Nephrogenic diabetes insipidus: Difference between revisions
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{{Short description|Impaired renal function disease}} |
{{Short description|Impaired renal function disease}} |
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{{Distinguish|Central diabetes insipidus}} |
{{Distinguish|Central diabetes insipidus}} |
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{{verification|date=October 2024}} |
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{{Infobox medical condition (new) |
{{Infobox medical condition (new) |
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| name = Nephrogenic diabetes insipidus |
| name = Nephrogenic diabetes insipidus |
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'''Nephrogenic diabetes insipidus''', recently renamed '''arginine vasopressin resistance''' (AVP-R) and previously known as '''renal diabetes insipidus''', is a form of [[diabetes insipidus]] primarily due to pathology of the [[kidney]]. This is in contrast to central or [[Central diabetes insipidus|neurogenic diabetes insipidus]], which is caused by insufficient levels of [[vasopressin]] (also called antidiuretic hormone, ADH). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to vasopressin, leading to a decrease in the ability of the kidney to concentrate the [[urine]] by [[Reabsorption|removing free water]]. |
'''Nephrogenic diabetes insipidus''', recently renamed '''arginine vasopressin resistance''' (AVP-R) and previously known as '''renal diabetes insipidus''', is a form of [[diabetes insipidus]] primarily due to pathology of the [[kidney]]. This is in contrast to central or [[Central diabetes insipidus|neurogenic diabetes insipidus]], which is caused by insufficient levels of [[vasopressin]] (also called antidiuretic hormone, ADH). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to vasopressin, leading to a decrease in the ability of the kidney to concentrate the [[urine]] by [[Reabsorption|removing free water]]. |
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==Signs and symptoms== |
==Signs and symptoms== |
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The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with [[polydipsia]] (excessive thirst) and [[polyuria]] (excretion of a large amount of dilute urine). Dehydration is common, and incontinence can occur secondary to chronic bladder distension.<ref>{{Cite web|url=http://www.patient.co.uk/showdoc/40001780/|title=Diabetes Insipidus. Diabetes symptoms and information|website=www.patient.co.uk|language=en-GB|access-date=2018-05-18}}</ref> On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, antidiuretic hormone levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then [[hypernatremia]] will ensue with its neurologic symptoms. |
The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with [[polydipsia]] (excessive thirst) and [[polyuria]] (excretion of a large amount of dilute urine). Dehydration is common, and incontinence can occur secondary to chronic bladder distension.<ref>{{Cite web|url=http://www.patient.co.uk/showdoc/40001780/|title=Diabetes Insipidus. Diabetes symptoms and information|website=www.patient.co.uk|language=en-GB|access-date=2018-05-18}}</ref> On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, antidiuretic hormone levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then [[hypernatremia]] will ensue with its neurologic symptoms. |
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==Causes== |
==Causes== |
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Nephrogenic diabetes insipidus is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including [[amyloidosis]],<ref name="4typneph">{{Cite web | last = Wildin | first = Robert | title = What is NDI? | publisher = The Diabetes Inspidus Foundation | year = 2006 |url=http://www.diabetesinsipidus.org/4_types_nephrogenic_di.htm |work=Nephrogenic Diabetes Insipidus |access-date=2009-04-04 |url-status=dead |archive-url=https://web.archive.org/web/20090401234459/http://diabetesinsipidus.org/4_types_nephrogenic_di.htm |archive-date=2009-04-01 }}</ref> [[polycystic kidney disease]],<ref name="NIHpub">{{Cite news|url=http://kidney.niddk.nih.gov/kudiseases/pubs/insipidus/index.htm|title=Diabetes Insipidus|work=National Institute of Diabetes and Digestive and Kidney Diseases|access-date=2018-05-18|language=en-US|archive-url=https://web.archive.org/web/20110608142320/http://kidney.niddk.nih.gov/kudiseases/pubs/insipidus/index.htm|archive-date=2011-06-08|url-status=dead}}</ref> electrolyte imbalance,<ref name="pmid8621781">{{cite journal |vauthors=Marples D, Frøkiaer J, Dørup J, Knepper MA, Nielsen S |title=Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex |journal=Journal of Clinical Investigation |volume=97 |issue=8 |pages=1960–8 |date=April 1996 |pmid=8621781 |pmc=507266 |doi=10.1172/JCI118628 }}</ref><ref name="pmid185584">{{cite journal |vauthors=Carney S, Rayson B, Morgan T |title=A study in vitro of the concentrating defect associated with hypokalaemia and hypercalcaemia |journal=Pflügers Archiv |volume=366 |issue=1 |pages=11–7 |date=October 1976 |pmid=185584 |doi= 10.1007/BF02486556|s2cid=29761514 }}</ref> or some other kidney defect.<ref name="4typneph"/> |
