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Tolvaptan, sold under the brand name Samsca among others, is an aquaretic drug that functions as a selective, competitive vasopressin receptor 2 (V 2) antagonist used to treat hyponatremia (low blood sodium levels) associated with congestive heart failure, cirrhosis, and the syndrome of inappropriate antidiuretic hormone (SIADH).
Tolvaptan phosphate is a drug used for the treatment of cardiac edema. It is a prodrug of tolvaptan , [ 1 ] [ 2 ] formulated as the salt tolvaptan sodium phosphate, for intravenous administration .
In 2014, Japan was the first country in the world to approve a pharmacological treatment for ADPKD [33] followed by Canada and Europe, which approved the drug tolvaptan for ADPKD patients in the beginning of 2015. The USA FDA approved the use of tolvaptan in the treatment of ADPKD in 2018. [41]
Clinical studies in patients with X-linked NDI showed that the selective V 1 R antagonist relcovaptan (SR49059, Sanofi-Aventis) significantly increased urine osmolality and decreased 24-hour urine flow. [9] Thus V 1 R and/or V 2 R antagonists may serve as molecular chaperones to mitigate misfolding defects in selected patients with type 2 NDI. [9]
Vasopressin receptor antagonists that are selective for the V2 receptor include: . Tolvaptan (FDA-approved); Lixivaptan; Mozavaptan; Satavaptan; Their main uses are in hyponatremia, such as that caused by syndrome of inappropriate antidiuretic hormone (SIADH) and heart failure, however these agents should be avoided in patients with cirrhosis.
However, tolvaptan therapy is associated with potentially life-threatening liver toxicity in patients with ADPKD. [10] Because of the risk of liver toxicity, in the US, tolvaptan is only available for ADPKD under a restricted distribution program (a Risk Evaluation and Mitigation Strategies (REMS program).
In a recent long-term study, patients using Tolvaptan had a 6.4% higher kidney function after 5 years compared to standard of care. [25] In 2019, a team of researchers at UCSB found that a ketogenic diet might be able to halt, or even reverse progression in mice, [26] and the results of a first human case series study are showing potential ...
Almost a century after the pioneering work of Claude Bernard (1813–1878) in animals, Peters et al, in 1950, reported three patients seen at Yale New Haven Hospital with hyponatremia associated with varying cerebral pathologies and severe dehydration. In each patient, urine sodium losses persisted despite hyponatremia and a high-salt diet.
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