Novel Vasopressin V1A and V2 Antagonist (Conivaptan) Increases Serum Sodium Concentration and Effective Water Clearance in Patients with Hyponatremia

2004 ◽  
Vol 10 (4) ◽  
pp. S27 ◽  
Author(s):  
Joseph G. Verbalis ◽  
Joseph G. Bisaha ◽  
Neila Smith
2020 ◽  
pp. 4729-4747
Author(s):  
Michael L. Moritz ◽  
Juan Carlos Ayus

Water intake and the excretion of water are tightly regulated processes that are able to maintain a near-constant serum osmolality. Sodium disorders (dysnatraemias—hyponatraemia or hypernatraemia) are almost always due to an imbalance between water intake and water excretion. Understanding the aetiology of sodium disorders depends on understanding the concept of electrolyte-free water clearance—this is a conceptual amount of water that represents the volume that would need to be subtracted (if electrolyte-free water clearance is positive) or added (if negative) to the measured urinary volume to make the electrolytes contained within the urine have the same tonicity as the plasma electrolytes. It is the concentration of the electrolytes in the urine, not the osmolality of the urine, which ultimately determines the net excretion of water. Hyponatraemia (serum sodium concentration <135 mmol/litre) is a common electrolyte disorder. It is almost invariably due to impaired water excretion, often in states where antidiuretic hormone release is (1) a normal response to a physiological stimulus such as pain, nausea, volume depletion, postoperative state, or congestive heart failure; or (2) a pathophysiological response as occurs with thiazide diuretics, other types of medications, or in the syndrome of inappropriate diuresis; with both often exacerbated in hospital by (3) inappropriate iatrogenic administration of hypotonic fluids. Hypernatraemia (serum sodium concentration >145 mmol/litre) is a common electrolyte disorder that occurs when water intake is inadequate to keep up with water losses. Since the thirst mechanism is such a powerful stimulus, hypernatraemia almost invariably occurs in the context of an illness and care that restricts the patient’s access to water. This chapter discusses the clinical features, management, and prevention of hyponatraemia and hypernatraemia.


2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.


1980 ◽  
Vol 8 (3) ◽  
pp. 349-352 ◽  
Author(s):  
Luen Bik To ◽  
P. J. Phillips

Eighteen patients with hyperosmolar non-ketotic diabetic coma were studied retrospectively to identify factors affecting prognosis and to review treatment. This condition affected older women two-thirds of whom were unrecognised diabetics. Eight (44%) died. Mortality correlated with age above 60, uraemia and hyperosmolarity, but not with the degree or rate of fall of hyperglycaemia. Hyperglycaemia responded to rehydration and insulin, but in all patients serum osmolarity remained high for several days. In 14 patients (78%) the serum sodium concentration initially increased and in four (22 %) serum osmolarity increased. This persistence or worsening of the hyperosmolar state can be avoided without the risk of cerebal oedema by replacing the fluid and electrolyte deficits over 48 hours and using 5% dextrose for the water deficit.


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