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Coexistence of Central Diabetes Insipidus and Salt Wasting: the Difficulties in Diagnosis, Changes In EDITORIAL COMMITTEE Tomas Berl, Editor William Henrich Mark Paller Fred Silva Denver, CO Toledo, OH Minneapolis, MN Oklahoma City, OK Nephrology Trainee Program, St. Michael’s Hospital, University of Toronto St. Michael’s Hospital is a major teaching center of the University of Toronto located in downtown Toronto. The nephrology training program at St. Michael’s offers a broad-based clinical experience coupled with the opportunity to work in a variety of basic research and clinical investigation sethngs. The program is designed for individuals who seek to pursue careers in nephrology with a major scholarly component. The patient population includes an excellent mix of general nephrology. One of the major areas of emphasis is the application of basic principles of physiology of acid-base and electrolyte disorders to the bedside. St. Michael’s Hospital also offers in-depth exposure to general nephrology. hemodialysis. continuous ambulatory peritoneal dialysis. and kidney transplantation. with an emphasis on ambulatory care. The outpatient clinics include general nephrology. progressive renal disease (predialysis). and a multidisciplinary diabetic complication clinic. There is a very active renal consultation and teaching service. Trainees are encouraged to spend part of their training time with a staff nephrologist in the area of fluid-electrolyte and acid-base physiology. delivery of hemodialysis care. or clinical kidney transplantation. In addition. there are opportunities to participate in laboratory projects in molecular medicine, acid-base and electrolyte physiology. and transplantation immunology. The clinical experience is complemented by a formal didactic program with structured rounds in clinical nephrology. renal physiology. molecular medicine. renal biopsy rounds. journal club, and a course (1 h/wk) designed to review all of the important areas of nephrology. followed by a weekly citywide nephrology grand rounds. which includes basic science and clinical presentations. with one visiting professor per month, under the auspices of the University of Toronto nephrology training program. Coexistence of Central Diabetes Insipidus and Salt Wasting: The Difficulties in Diagnosis, Changes in Natrem ia , a nd Treatment1 Sheila Laredo, Ken Yuen, Brian Sonnenberg, and Mitchell L. Halperin2 the osmole excretion rate early on revealed the co- S. Laredo. K. Yuen, B. Sonnenberg. ML. Halperin. Renal existence of central Dl and an osmotic diuresis. The Division. Department of Medicine. St. Michael’s Hospi- osmoles excreted were largely Na salts; after antidi- tal. Toronto. Ontario, Canada uretic hormone acted, this electrolyte diuresis caused (J. Am. Soc. Nephrol. 1996; 7:2527-2532) the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was ABSTRACT contracted. The tool to explain the basis for the dys- Both central diabetes insipidus (Dl) and a high rate of natremias was a tonicity balance. Hypernatremia, excretion of sodium (Na) and chloride (Cl) contrib- which developed before treatment of central Dl, was uted to the development of polyuria and dysnatre- primarily a result of a positive balance for Na rather mia in two patients during the acute postoperative than a large negative balance for water. Moreover, period after neurosurgery. To minimize difficulties in hyponatremia that developed once antidiuretic hor- diagnosis and projections for therapy, two available mone acted was primarily a result of a negative (but not often used) clinical tools were helpful. First, balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further 1 Received September 27, 1995. Accepted April 10, 1996. 2 Correspondence to Dr. ML. Halperin, St. Michael’s Hospital, 38 Shuter Street, decline in the plasma Na concentration, either the Na Toronto, Ontario M5B 1A6, Canada. concentration in the urine should be decreased by 1046.6673/07 12.2527$03.OO/O provision of urea or a loop diuretic while replacing all Journal of the American Society of Nephrology Copyright © 1996 by the American Society of Nephrology unwanted water and electrolyte losses; alternatively, Journal of the American Society of Nephrology 2527 Salt- and Water-Wasting the fluid infused should have a similar Na concentra- anterior communicating artery as well as smaller tion and volume as the urine (infuse hypertonic sa- aneurysms in the right posterior communicating and line). left ophthalmic arteries were identified on computed tomography scan. Her subarachnoid hemorrhage ex- Key Words: Cerebral salt wasting. hypernatremia. hyponatre- tended into the interhemispheric region around the mia, natriuretic factors. sodium lamina terminalis and into the carotid cisterns bilat- eralby. D erangements in the plasma sodium (Na) concen- Preoperatively, she was given dibantin (800 mg) and tration are commonly observed after surgery. Decadron (Dexamethasone; Merck-Sharpe & Dohme, especially with procedures that involve the pituitary Pointe Claire, Dorvab, Quebec, Canada; 4 mg). The gland (reviewed in Reference 1 ). Our purpose in this bleeding aneurysm was clipped, the procedure was article is to provide a rationale to understand the basis thought to be without complication. and an unevent- for these dysnatremias and the expected change in ful recovery was anticipated. During surgery, she urine composition once antidiuretic hormone (ADH) is received mannitol (50 g). Decadron ( 1 0 mg), and 3 L of given. The analysis will be to focus initially on two Ringer’s lactate. In the subsequent 10 h. balance Issues. First, by examining the urine osmolality. cal- studies were carried out. During that time, her plasma culating the osmole excretion rate, and comparing it Na concentration rose from 136 to 155 mM. She to usual values (approximately 0.5 mosmol/min), one received a total of 839 mmol of NaC1 in a volume of 7.3 can determine why the urine flow rate is high. In this L. Polyuria was evident in that her urine output was regard, it is Important to know that there is usually 7.4 L (average flow rate of 12.3 mL/min) (Figure 1). little diurnal variation in the rate of excretion of urea, Because of the very high urine flow rate, low urine the principal urine osmole (2). Second, to determine osmolality (120 mosmob/kg H20, (Na) 37 mM, (K) 13 the basis for dysnatremia and to define therapy, ex- mM), and the development of hypernatremia, a diag- ternal balances for water and solutes that affect water nosis of central DI was made. This diagnosis was movement across cell membranes were calculated. confirmed when deamino-8-D-arginine vasopressin The sobutes in the body and the urine that affect water (DDAVP. Desmopressin; Ferring, North York, Ontario, distribution across the extracellular fluid (ECF):intra- Canada; 4 j.Lg) was administered and caused a prompt cellular fluid (ICF) interface are Na and potassium (K) rise in urine osmolality from 120 to 379 mosmol/kg salts (3). We shall call this a “tonicity balance.” Be- H20, together with a fall in urine flow rate (but to only cause urea readily crosses cell membranes, as well as 8 mL/min). Over the next several hours, more DDAVP inner medullary collecting duct (IMCD) membranes was given because of the false impression that there when ADH acts (reviewed in Reference 4), urea should was resistance to its actions (high urine flow rate). not affect water movement across these membranes It is important to recognize that the total urine and it is not included in the tonicity balance. volume of 7.4 L represents the excretion of 2.5 L of The presence of a high rate of Na excretion after isotonic saline and 5 L of electrolyte-free water; this neurosurgery is a common observation (reviewed in Reference 5). If both central diabetes insipidus (DI) and a high rate of excretion of NaC1 occur simubta- 10 hr before DDAVP 24 hr after DDAVP: neousby, this can have a profound effect on the plasma Na concentration as webb as on the urine flow rate and Water: 7.3 1 Water. 13.5 1 composition. In this setting, it is more difficult to Na+K: 839 mmol Na + K: 3165 mmol interpret the urinary findings. The focus of this pre- sentation is two patients who presented with dys- natremia, pobyuria. and an acute fall in ECF volume [Na] after a recent neurosurgicab procedure. Both patients had central DI at a time when they also had a barge natriuresis. Possible explanations for these findings Water: 7.4 L Water: 14.28 1 and a strategy for treatment will be presented. Na + K: 370 mmol Na + K: 2042 mmol Osmolality: 120 mosm/L Osmolality: 379 mosm/1 Balance Na + K: + 469 mmol Balance Na + K: . 877 mmol CASES Figure 1 . Tonicity balance in Patient 1 . A tonicity balance was Patient 1 calculated in the 10 h before treatment of central DI with DDAVP. The osmole excretion rate was close to 1.5 mosmol! A 42-yr-old previously healthy female (weight, 52 kg mm. The reason the plasma (Na) rose from 136 to 155 mM I 1 14 bbl) had developed a headache that had increased was a positive balance for Na + K of 469 mmol because in severity over 3 days. Nausea and vomiting began water balance was close to neutral. Balance data are just prior to her arrival in the hospital. She was provided for the 24-h period after DDAVP was given, in which somewhat drowsy. yet was easily awakened through- the plasma Na fell from 155 to 123 mM. The fall in plasma out the period before neurosurgery. The physical ex- (Na) was almost exclusively the result of negative balance amination, including the neurological portion, did not for Na (K input was 115 mmol and K loss was 172 mmol), identify a specific local lesion. An aneurysm in the again because water balance was close to neutral. 2528 Volume 7 ‘ Number 12 . 1996 Laredo et aI excretion occurred at a time when much less electro- cabby to 3 to 4 mosmob/min and the urine volume lyte-free water was administered (Figure 1 ).
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