fluids and stabilization of serum electrolytes. In 3 patients, fludrocortisone treatment was complicated by hypokalemia, and in 1 patient by hypertension, which necessitated a dose reduction or brief cessation of therapy. Duration of therapy was 4 to 125 days. Cerebral salt wasting presents considerable management challenges; however, fludrocortisone therapy can be an effective adjunct to treatment.

PMID 17101713  Pediatrics. 2006 Dec;118(6):e1904-8. doi: 10.1542/peds.・・・
著者: Soichi Sano, Keiko Yamagami, Takashi Morikawa, Katsunobu Yoshioka
雑誌名: Intern Med. 2010;49(2):161-5. Epub 2010 Jan 15.
Abstract/Text Central diabetes insipidus (CDI) could occurs in patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML), because of infiltration of leukemic cells into the neurohypophysis or some other reason and it is closely associated with abnormalities of chromosome 7. We report a case of MDS with abnormalities of chromosome 7, presenting as CDI followed by deterioration of polyuria and hyponatremia with a decreased extracellular fluid volume. Magnetic resonance imaging (MRI) revealed symmetrically enhanced lesions in the hypothalamus. Fludrocortisone treatment normalized his serum sodium level and cerebral salt wasting syndrome (CSWS) was suspected.

PMID 20075582  Intern Med. 2010;49(2):161-5. Epub 2010 Jan 15.
著者: Halil Ozdemir, Zehra Aycan, Aydan Degerliyurt, Ayse Metin
雑誌名: Turk Neurosurg. 2010 Jan;20(1):100-2.
Abstract/Text Hyponatremia is the most frequent electrolyte disorder in critically ill neurological patients. The major differential diagnoses in this situation are the syndrome of inappropriate antidiuretic hormone secretion, marked by inappropriate retention of free water, and cerebral salt wasting, characterized by excessive urinary loss of sodium and resulting in polyuria and extracellular volume contraction. Cerebral salt wasting is a syndrome of hyponatremia due to increased urine output and excessive natriuresis described in patients with central nervous system disease. Although cerebral salt wasting has been well described in neurosurgical patients, data regarding pediatric patients is sparse. We present a 34-month-old boy with lissencephaly who developed cerebral salt wasting after brain biopsy. The patient was treated with hypertonic saline and multiple antiepileptic drugs. Fludrocortisone supplementation effectively treated cerebral salt wasting.

PMID 20066633  Turk Neurosurg. 2010 Jan;20(1):100-2.
著者: L Nagotkar, P Shanbag, N Dasarwar
雑誌名: Indian Pediatr. 2008 Jul;45(7):598-601.
Abstract/Text Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction in the presence of cerebral pathology. Diagnosis can be difficult and therapy is challenging. We report two children with tuberculous meningitis and hydrocephalus who developed cerebral salt wasting following neurosurgical intervention. The first patient was managed with rigorous salt and water replacement whereas the second patient required the addition of fludrocortisone for control of salt-wasting.

PMID 18695284  Indian Pediatr. 2008 Jul;45(7):598-601.
著者: Akram Askar, Nauman Tarif
雑誌名: Saudi J Kidney Dis Transpl. 2007 Mar;18(1):95-9.
Abstract/Text Hyponatremia secondary to the syndrome of inappropriate anti-diuretic hormone secretion is commonly observed in patients with various neurological disorders. Cerebral salt wasting (CSW), although uncommon, has also been reported to frequently result in hyponatremia. Here, we report a case of CSW in a patient with head trauma without evidence of cerebrovascular injury or brain edema. He was diagnosed on the basis of high fractional excretion of urinary sodium and uric acid along with extremely low serum uric acid. Improvements in serum sodium levels after saline hydration and fludrocortisone administration further supported the diagnosis, even in the presence of normal brain and atrial natriuretic peptide levels.

PMID 17237900  Saudi J Kidney Dis Transpl. 2007 Mar;18(1):95-9.
著者: M J Hannon, L A Behan, M M C O'Brien, W Tormey, S G Ball, M Javadpour, M Javadpur, M Sherlock, C J Thompson
雑誌名: J Clin Endocrinol Metab. 2014 Jan;99(1):291-8. doi: 10.1210/jc.2013-3032. Epub 2013 Dec 20.
Abstract/Text CONTEXT: Hyponatremia is common after acute subarachnoid hemorrhage (SAH) but the etiology is unclear and there is a paucity of prospective data in the field. The cause of hyponatremia is variously attributed to the syndrome of inappropriate antidiuresis (SIAD), acute glucocorticoid insufficiency, and the cerebral salt wasting syndrome (CSWS).
OBJECTIVE: The objective was to prospectively determine the etiology of hyponatremia after SAH using sequential clinical examination and biochemical measurement of plasma cortisol, arginine vasopressin (AVP), and brain natriuretic peptide (BNP).
DESIGN: This was a prospective cohort study.
SETTING: The setting was the National Neurosurgery Centre in a tertiary referral centre in Dublin, Ireland.
PATIENTS: One hundred patients with acute nontraumatic aneurysmal SAH were recruited on presentation.
INTERVENTIONS: Clinical examination and basic biochemical evaluation were performed daily. Plasma cortisol at 0900 hours, AVP, and BNP concentrations were measured on days 1, 2, 3, 4, 6, 8, 10, and 12 following SAH. Those with 0900 hours plasma cortisol<300 nmol/L were empirically treated with iv hydrocortisone.
MAIN OUTCOME MEASURES: Plasma sodium concentration was recorded daily along with a variety of clinical and biochemical criteria. The cause of hyponatremia was determined clinically. Later measurement of plasma AVP and BNP concentrations enabled a firm biochemical diagnosis of the cause of hyponatremia to be made.
RESULTS: Forty-nine of 100 developed hyponatremia<135 mmol/L, including 14/100<130 mmol/L. The cause of hyponatremia, and determined by both clinical examination and biochemical hormone measurement, was SIAD in 36/49 (71.4%), acute glucocorticoid insufficiency in 4/49 (8.2%), incorrect iv fluids in 5/49 (10.2%), and hypovolemia in 5/49 (10.2%). There were no cases of CSWS.
CONCLUSIONS: The most common cause of hyponatremia after acute nontraumatic aneurysmal SAH is SIAD. Acute glucocorticoid insufficiency accounts for a small but significant number of cases. We found no cases of CSWS.

