Describe the treatment principle of DI.
Treat the underlying condition, ensure sufficient fluid intake, and initiate a low-sodium, low-protein diet.
How is the central DI treated?
Desmopressin: synthetic vasopressin without vasoconstrictive effects
Administration: intranasal (preferred), subcutaneous, or oral
Important side effect: hyponatremia
Alternative medication: chlorpropamide
How is the nephrogenic DI treated?
Discontinuation of the causative agent (e.g., lithium, demeclocycline) in medication-induced NDI
Thiazide diuretics
NSAIDs (e.g., indomethacin)
Amiloride
Indicated in patients with lithium-induced NDI
Amiloride blocks lithium entry through the sodium channel.
Why is desmopressin used instead of vasopressin?
Vasopressin is generally not used therapeutically because its half-life is too short compared to desmopressin and terlipressin. In contrast to terlipressin (which is used in patients with esophageal varices), desmopressin has no effect on the vascular wall and does not cause vasoconstriction.
What is the effect of chlorpropamide?
Increases ADH secretion and strengthens the effect of ADH
What is the rationale behind the use of thiazide diuretics?
Thiazide diuretics lead to sodium depletion, which causes sodium and water reabsorption in the proximal tubules. As a result, less water reaches the ADH-sensitive distal collecting tubules and volume of urine decreases.
What is the rationale behind the use of NSAIDs?
While NSAIDs may be contraindicated in renal disease due to their potentially nephrotoxic effects, experimental studies have shown that NSAIDs can increase the integration of aquaporin 2 water channels into the collective ducts and Na-K-2Cl cotransporter type 2 (NKCC2) in the thick ascending limb, reducing diuresis. Nevertheless, NSAID treatment in patients with renal disease must be carefully considered.
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