scholarly journals The role of amiloride in managing patients with lithium-induced nephrogenic diabetes insipidus

2016 ◽  
Vol 47 (5) ◽  
pp. 389-392 ◽  
Author(s):  
Misha Lodin ◽  
James Dwyer
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus

scholarly journals Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus

JCI Insight ◽  
2017 ◽  
Vol 2 (7) ◽  
Author(s):  
Søren Brandt Poulsen ◽  
Tina Bøgelund Kristensen ◽  
Heddwen L. Brooks ◽  
Donald E. Kohan ◽  
Timo Rieg ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Adenylyl Cyclase ◽  
Nephrogenic Diabetes Insipidus

scholarly journals Physiology and Pathophysiology of Renal Aquaporins

1999 ◽  
Vol 10 (3) ◽  
pp. 647-663
Author(s):  
SØREN NIELSEN ◽  
TAE-HWAN KWON ◽  
BIRGITTE MØNSTER CHRISTENSEN ◽  
DOMINIQUE PROMENEUR ◽  
JØRGEN FRØKIÆR ◽  
...  
Keyword(s):  
Water Balance ◽  
Diabetes Insipidus ◽  
Proximal Tubule ◽  
Nephrogenic Diabetes Insipidus ◽  
Collecting Duct ◽  
Water Channels ◽  
Apical Plasma Membrane ◽  
Water Reabsorption ◽  
Balance Disorders

Abstract. The discovery of aquaporin membrane water channels by Agre and coworkers answered a long-standing biophysical question of how water specifically crosses biologic membranes, and provided insight, at the molecular level, into the fundamental physiology of water balance and the pathophysiology of water balance disorders. Of nine aquaporin isoforms, at least six are known to be present in the kidney at distinct sites along the nephron and collecting duct. Aquaporin-1 (AQP1) is extremely abundant in the proximal tubule and descending thin limb, where it appears to provide the chief route for proximal nephron water reabsorption. AQP2 is abundant in the collecting duct principal cells and is the chief target for vasopressin to regulate collecting duct water reabsorption. Acute regulation involves vasopressin-regulated trafficking of AQP2 between an intracellular reservoir and the apical plasma membrane. In addition, AQP2 is involved in chronic/adaptational regulation of body water balance achieved through regulation of AQP2 expression. Importantly, multiple studies have now identified a critical role of AQP2 in several inherited and acquired water balance disorders. This concerns inherited forms of nephrogenic diabetes insipidus and several, much more common acquired types of nephrogenic diabetes insipidus where AQP2 expression and/or targeting are affected. Conversely, AQP2 expression and targeting appear to be increased in some conditions with water retention such as pregnancy and congestive heart failure. AQP3 and AQP4 are basolateral water channels located in the kidney collecting duct, and AQP6 and AQP7 appear to be expressed at lower abundance at several sites including the proximal tubule. This review focuses mainly on the role of AQP2 in water balance regulation and in the pathophysiology of water balance disorders.

SALT AND WATER METABOLISM AND NEUROHYPOPHYSEAL VASOPRESSOR ACTIVITY IN MICE WITH HEREDITARY NEPHROGENIC DIABETES INSIPIDUS

1972 ◽  
Vol 69 (3) ◽  
pp. 434-444 ◽  
Author(s):  
D. V. Naik
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Urine Osmolality ◽  
Water Metabolism ◽  
Urine Sodium ◽  
Adh Activity ◽  
Vasopressor Activity ◽  
Sodium And Potassium ◽  
Total Excretion

ABSTRACT Three genotypes of mice, VII Os/+, DI +/+ and DI Os/+, with nephrogenic (vasopressin resistant) diabetes insipidus (DI) are compared to a normal VII +/+ strain with respect to water intake, urine output, urine osmolality, urine sodium and potassium, and the extractable vasopressor (ADH) activity from the neurohypophysis. From the results obtained, it is confirmed that the severely diabetic DI Os/+ mice produce large volumes of dilute, hypotonic urine and have a 2½ fold vasopressor increase as compared to normal VII +/+ mice, whereas, the mildly diabetic VII Os/+ and DI +/+ stand in between the DI Os/+ and VII +/+ with intermediate volumes of hypertonic urine and a vasopressor increase of 1⅓ and 1½ fold respectively. Further, a parallelism between the severity of diabetes insipidus and increased vasopressor activity is demonstrated in this study. The total excretion of sodium in the urine of VII Os/+ and DI Os/+ is higher than that of the VII +/+ and DI +/+ mice. This natriuresis is associated with Os gene and furthermore, its possible hypothalamic involvement is discussed. The increase of ADH in these hereditary nephrogenic diabetes insipidus mice is a new syndrome and the possible role of other factors involved is discussed.