PMID 24248182  J Clin Endocrinol Metab. 2014 Jan;99(1):291-8. doi: 10.・・・
著者: R Boton, M Gaviria, D C Batlle
雑誌名: Am J Kidney Dis. 1987 Nov;10(5):329-45.
Abstract/Text From the analysis of several studies published from 1979 to 1986 comprising 1,172 patients, we estimated that glomerular filtration rate (GFR) was normal in 85% of unselected patients on chronic lithium therapy. The remaining 15% of patients displayed only mild reduction in GFR, clustering at approximately 60 mL/min. Thus, the data available to date do not support earlier concerns that long-term lithium therapy could eventuate into renal insufficiency. The most prevalent renal effect of lithium is impairment of concentrating ability, which we estimated to be present in at least 54% of 1,105 unselected patients on chronic lithium therapy. This defect translated into overt polyuria in only 19% of unselected cases. A renal lesion confined to the collecting tubule has been described in humans who have taken lithium for short periods of time. This lesion may represent the collecting tubule's response to the intracellular accumulation of lithium, which interferes with cAMP formation and results in an early and probably reversible inhibition of antidiuretic hormone (ADH)-mediated water transport. However, long-term lithium therapy may induce a progressive and partly irreversible defect in concentrating ability. The potential risk for dehydration associated with lithium-induced polyuria, as well as the discomfort inherent to this side effect, deserves evaluation and consideration for therapeutic intervention. Amiloride has additional advantages over conventional treatment of nephrogenic diabetes insipidus using thiazide diuretics. The action of amiloride on ADH-mediated water transport seems specific in as much as it is capable of preventing the uptake of lithium in high resistance epithelia and thereby prevents the inhibitory effect of intracellular lithium on water transport. Unlike thiazides, amiloride has a weak natriuretic effect and is less likely to increase plasma lithium levels by causing volume contraction. In addition, amiloride, by conserving potassium, obviates the need for potassium supplementation that is usually required to prevent hypokalemia when thiazides are used to treat lithium-induced polyuria. Since amiloride may prevent chronic intracellular lithium accumulation in the collecting tubule, future studies should elucidate whether amiloride also has a role in preventing lithium-induced chronic tubulo-interstitial damage.

PMID 3314489  Am J Kidney Dis. 1987 Nov;10(5):329-45.
著者: L E Earley, J Orloff
雑誌名: J Clin Invest. 1962 Nov;41(11):1988-97. doi: 10.1172/JCI104657.
Abstract/Text
PMID 16695887  J Clin Invest. 1962 Nov;41(11):1988-97. doi: 10.1172/JC・・・
著者: J K Maesaka, N Miyawaki, T Palaia, S Fishbane, J H C Durham
雑誌名: Kidney Int. 2007 Apr;71(8):822-6. doi: 10.1038/sj.ki.5002093. Epub 2007 Feb 21.
Abstract/Text
PMID 17311074  Kidney Int. 2007 Apr;71(8):822-6. doi: 10.1038/sj.ki.50・・・
著者: J de Leon, C Verghese, J I Tracy, R C Josiassen, G M Simpson
雑誌名: Biol Psychiatry. 1994 Mar 15;35(6):408-19.
Abstract/Text Polydipsia among chronic psychiatric patients is poorly understood and underdiagnosed. It may have three stages: simple polydipsia, polydipsia with water intoxication, and physical complications. Epidemiological surveys have used staff reports and polyuria measures to identify polydipsic patients. Water intoxication has been screened by chart review, weight, or serum sodium data. According to these surveys, polydipsia, not explained by medically induced polyuria, may be present in more than 20% of chronic inpatients. Up to 5% of chronic inpatients had episodes of water intoxication although mild cases may have been missed. Single time point surveys show that 29% of polydipsic patients had presented water intoxication. Methodologically limited clinical studies suggest that polydipsia with water intoxication rather than simple polydipsia may be associated with poor prognosis in schizophrenia. Epidemiological surveys found polydipsia with water intoxication to be associated with chronicity, schizophrenia, smoking, some medications, male gender, and white race. New pathophysiological models need to elucidate these findings.

PMID 8018788  Biol Psychiatry. 1994 Mar 15;35(6):408-19.
著者: Brian Dundas, Melissa Harris, Meera Narasimhan
雑誌名: Curr Psychiatry Rep. 2007 Jun;9(3):236-41.
Abstract/Text Psychogenic polydipsia (PPD), a clinical disorder characterized by polyuria and polydipsia, is a common occurrence in inpatients with psychiatric disorders. The underlying pathophysiology of this syndrome is unclear, and multiple factors have been implicated, including a hypothalamic defect and adverse medication effects. Hyponatremia in PPD can progress to water intoxication and is characterized by symptoms of confusion, lethargy, and psychosis, and seizures or death. Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities.

PMID 17521521  Curr Psychiatry Rep. 2007 Jun;9(3):236-41.

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