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Arginine vasopressin resistance (AVP-R, formerly called nephrogenic diabetes insipidus) is uncommon disease entity which accounts for about 2% of hypotonic polyuria and characterized by the inability of the kidneys to respond to vasopressin. Acquired AVP-R includes drug-induced AVP-R, and typical causative drugs are lithium, demeclocycline, amphotericin B, and rifampicin.
We report a rare case of fluconazole drug-induced AVP-R.
A 52-year-old woman with type I diabetes was admitted to our hospital because of impaired consciousness. The patient had been in her usual state of health until 2 days before the admission, and her diabetic medications included dapagliflozin, insulin, and metformin. Examinations have revealed diabetic ketoacidosis (DKA), multiple cerebral atherosclerotic infarctions, and intrapelvic infection of unknown etiology. DKA was rapidly treated with continuous hydration, insulin, and electrolytes corrections. Acute brain infarction treatments have failed to reverse the impaired consciousness and the patient became under continuous intravenous hyperalimentation (IVH) management and insulin treatment. Broad spectrum antibiotics, meropenem and daptomycin, were introduced and continued to control the infection. Obesity of body-mass index 35.0, the underlying diabetes, malnutrition, and long-term antibiotic usage led to the development of Candida Albicans invasive infection including dermatitis, endophthalmitis, and bloodstream infection. Initially, micafungin 150 mg q12hr was introduced and then stopped due to liver dysfunction. Fluconazole (FCZ) 400 mg q24hr followed to manage systemic C. Albicans infection. The urine volume which had been stable around 1,500 mL per day gradually increased, and on day 4 after FCZ initiation, polyuria and hypernatremia developed. Urine volume measured up to 3,500 mL per day without any change of hydration composition; The urine specific gravity became less than 1.005 and the serum sodium elevated to 158 mmol/L. The water-deprivation test was impossible to be performed due to her consciousness level. Desmopressin administration did not increase urine osmolality or reduce urine volume, which demonstrated renal unresponsiveness. The level of plasma antidiuretic hormone was detectable, 1.9 pg/mL, which excluded central AVP-deficiency. FCZ cessation rapidly recovered the urinary concentrating ability. The diagnosis was AVP-R caused by FCZ.
Drug induced AVP-R varies in its pathologic mechanistic; Whereas lithium is known to disrupt aquaporin-2 water channel function in the collecting ducts, amphotericin B is reported to decrease aquapotin-2 protein expression. FCZ has been rarely reported to cause AVP-R, and its mechanistic is unclear. Careful continuous observation of urinary concentration and serum sodium level are important to quickly diagnose and treat drug-induced AVP-R.