Nephrogenic diabetes insipidus is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including [[amyloidosis]],<ref name="4typneph">{{Cite web | last = Wildin | first = Robert | title = What is NDI? | publisher = The Diabetes Inspidus Foundation | year = 2006 |url=http://www.diabetesinsipidus.org/4_types_nephrogenic_di.htm |work=Nephrogenic Diabetes Insipidus |access-date=2009-04-04 |url-status=dead |archive-url=https://web.archive.org/web/20090401234459/http://diabetesinsipidus.org/4_types_nephrogenic_di.htm |archive-date=2009-04-01 }}</ref> [[polycystic kidney disease]],<ref name="NIHpub">{{Cite news|url=http://kidney.niddk.nih.gov/kudiseases/pubs/insipidus/index.htm|title=Diabetes Insipidus|work=National Institute of Diabetes and Digestive and Kidney Diseases|access-date=2018-05-18|language=en-US|archive-url=https://web.archive.org/web/20110608142320/http://kidney.niddk.nih.gov/kudiseases/pubs/insipidus/index.htm|archive-date=2011-06-08|url-status=dead}}</ref> electrolyte imbalance,<ref name="pmid8621781">{{cite journal |vauthors=Marples D, Frøkiaer J, Dørup J, Knepper MA, Nielsen S |title=Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex |journal=Journal of Clinical Investigation |volume=97 |issue=8 |pages=1960–8 |date=April 1996 |pmid=8621781 |pmc=507266 |doi=10.1172/JCI118628 }}</ref><ref name="pmid185584">{{cite journal |vauthors=Carney S, Rayson B, Morgan T |title=A study in vitro of the concentrating defect associated with hypokalaemia and hypercalcaemia |journal=Pflügers Archiv |volume=366 |issue=1 |pages=11–7 |date=October 1976 |pmid=185584 |doi= 10.1007/BF02486556|s2cid=29761514 }}</ref> or some other kidney defect.<ref name="4typneph"/> |
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The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are [[lithium (medication)|lithium]] toxicity and [[hypercalcemia|high blood calcium]]. About 80% of lithium ingested appears to affect the [[proximal tubule]]s by entering the collecting tubule cells through sodium channels, accumulating and interfering with the normal response to antidiuretic hormone in a mechanism that is not yet fully understood.<ref name="Davis Desmond Berk pp. 897–903">{{cite journal | last1=Davis | first1=Justin | last2=Desmond | first2=Michael | last3=Berk | first3=Michael | title=Lithium and nephrotoxicity: Unravelling the complex pathophysiological threads of the lightest metal | journal=Nephrology | publisher=Wiley | volume=23 | issue=10 | date=2018-09-24 | issn=1320-5358 | doi=10.1111/nep.13263 | pages=897–903| pmid=29607573 | s2cid=4552345 | doi-access=free | hdl=11343/283773 | hdl-access=free }}</ref> High blood calcium causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the [[calcium-sensing receptor]]. |
The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are [[lithium (medication)|lithium]] toxicity and [[hypercalcemia|high blood calcium]]. About 80% of lithium ingested appears to affect the [[proximal tubule]]s by entering the collecting tubule cells through sodium channels, accumulating and interfering with the normal response to antidiuretic hormone in a mechanism that is not yet fully understood.<ref name="Davis Desmond Berk pp. 897–903">{{cite journal | last1=Davis | first1=Justin | last2=Desmond | first2=Michael | last3=Berk | first3=Michael | title=Lithium and nephrotoxicity: Unravelling the complex pathophysiological threads of the lightest metal | journal=Nephrology | publisher=Wiley | volume=23 | issue=10 | date=2018-09-24 | issn=1320-5358 | doi=10.1111/nep.13263 | pages=897–903| pmid=29607573 | s2cid=4552345 | doi-access=free | hdl=11343/283773 | hdl-access=free }}</ref> High blood calcium causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the [[calcium-sensing receptor]]. |
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===Osmotic=== |
===Osmotic=== |
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Other causes of acquired nephrogenic diabetes insipidus include [[hypokalemia]] (low blood potassium), post-obstructive polyuria, [[sickle cell disease]] or trait, amyloidosis, [[Sjögren syndrome]], renal cystic disease, [[Bartter syndrome]], and various medications ([[amphotericin B]], [[orlistat]], [[ifosfamide]], [[ofloxacin]], [[cidofovir]], [[vasopressin receptor antagonist#Vaptans|vaptan]]s). |