Role of cAMP-phosphodiesterase isozymes in pathogenesis of murine nephrogenic diabetes insipidus

1991 ◽  
Vol 261 (2) ◽  
pp. F345-F353 ◽  
Author(s):  
S. Homma ◽  
S. M. Gapstur ◽  
A. Coffey ◽  
H. Valtin ◽  
T. P. Dousa
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Camp Phosphodiesterase ◽  
Pde Inhibitors ◽  
Collecting Ducts ◽  
Camp System ◽  
And Control ◽  
Camp Levels ◽  
Normal Controls

To test the hypothesis that rapid adenosine 3',5'-cyclic monophosphate (cAMP) catabolism via cyclic 3',5'-nucleotide phosphodiesterase (PDE) is a cause of the unresponsiveness to vasopressin (VP) in mice with hereditary nephrogenic diabetes insipidus (NDI), we investigated properties of PDEs and other aspects of the VP-dependent cAMP-signaling system in segments of collecting ducts [inner medullary (IMCD), cortical (CCD), and outer medullary (OMCD) ducts] microdissected from control mice and mice with NDI. The activity of cAMP-PDE, but not of cGMP-PDE, was markedly higher in IMCD (+109%), and to a lesser degree in OMCD (+41%) and CCD (+27%), of NDI mice than in normal controls. The cAMP-PDE in IMCD of NDI mice was more sensitive to inhibition by the PDE isozyme-specific inhibitors rolipram and cilostamide, but not by 3-isobutyl-1-methylxanthine, than was the cAMP-PDE in controls. Levels of cAMP in intact IMCD and CCD from NDI mice completely failed to increase in response to 10(-6) M VP. Incubation with rolipram alone, but not with cilostamide alone, restored VP-dependent cAMP accumulation in IMCD of NDI mice to the levels found in control mice; addition of cilostamide further enhanced the effect of rolipram. Analogous (but quantitatively lesser) anomalies of the VP-dependent cAMP system, including the effects of PDE inhibitors, were observed also in CCD of NDI mice. However, the activity of VP-stimulated adenylate cyclase assayed in permeabilized IMCD did not differ in NDI and control mice. These results indicate that anomalously high activities of low-Km cAMP-PDE isozymes account for the failure of collecting ducts of NDI mice to increase cAMP levels in response in VP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Congenital nephrogenic diabetes insipidus accompanied with central nephrogenic diabetes secondary to pituitary surgery -a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wei Zhang ◽  
Yimin Shen ◽  
Yuezhong Ren ◽  
Yvbo Xin ◽  
Lijun Wang
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Direct Detection ◽  
Urine Volume ◽  
Pituitary Surgery ◽  
Accurate Method ◽  
Heterozygous Mutation ◽  
Case Presentation ◽  
Congenital Nephrogenic Diabetes Insipidus

Abstract Background Diabetes insipidus (DI) can be a common cause of polydipsia and polyuria. Here, we present a case of congenital nephrogenic diabetes insipidus (CNDI) accompanied with central diabetes insipidus (CDI) secondary to pituitary surgery. Case presentation A 24-year-old Chinese woman came to our hospital with the complaints of polydipsia and polyuria for 6 months. Six months ago, she was detected with pituitary apoplexy, and thereby getting pituitary surgery. However, the water deprivation test demonstrated no significant changes in urine volume and urine gravity in response to fluid depression or AVP administration. In addition, the genetic results confirmed a heterozygous mutation in arginine vasopressin receptor type 2 (AVPR2) genes. Conclusions She was considered with CNDI as well as acquired CDI secondary to pituitary surgery. She was given with hydrochlorothiazide (HCTZ) 25 mg twice a day as well as desmopressin (DDAVP, Minirin) 0.1 mg three times a day. There is no recurrence of polyuria or polydipsia observed for more than 6 months. It can be hard to consider AVPR2 mutation in female carriers, especially in those with subtle clinical presentation. Hence, direct detection of DNA sequencing with AVPR2 is a convenient and accurate method in CNDI diagnosis.

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