Acetazolamide Attenuates Lithium–Induced Nephrogenic Diabetes Insipidus

Groot, Theun de; Sinke, Anne P.; Kortenoeven, Marleen L. A.; Alsady, Mohammad; Baumgarten, Ruben; Devuyst, Olivier; Loffing, Johannes; Wetzels, Jack F.M.; Deen, Peter M.T.

doi:10.1681/asn.2015070796

Cited by 44 publications

(29 citation statements)

References 72 publications

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“…These side effects were not observed in the acetazolamide-treated mice with lithium-induced NDI. de Groot et al 3 also found that acetazolamide treatment of mice with lithium-induced NDI reduces inulin clearance, reduces the cortical expression of the sodium/hydrogen exchanger 3, and reduces the increase in urinary prostaglandin E 2 observed in mice with lithium-induced NDI.…”

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confidence: 93%

“…de Groot et al 3 found that, in mice with lithium-induced NDI, treatment with either acetazolamide or thiazide/amiloride resulted in a similar reduction of polyuria, increase in urine osmolality, and increase in AQP2 protein abundance. However, the side effects of the two treatment regimens were different.…”

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confidence: 98%

“…Thus, Mamenko et al 2 identified a novel genetic mutation and a novel physiologic mechanism for NDI through SOCE and STIM1 and elucidated an important role for Ca 21 signaling in the urinary concentrating mechanism. 2 The paper in JASN by de Groot et al 3 addressed a different aspect of NDI: a new therapeutic approach to lithiuminduced NDI. Lithium is used to treat manic depressive illness (reviewed in ref.…”

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confidence: 99%

“…de Groot et al 3 tested this hypothesis directly in lithiumtreated mice by comparing acetazolamide with thiazide/ amiloride therapy. de Groot et al 3 found that, in mice with lithium-induced NDI, treatment with either acetazolamide or thiazide/amiloride resulted in a similar reduction of polyuria, increase in urine osmolality, and increase in AQP2 protein abundance.…”

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Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus

Sands

2015

JASN

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showed that the SHR-A3 rat has a novel truncating mutation in the gene encoding stromal interaction molecule 1 (STIM1), which is the endoplasmic reticulum Ca 21 sensor that triggers SOCE. Mamenko et al. 2 used whole-genome sequencing to uncover this novel mutation in the STIM1 gene. Mamenko et al. 2 made this discovery using a clever approach: they crossed SHR-A3 rats with a very closely related rat, the SHR-B2. The SHR-B2 rat shares 87% of its genome with the SHR-A3 rat but lacks the STIM1 mutation present in the SHR-A3 rat. Mamenko et al. 2 found a significant relationship between the inheritance of the STIM1 SHR-A3 mutant allele and the production of dilute urine.In addition to finding the mutation, Mamenko et al. 2 performed physiologic studies to show that the STIM1 mutation present in SHR-A3 rats resulted in increased urine volume, polydipsia, hypertonic plasma, and impaired urinary concentrating ability accompanied by elevated vasopressin levels (i.e., NDI). Mamenko et al. 2 used split-open collecting ducts from SHR-A3 rats and found decreased basal intracellular Ca 21 levels and a major defect in SOCE, which results in a failure of vasopressin to induce a sustained intracellular Ca 21 mobilization in SHR-A3 rat collecting ducts. This led to a reduction in AQP2 protein abundance and an increase in the intracellular retention of AQP2, thereby resulting in less AQP2 in the apical plasma membrane where it is needed to reabsorb water in collecting ducts from SHR-A3 rats. Mamenko et al. 2 used cultured cells to show that STIM1 knockdown reduces SOCE and basal intracellular Ca 21 levels and prevents vasopressinmediated translocation of AQP2 to the plasma membrane. Thus, Mamenko et al. 2 identified a novel genetic mutation and a novel physiologic mechanism for NDI through SOCE and STIM1 and elucidated an important role for Ca 21 signaling in the urinary concentrating mechanism. 2 The paper in JASN by de Groot et al. 3 addressed a different aspect of NDI: a new therapeutic approach to lithiuminduced NDI. Lithium is used to treat manic depressive illness (reviewed in ref. 4). Lithium enters cells by substituting for sodium on several transport proteins that normally transport sodium. However, the pathways for transporting lithium out of cells are more limited, resulting in intracellular lithium accumulation. Lithium inhibits adenylyl cyclase in the collecting duct. Vasopressin, through the V 2 R, activates adenylyl cyclase, stimulates cAMP production, and activates protein kinase A, which in turn, phosphorylates both AQP2 and the urea transporter-A1 and increases their apical plasma membrane accumulation (reviewed in ref. 5). Thus, by inhibiting the adenylyl cyclase-cAMP-protein kinase A signal transduction pathway, lithium disrupts the activation of vasopressinsensitive transport proteins in the collecting duct, which results in polyuria and NDI. In addition, chronic lithium therapy decreases both AQP2 and urea transporter-A1 protein abundance, further contributing to NDI. 6,7 Conventional therapy for lithium-ind...

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Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus

Sands

2015

JASN

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“…2 Acetazolamide monotherapy was as effective as the combination of hydrochlorothiazide and amiloride in reducing polyuria in an animal model of lithium-induced nephrogenic diabetes insipidus but had fewer side effects. 3 Acetazolamide reduces the glomerular filtration rate by means of tubuloglomerular feedback and reduces renal prostaglandin secretion; both effects attenuate polyuria induced by nephrogenic diabetes insipidus.…”

Section: Acetazolamide In Lithium-induced Nephrogenic Diabetes Insipidusmentioning

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Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus

Gordon¹,

Vantzelfde²,

Francis³

2016

N Engl J Med

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Folic acid‐induced animal model of kidney disease

2021

Anim Models and Exp Med

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Kidney disease may be generally classified clinically into two categories: acute kidney injury (AKI) and chronic kidney disease (CKD), both of which are tightly interconnected. 1-3 AKI can often develop in clinical settings in critically ill patients, leading to increased morbidity and mortality. 4,5 AKI is manifested by a rapid decline in the glomerular filtration rates (GFRs) 6 and its pathogenesis is complex, involving ischemia, sepsis, drug toxicity, and trauma. 7 If left unmanaged, AKI can develop into CKD, which is characterized by a progressive decrease in GFR, culminating in a gradual loss of renal function. 8 The transition from AKI to CKD can also be hastened by numerous risk factors such as obesity, hypertension, diabetes, and chronic inflammation. 9-11 Currently, there are no effective treatments for either AKI or CKD, stressing a continual need to elucidate the underlying pathological mechanisms of AKI and CKD. In this regard, animal models of kidney disease have been invaluable in that utilization of these animal models not only facilitates our understanding of the

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Acetazolamide Attenuates Lithium–Induced Nephrogenic Diabetes Insipidus

Cited by 44 publications

References 72 publications

Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus

Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus

Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus

Folic acid‐induced animal model of kidney disease

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