Other causes of acquired nephrogenic diabetes insipidus include [[hypokalemia]] (low blood potassium), post-obstructive polyuria, [[sickle cell disease]] or trait, amyloidosis, [[Sjögren syndrome]], renal cystic disease, [[Bartter syndrome]], and various medications ([[amphotericin B]], [[orlistat]], [[ifosfamide]], [[ofloxacin]], [[cidofovir]], [[vasopressin receptor antagonist#Vaptans|vaptan]]s). |
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In addition to kidney and systemic disorders, nephrogenic diabetes insipidus can present itself as a side effect of some [[medication|medications.]] The most common and well known of these medications is lithium,<ref name="pmid2989335">{{cite journal |vauthors=Christensen S, Kusano E, Yusufi AN, Murayama N, Dousa TP |title=Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats |journal=Journal of Clinical Investigation |volume=75 |issue=6 |pages=1869–79 |date=June 1985 |pmid=2989335 |pmc=425543 |doi=10.1172/JCI111901 }}</ref> although there are many other medications that cause this effect with lesser frequency.<ref name="4typneph"/> |
In addition to kidney and systemic disorders, nephrogenic diabetes insipidus can present itself as a side effect of some [[medication|medications.]] The most common and well known of these medications is lithium,<ref name="pmid2989335">{{cite journal |vauthors=Christensen S, Kusano E, Yusufi AN, Murayama N, Dousa TP |title=Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats |journal=Journal of Clinical Investigation |volume=75 |issue=6 |pages=1869–79 |date=June 1985 |pmid=2989335 |pmc=425543 |doi=10.1172/JCI111901 }}</ref> although there are many other medications that cause this effect with lesser frequency.<ref name="4typneph"/> |
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Recently, lab assays for antidiuretic hormone are available and can aid in diagnosis. If the patient is able to rehydrate properly, sodium concentration should be nearer to the maximum of the normal range. This, however, is not a diagnostic finding, as it depends on patient hydration.{{cn|date=April 2021}} |
Recently, lab assays for antidiuretic hormone are available and can aid in diagnosis. If the patient is able to rehydrate properly, sodium concentration should be nearer to the maximum of the normal range. This, however, is not a diagnostic finding, as it depends on patient hydration.{{cn|date=April 2021}} |
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[[Desmopressin]] can also be used; if the patient is able to concentrate urine following administration of desmopressin, then the cause of the diabetes insipidus is neurogenic diabetes insipidus; if no response occurs to desmopressin, then the cause is likely to be nephrogenic. |
[[Desmopressin]] can also be used; if the patient is able to concentrate urine following administration of desmopressin, then the cause of the diabetes insipidus is neurogenic diabetes insipidus; if no response occurs to desmopressin, then the cause is likely to be nephrogenic. |
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==Treatment== |
==Treatment== |
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Persons with nephrogenic diabetes insipidus must consume enough fluids to equal the amount of urine produced. Any underlying cause such as high blood calcium must be corrected to treat nephrogenic diabetes insipidus. The first line of treatment is [[hydrochlorothiazide]] and [[amiloride]].<ref name="pmid10332005">{{cite journal |vauthors=Kirchlechner V, Koller DY, Seidl R, Waldhauser F |title=Treatment of nephrogenic diabetes insipidus with hydrochlorothiazide and amiloride |journal=Archives of Disease in Childhood |volume=80 |issue=6 |pages=548–52 |date=June 1999 |pmid=10332005 |pmc=1717946 |doi= 10.1136/adc.80.6.548}}</ref> Patients may also consider a low-salt and low-protein diet. |
Persons with nephrogenic diabetes insipidus must consume enough fluids to equal the amount of urine produced. Any underlying cause such as high blood calcium must be corrected to treat nephrogenic diabetes insipidus. The first line of treatment is [[hydrochlorothiazide]] and [[amiloride]].<ref name="pmid10332005">{{cite journal |vauthors=Kirchlechner V, Koller DY, Seidl R, Waldhauser F |title=Treatment of nephrogenic diabetes insipidus with hydrochlorothiazide and amiloride |journal=Archives of Disease in Childhood |volume=80 |issue=6 |pages=548–52 |date=June 1999 |pmid=10332005 |pmc=1717946 |doi= 10.1136/adc.80.6.548}}</ref> Patients may also consider a low-salt and low-protein diet. |
