{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:45:44Z","timestamp":1786135544834,"version":"build-2736575974"},"reference-count":73,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:p>To reduce lithium\u2013induced nephrogenic diabetes insipidus (lithium-NDI), patients with bipolar disorder are treated with thiazide and amiloride, which are thought to induce antidiuresis by a compensatory increase in prourine uptake in proximal tubules. However, thiazides induced antidiuresis and alkalinized the urine in lithium-NDI mice lacking the sodium-chloride cotransporter, suggesting that inhibition of carbonic anhydrases (CAs) confers the beneficial thiazide effect. Therefore, we tested the effect of the CA\u2013specific blocker acetazolamide in lithium-NDI. In collecting duct (mpkCCD) cells, acetazolamide reduced the cellular lithium content and attenuated lithium-induced downregulation of aquaporin-2 through a mechanism different from that of amiloride. Treatment of lithium-NDI mice with acetazolamide or thiazide\/amiloride induced similar antidiuresis and increased urine osmolality and aquaporin-2 abundance. Thiazide\/amiloride-treated mice showed hyponatremia, hyperkalemia, hypercalcemia, metabolic acidosis, and increased serum lithium concentrations, adverse effects previously observed in patients but not in acetazolamide-treated mice in this study. Furthermore, acetazolamide treatment reduced inulin clearance and cortical expression of sodium\/hydrogen exchanger 3 and attenuated the increased expression of urinary PGE2 observed in lithium-NDI mice. These results show that the antidiuresis with acetazolamide was partially caused by a tubular-glomerular feedback response and reduced GFR. The tubular-glomerular feedback response and\/or direct effect on collecting duct principal or intercalated cells may underlie the reduced urinary PGE2 levels with acetazolamide, thereby contributing to the attenuation of lithium-NDI. In conclusion, CA activity contributes to lithium-NDI development, and acetazolamide attenuates lithium-NDI development in mice similar to thiazide\/amiloride but with fewer adverse effects.<\/jats:p>","DOI":"10.1681\/asn.2015070796","type":"journal-article","created":{"date-parts":[[2015,11,16]],"date-time":"2015-11-16T22:19:10Z","timestamp":1447712350000},"page":"2082-2091","source":"Crossref","is-referenced-by-count":46,"title":["Acetazolamide Attenuates Lithium\u2013Induced Nephrogenic Diabetes Insipidus"],"prefix":"10.1681","volume":"27","author":[{"given":"Theun","family":"de Groot","sequence":"first","affiliation":[{"name":"Physiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne P.","family":"Sinke","sequence":"additional","affiliation":[{"name":"Physiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marleen L.A.","family":"Kortenoeven","sequence":"additional","affiliation":[{"name":"Physiology 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