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Use of Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus: a Case Report

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Use of Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus: a Case Report ID: 17-0154 10.1530/EDM-17-0154 R A Macau, T N da Silva and Acetazolamide in lithium ID: 17-0154; February 2018 others nephrogenic DI DOI: 10.1530/EDM-17-0154 Use of acetazolamide in lithium-induced nephrogenic diabetes insipidus: a case report Ricardo A Macau1,*, Tiago Nunes da Silva2,*, Joana Rego Silva1, Ana Gonçalves Ferreira2 and Pedro Bravo1 Correspondence should be addressed 1Nephrology Department, Hospital Garcia de Orta and 2Endocrinology Department, Hospital Garcia de Orta, to R A Macau or T N da Silva Almada, Portugal Email ricardoandremacau@gmail. com or tiago_fcml@yahoo. *(R A Macau and T N da Silva contributed equally to this work) com Summary Lithium-induced nephrogenic diabetes insipidus (Li-NDI) is a rare and difficult-to-treat condition. A study in mice and two recent papers describe the use of acetazolamide in Li-NDI in 7 patients (a case report and a 6 patient series). We describe the case of a 63-year-old woman with bipolar disorder treated with lithium and no previous history of diabetes insipidus. She was hospitalized due to a bowel obstruction and developed severe dehydration after surgery when she was water deprived. After desmopressin administration and unsuccessful thiazide and amiloride treatment, acetazolamide was administrated to control polyuria and hydroelectrolytic disorders without significant side effects. To our knowledge, this is the third publication on acetazolamide use in Li-NDI patients. Learning points: • Treatment of lithium-induced nephrogenic diabetes insipidus might be challenging. • Vasopressin, amiloride and thiazide diuretics have been used in lithium-induced nephrogenic diabetes insipidus treatment. • Acetazolamide might be an option to treat lithium-induced nephrogenic diabetes insipidus patients who fail to respond to standard treatment. • The use of acetazolamide in lithium-induced nephrogenic diabetes insipidus must be monitored, including its effects on glomerular filtration rate. Background Diabetes insipidus (DI) is a rare condition in which therapy. The latter is the most common form of NDI, patients excrete large quantities of diluted urine (up and is known as lithium-induced NDI (Li-NDI) (1, 2, 3, to 1 litre per hour in the most severe cases), leading to 4, 5, 6, 7). Lithium enters cells through several (sodium) dehydration in the absence of adequate water intake. It transporters, but there is limited transportation out of cells, can be either central (resulting from failure to synthesize resulting in intracellular accumulation. Some controversy or secrete vasopressin from the hypothalamus or posterior exists regarding the pathogenicity of intracellular lithium pituitary) or nephrogenic (resulting from kidney inability damage (8). One model proposes that intracellular lithium to respond to vasopressin). Nephrogenic diabetes insipidus inhibits adenylyl cyclase in the collecting duct, disrupting (NDI) can result from genetic causes, such as mutations the activation of vasopressin-sensitive transport proteins, in the V2-vasopressin receptor (V2R) or the aquaporin-2 thus resulting in polyuria and NDI (9). In addition, (AQP2) water channel, or acquired causes, such as lithium chronic lithium therapy decreases both AQP2 and urea This work is licensed under a Creative Commons © 2018 The authors http://www.edmcasereports.com Attribution-NonCommercial-NoDerivs 3.0 Published by Bioscientifica Ltd Unported License. Downloaded from Bioscientifica.com at 09/25/2021 05:05:26AM via free access PROOF ONLY R A Macau, T N da Silva and Acetazolamide in lithium ID: 17-0154; February 2018 others nephrogenic DI DOI: 10.1530/EDM-17-0154 transporter-A1 protein expression, further contributing to not increased urine osmolality or decreased urine output NDI (10). However, lithium-induced downregulation of significantly. In mice, acetazolamide partially reversed AQP2 and development of NDI may occur independently lithium-induced polyuria and increased urine osmolality. of adenylyl cyclase activity (11). The decrease in urine output in mice was associated to a The management of Li-NDI is challenging, even after decreased glomerular filtration rate (GFR), which warrants lithium discontinuation. Thiazide diuretics, amiloride against acetazolamide application in first line without and reduced sodium intake have been used as standard further studies (18). therapy. Thiazide diuretics block the sodium–chloride Case presentation cotransporter (NCC) in the distal convoluted tubule and thus exaggerate the hypovolemia and increase an already A 63-year-old woman with bipolar disorder on long-term activated renin–angiotensin–aldosterone system (RAAS) lithium therapy (400 mg/tid for 8 