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Thiazide diuretics cause a mild decrease in extracellular fluid volume through natriuresis and diuresis which in turn increases the [[Proximal convoluted tubule|proximal]] absorption of sodium and water, lowering urine output.<ref>{{cite web|url=https://www.uptodate.com/contents/mechanism-of-action-of-diuretics#H4|title=Mechanism of action of diuretics|date=November 30, 2022|accessdate=August 19, 2024|website=[[UpToDate]]|first1=Craig|last1=Brater|first2=David|last2=H Ellison|url-access=subscription}}</ref> |
Thiazide diuretics cause a mild decrease in extracellular fluid volume through natriuresis and diuresis which in turn increases the [[Proximal convoluted tubule|proximal]] absorption of sodium and water, lowering urine output.<ref>{{cite web|url=https://www.uptodate.com/contents/mechanism-of-action-of-diuretics#H4|title=Mechanism of action of diuretics|date=November 30, 2022|accessdate=August 19, 2024|website=[[UpToDate]]|first1=Craig|last1=Brater|first2=David|last2=H Ellison|url-access=subscription}}</ref> |
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High serum osmolarity stimulates polydipsia in an attempt to dilute the serum back to normal and provide free water for excreting the excess serum solutes. However, since the patient is unable to concentrate urine to excrete the excess solutes, the resulting urine fails to decrease serum osmolarity and the cycle repeats itself, hence polyuria. |
High serum osmolarity stimulates polydipsia in an attempt to dilute the serum back to normal and provide free water for excreting the excess serum solutes. However, since the patient is unable to concentrate urine to excrete the excess solutes, the resulting urine fails to decrease serum osmolarity and the cycle repeats itself, hence polyuria. |
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== Etymology == |
== Etymology == |
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The name of the disease comes from: |
The name of the disease comes from: |
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* ''diabetes'': from {{ |
* ''diabetes'': from {{langx|la|diabetes}}, from {{langx|grc|διαβήτης}} ''diabḗtēs'' "a passer-through; siphon", from Greek διαβαίνειν ''diabaínein'' "to pass through", from δια- ''dia-'' "through" + βαίνειν ''baínein'' "to go". |
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* ''insipidus'': from [[Late Latin]]: ''insipidus'' "tasteless," from Latin ''in-'' "not" + ''sapidus'' "tasty", from ''sapere'' "to taste". |
* ''insipidus'': from [[Late Latin]]: ''insipidus'' "tasteless," from Latin ''in-'' "not" + ''sapidus'' "tasty", from ''sapere'' "to taste". |
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This is because patients experience polyuria (an excretion of over 2.5 liters of urine per day), and the urine does not have an elevated [[glucose]] concentration, as opposed to [[diabetes mellitus]]. The two diseases were named (in ancient times) for the fact that one features polyuria in which the urine tastes sweet, whereas the other features polyuria in which the urine tastes unremarkable.{{cn|date=April 2021}} |
This is because patients experience polyuria (an excretion of over 2.5 liters of urine per day), and the urine does not have an elevated [[glucose]] concentration, as opposed to [[diabetes mellitus]]. The two diseases were named (in ancient times) for the fact that one features polyuria in which the urine tastes sweet, whereas the other features polyuria in which the urine tastes unremarkable.{{cn|date=April 2021}} |
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Latest revision as of 14:56, 25 October 2024
 | This article needs additional citations for verification. (October 2024) |
| Nephrogenic diabetes insipidus | |
|---|---|
| Other names | arginine vasopressin resistance; AVP-R; renal diabetes insipidus |
| Specialty | Nephrology, endocrinology, urology  |
| Symptoms | Polyuria, nocturia, and polydipsia. |
| Complications | Dehydration, seizures |
| Diagnostic method | Urine tests, blood tests, fluid deprivation test |
| Differential diagnosis | AVP-D (central), Diabetes mellitus |
| Treatment | Drinking sufficient fluids |
| Medication | thiazides, aspirin |
| Frequency | 3 per 100,000 per year |
Nephrogenic diabetes insipidus, recently renamed arginine vasopressin resistance (AVP-R) and previously known as renal diabetes insipidus, is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central or neurogenic diabetes insipidus, which is caused by insufficient levels of vasopressin (also called antidiuretic hormone, ADH). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to vasopressin, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water.
