Chapter 046. Sodium and Water (Part 10)

Figure 46-2Many causes of hypernatremia are associated with polyuria and a submaximal urine osmolality. The product of the urine volume and osmolality, i.e., the solute excretion rate, is helpful in determining the basis of the polyuria (see above). To maintain a steady state, total solute excretion must equal solute production. As stated above, individuals eating a normal diet generate ~600 mosmol/d. Therefore, daily solute excretion in excess of 750 mosmol defines an osmotic diuresis.
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Chapter 046. Sodium and Water (Part 10) Chapter 046. Sodium and Water (Part 10)Figure 46-2 Many causes of hypernatremia are associated with polyuria and asubmaximal urine osmolality. The product of the urine volume and osmolality,i.e., the solute excretion rate, is helpful in determining the basis of the polyuria(see above). To maintain a steady state, total solute excretion must equal soluteproduction. As stated above, individuals eating a normal diet generate ~600mosmol/d. Therefore, daily solute excretion in excess of 750 mosmol defines anosmotic diuresis. This can be confirmed by measuring the urine glucose and urea.In general, both CDI and NDI present with polyuria and hypotonic urine (urineosmolality The therapeutic goals are to stop ongoing water loss by treating theunderlying cause and to correct the water deficit. The ECF volume should berestored in hypovolemic patients. The quantity of water required to correct thedeficit can be calculated from the following equation: In hypernatremia due to water loss, total body water is approximately 50and 40% of lean body weight in men and women, respectively. For example, a 50-kg woman with a plasma Na+ concentration of 160 mmol/L has an estimated free-water deficit of 2.9 L {[(160 – 140) ÷ 140] x (0.4 x 50)}. As in hyponatremia,rapid correction of hypernatremia is potentially dangerous. In this case, a suddendecrease in osmolality could potentially cause a rapid shift of water into cells thathave undergone osmotic adaptation. This would result in swollen brain cells andincrease the risk of seizures or permanent neurologic damage. Therefore, the waterdeficit should be corrected slowly over at least 48–72 h. When calculating the rateof water replacement, ongoing losses should be taken into account, and the plasmaNa+ concentration should be lowered by 0.5 mmol/L per h and by no more than 12mmol/L over the first 24 h. The safest route of administration of water is by mouth or via a nasogastrictube (or other feeding tube). Alternatively, 5% dextrose in water or half-isotonicsaline can be given intravenously. The appropriate treatment of CDI consists ofadministering desmopressin intranasally (Chap. 334). Other options for decreasingurine output include a low-salt diet in combination with low-dose thiazide diuretictherapy. In some patients with partial CDI, drugs that either stimulate AVP secretionor enhance its action on the kidney have been useful. These includechlorpropamide, clofibrate, carbamazepine, and nonsteroidal anti-inflammatorydrugs (NSAIDs). The concentrating defect in NDI may be reversible by treating theunderlying disorder or eliminating the offending drug. Symptomatic polyuria dueto NDI can be treated with a low-Na+ diet and thiazide diuretics, as describedabove. This induces mild volume depletion, which leads to enhanced proximalreabsorption of salt and water and decreased delivery to the site of action of AVP,the collecting duct. By impairing renal prostaglandin synthesis, NSAIDs potentiate AVP actionand thereby increase urine osmolality and decrease urine volume. Amiloride maybe useful in patients with NDI who need to be on lithium. The nephrotoxicity oflithium requires the drug to be taken up into collecting duct cells via the amiloride-sensitive Na+ channel.