years) and no other further. This mechanism stimulates proximal tubule relevant medical history was admitted to the emergency sodium and water reabsorption resulting in less volume room with diffuse abdominal pain and constipation for delivery to the distal nephron (1, 2, 3, 12, 13, 14). Other ten days. She had polydipsia (water intake estimated of data suggested that thiazides' beneficial effect in lithium- 5 litre per day) and polyuria for years that had not been induced NDI may derive from inhibition of CA, both investigated. On admission, her clinical examination by direct vascular effects (15) and also anti-diuresis and revealed abdominal distension. Laboratory values alkalinization of urine in Li-NDI mice lacking NCC (14). showed: mild anaemia (haemoglobin: 114 g/L; reference Amiloride inhibits lithium entry into renal collecting duct range (RR): 115-180 g/dL), mild renal insufficiency cells through the epithelial sodium channel (ENaC) (1, 8, (creatinine: 1.3 mg/dL;RR: 0.5- 0.9 mg/dL) and a normal 10, 12). Non-steroidal anti-inflammatory drugs have been sodium of 140 mmol/L (RR: 135–145). Abdominal CT used but they are nephrotoxic (1, 2, 3, 5, 8, 12). showed a stenotic lesion in the cecum and ascending In an animal model of Li-NDI, acetazolamide (a CA) colon, a probable metastatic lesion in the liver and was as effective as the combination of hydrochlorothiazide bowel distention. An urgent right hemicolectomy plus and amiloride in reducing polyuria and increasing urine metastectomy and ileostomy were performed, and osmolality and AQP2 abundance. Acetazolamide also the patient was admitted to the surgical ward. Over showed fewer side effects. In particular, the thiazide/ the next two days, her mental status progressively amiloride-treated mice developed hyponatraemia, worsened, alongside increasing polyuria (from 650 to hyperkalaemia, hypercalcaemia, metabolic acidosis and 2800 to 3620 mL/day), increasing natremia (140 up to increased serum lithium concentrations, and these side 171 and then up to 181 mmol/L) and increasing serum effects were not observed in the acetazolamide-treated osmolality (up to 379 mosmol/kg; RR: 275–295). Urinary mice. Groot and coworkers concluded that the reduction osmolality achieved a maximum value of 303 mosmol/ in polyuria after acetazolamide treatment was partially Kg (RR: 300–900). Lithium concentration was in the caused by a tubular-glomerular feedback response and supra-therapeutic range (1.46 mmol/L; RR: 0.6–1.2) reduced glomerular filtration rate (GFR), which also and was stopped. She was diagnosed with Li-NDI and contributed to the reduction in urinary prostaglandin E2 transferred to the intensive care unit (ICU) where she levels and to the amelioration of the Li-NDI (16). was ventilated for airway protection due to impaired Supported by this model, Gordon and coworkers consciousness. Standard therapy with 5% IV dextrose, recently reported the first case of acetazolamide hydrochlorothiazide 50 plus amiloride 5 mg and treatment to a 49-year-old patient with severe Li-NDI desmopressin 2 mg IV bid was initiated. No significant (after elective surgery and water depriving), resistant reduction in the urine output was observed after each to hydrochlorothiazide treatment and other measures. desmopressin treatment and on day 8 after surgery, Following treatment with acetazolamide, daily urine the patient maintained polyuria (4200 mL/day) and output decreased, urinary osmolality increased and hypernatraemia (154 mmol/L, Fig. 1). of serum sodium levels normalized. No major adverse effects were observed (17). Groot and coworkers recently Treatment published a series of mice and 6 human patients with Li-NDI. Two patients withdrew from the study due to Following the publication of a recent report of successful side effects. In the remaining patients, acetazolamide did Li-ND treatment with acetazolamide (15), the drug was http://www.edmcasereports.com 2 Downloaded from Bioscientifica.com at 09/25/2021 05:05:26AM via free access R A Macau, T N da Silva and Acetazolamide in lithium ID: 17-0154; February 2018 others nephrogenic DI DOI: 10.1530/EDM-17-0154 Figure 1 Daily urinary output during the admission. Surgery was performed on May 25th (*), acetazolamide was started on June 6th (**), stopped on Figure 2 June 9th along with the other diuretics (***), restarted in monotherapy Creatinine as a marker of GFR during hospitalization. Surgery was on June 11th (**), stopped again on June 27th (***) and restarted again performed on May 25th (*), acetazolamide was started on June 6th (**), on July 4th (**). stopped on June 9th along with the other diuretics (***), restarted in monotherapy on June 11th (**), stopped again on June 27th (***) and started at 500 mg b.I.d. A progressive reduction of the restarted again on July 4th (**). The patient was discharged on the 7th of urinary output was observed
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