Signs and symptoms
[edit]The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with polydipsia (excessive thirst) and polyuria (excretion of a large amount of dilute urine). Dehydration is common, and incontinence can occur secondary to chronic bladder distension.[1] On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, antidiuretic hormone levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms.
Causes
[edit]Acquired
[edit]Nephrogenic diabetes insipidus is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis,[2] polycystic kidney disease,[3] electrolyte imbalance,[4][5] or some other kidney defect.[2]
The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are lithium toxicity and high blood calcium. About 80% of lithium ingested appears to affect the proximal tubules by entering the collecting tubule cells through sodium channels, accumulating and interfering with the normal response to antidiuretic hormone in a mechanism that is not yet fully understood.[6] High blood calcium causes natriuresis (increased sodium loss in the urine) and water diuresis, in part by its effect through the calcium-sensing receptor.
Osmotic
[edit]Other causes of acquired nephrogenic diabetes insipidus include hypokalemia (low blood potassium), post-obstructive polyuria, sickle cell disease or trait, amyloidosis, Sjögren syndrome, renal cystic disease, Bartter syndrome, and various medications (amphotericin B, orlistat, ifosfamide, ofloxacin, cidofovir, vaptans).
In addition to kidney and systemic disorders, nephrogenic diabetes insipidus can present itself as a side effect of some medications. The most common and well known of these medications is lithium,[7] although there are many other medications that cause this effect with lesser frequency.[2]
Hereditary
[edit]This form of diabetes insipidus can also be hereditary due to defects in the following genes:
| Type | OMIM | Gene | Locus |
|---|---|---|---|
| NDI1 | 304800 | AVPR2 | Usually, the hereditary form of nephrogenic diabetes insipidus is the result of an X-linked genetic defect which causes the vasopressin receptor (also called the V2 receptor) in the kidney to not function correctly.[2][8] |
| NDI2 | 125800 | AQP2 | In more rare cases, a mutation in the "aquaporin 2" gene impedes the normal functionality of the kidney water channel, which results in the kidney being unable to absorb water. This mutation is often inherited in an autosomal recessive manner although dominant mutations are reported from time to time [2][9] |
Diagnosis
[edit]Differential diagnosis includes nephrogenic diabetes insipidus, neurogenic/central diabetes insipidus and psychogenic polydipsia. They may be differentiated by using the water deprivation test. Recently, lab assays for antidiuretic hormone are available and can aid in diagnosis. If the patient is able to rehydrate properly, sodium concentration should be nearer to the maximum of the normal range. This, however, is not a diagnostic finding, as it depends on patient hydration.[citation needed]
Desmopressin can also be used; if the patient is able to concentrate urine following administration of desmopressin, then the cause of the diabetes insipidus is neurogenic diabetes insipidus; if no response occurs to desmopressin, then the cause is likely to be nephrogenic.
Treatment
[edit]Persons with nephrogenic diabetes insipidus must consume enough fluids to equal the amount of urine produced. Any underlying cause such as high blood calcium must be corrected to treat nephrogenic diabetes insipidus. The first line of treatment is hydrochlorothiazide and amiloride.[10] Patients may also consider a low-salt and low-protein diet.
Thiazide diuretics cause a mild decrease in extracellular fluid volume through natriuresis and diuresis which in turn increases the proximal absorption of sodium and water, lowering urine output.[11]
High serum osmolarity stimulates polydipsia in an attempt to dilute the serum back to normal and provide free water for excreting the excess serum solutes. However, since the patient is unable to concentrate urine to excrete the excess solutes, the resulting urine fails to decrease serum osmolarity and the cycle repeats itself, hence polyuria.
Etymology
[edit]The name of the disease comes from:
- diabetes: from Latin: diabetes, from Ancient Greek: διαβήτης diabḗtēs "a passer-through; siphon", from Greek διαβαίνειν diabaínein "to pass through", from δια- dia- "through" + βαίνειν baínein "to go".
- insipidus: from Late Latin: insipidus "tasteless," from Latin in- "not" + sapidus "tasty", from sapere "to taste".
This is because patients experience polyuria (an excretion of over 2.5 liters of urine per day), and the urine does not have an elevated glucose concentration, as opposed to diabetes mellitus. The two diseases were named (in ancient times) for the fact that one features polyuria in which the urine tastes sweet, whereas the other features polyuria in which the urine tastes unremarkable.[citation needed]
Although they share part of their names, diabetes mellitus and diabetes insipidus are two separate conditions. Both cause excessive urination (hence the similarity in name), but whereas diabetes insipidus is a problem with the production of antidiuretic hormone (neurogenic diabetes insipidus) or the kidneys' response to antidiuretic hormone (nephrogenic diabetes insipidus), diabetes mellitus causes polyuria via osmotic diuresis, due to the high blood sugar leaking into the urine, taking excess water along with it.[citation needed]
References
[edit]- ^ "Diabetes Insipidus. Diabetes symptoms and information". www.patient.co.uk. Retrieved 2018-05-18.
- ^ a b c d e Wildin, Robert (2006). "What is NDI?". Nephrogenic Diabetes Insipidus. The Diabetes Inspidus Foundation. Archived from the original on 2009-04-01. Retrieved 2009-04-04.
- ^ "Diabetes Insipidus". National Institute of Diabetes and Digestive and Kidney Diseases. Archived from the original on 2011-06-08. Retrieved 2018-05-18.
- ^ Marples D, Frøkiaer J, Dørup J, Knepper MA, Nielsen S (April 1996). "Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex". Journal of Clinical Investigation. 97 (8): 1960–8. doi:10.1172/JCI118628. PMC 507266. PMID 8621781.
- ^ Carney S, Rayson B, Morgan T (October 1976). "A study in vitro of the concentrating defect associated with hypokalaemia and hypercalcaemia". Pflügers Archiv. 366 (1): 11–7. doi:10.1007/BF02486556. PMID 185584. S2CID 29761514.
- ^ Davis, Justin; Desmond, Michael; Berk, Michael (2018-09-24). "Lithium and nephrotoxicity: Unravelling the complex pathophysiological threads of the lightest metal". Nephrology. 23 (10). Wiley: 897–903. doi:10.1111/nep.13263. hdl:11343/283773. ISSN 1320-5358. PMID 29607573. S2CID 4552345.
- ^ Christensen S, Kusano E, Yusufi AN, Murayama N, Dousa TP (June 1985). "Pathogenesis of nephrogenic diabetes insipidus due to chronic administration of lithium in rats". Journal of Clinical Investigation. 75 (6): 1869–79. doi:10.1172/JCI111901. PMC 425543. PMID 2989335.
- ^ Online Mendelian Inheritance in Man (OMIM): Diabetes Insipidus, Nephrogenic, X-linked - 304800
- ^ Online Mendelian Inheritance in Man (OMIM): Diabetes Insipidus, Nephrogenic, Autosomal - 125800
- ^ Kirchlechner V, Koller DY, Seidl R, Waldhauser F (June 1999). "Treatment of nephrogenic diabetes insipidus with hydrochlorothiazide and amiloride". Archives of Disease in Childhood. 80 (6): 548–52. doi:10.1136/adc.80.6.548. PMC 1717946. PMID 10332005.
- ^ Brater, Craig; H Ellison, David (November 30, 2022). "Mechanism of action of diuretics". UpToDate. Retrieved August 19, 2024.