Diabetes insipidus medical therapy: Difference between revisions
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==Overview== | ==Overview== | ||
The hallmark symptoms of both central and nephrogenic diabetes insipidus (DI) are polyuria, nocturia, and polydipsia due to the concentrating defect. Treatment of central | The hallmark symptoms of both [[Central diabetes insipidus|central]] and [[nephrogenic diabetes insipidus]] (DI) are [[polyuria]], [[nocturia]], and [[polydipsia]] due to the concentrating defect. Treatment of [[central diabetes insipidus]] is primarily aimed at decreasing the urine output, usually by increasing the activity of [[antidiuretic hormone]] ([[ADH]], also called [[arginine vasopressin]] or [[AVP]]). However, [[nephrogenic diabetes insipidus]] (DI) results from resistance of the [[kidney]] to the actions of [[antidiuretic hormone]]([[ADH]]). As a result, patients with this disorder are not likely to have a good response to hormone administration (as [[DDAVP]]) or to drugs that increase either the renal response to [[ADH]] or [[ADH]] secretion and so other treatment options must be explored. | ||
However, nephrogenic diabetes insipidus (DI) results from resistance of the kidney to the actions of antidiuretic hormone(ADH). As a result, patients with this disorder are not likely to have a good response to hormone administration (as | |||
==Medical Therapy== | ==Medical Therapy== | ||
===Central Diabetes Insipidus=== | ===[[Central diabetes insipidus|Central Diabetes Insipidus]]=== | ||
*The mainstay of therapy for central diabetes insipidus is desmopressin. Fluid restriction should be observed. Dosing should be individualized to response.<ref name="pmid8877030">{{cite journal |vauthors=Lam KS, Wat MS, Choi KL, Ip TP, Pang RW, Kumana CR |title=Pharmacokinetics, pharmacodynamics, long-term efficacy and safety of oral 1-deamino-8-D-arginine vasopressin in adult patients with central diabetes insipidus |journal=Br J Clin Pharmacol |volume=42 |issue=3 |pages=379–85 |year=1996 |pmid=8877030 |pmc=2042683 |doi= |url=}}</ref><ref name="pmid8241672">{{cite journal |vauthors=Fjellestad-Paulsen A, Laborde K, Kindermans C, Czernichow P |title=Water-balance hormones during long-term follow-up of oral dDAVP treatment in diabetes insipidus |journal=Acta Paediatr. |volume=82 |issue=9 |pages=752–7 |year=1993 |pmid=8241672 |doi= |url=}}</ref> | *The mainstay of therapy for [[central diabetes insipidus]] is [[desmopressin]]. Fluid restriction should be observed. Dosing should be individualized to response.<ref name="pmid8877030">{{cite journal |vauthors=Lam KS, Wat MS, Choi KL, Ip TP, Pang RW, Kumana CR |title=Pharmacokinetics, pharmacodynamics, long-term efficacy and safety of oral 1-deamino-8-D-arginine vasopressin in adult patients with central diabetes insipidus |journal=Br J Clin Pharmacol |volume=42 |issue=3 |pages=379–85 |year=1996 |pmid=8877030 |pmc=2042683 |doi= |url=}}</ref><ref name="pmid8241672">{{cite journal |vauthors=Fjellestad-Paulsen A, Laborde K, Kindermans C, Czernichow P |title=Water-balance hormones during long-term follow-up of oral dDAVP treatment in diabetes insipidus |journal=Acta Paediatr. |volume=82 |issue=9 |pages=752–7 |year=1993 |pmid=8241672 |doi= |url=}}</ref> | ||
**IV, SubQ: US labeling: 2 to 4 mcg daily (0.5 to 1 mL) in 2 divided doses or one-tenth (1/10) of the maintenance intranasal dose. | **[[IV]], [[Subcutaneous|SubQ]]: US labeling: 2 to 4 mcg daily (0.5 to 1 mL) in 2 divided doses or one-tenth (1/10) of the maintenance [[Intranasal route|intranasal]] dose. | ||
**IM, IV, SubQ: Canadian labeling (DDAVP Injection only): 1 to 4 mcg (0.25 to 1 mL) once daily or one-tenth (1/10) of the maintenance intranasal dose. | **[[Intramuscular injection|IM]], [[IV]], [[Subcutaneous|SubQ]]: Canadian labeling ([[DDAVP]] Injection only): 1 to 4 mcg (0.25 to 1 mL) once daily or one-tenth (1/10) of the maintenance [[Intranasal route|intranasal]] dose. | ||
**Intranasal (100 mcg/mL nasal solution): Usual dose range: 10 to 40 mcg daily (0.1 to 0.4 mL) as a single dose or divided 2 to 3 times daily. | **[[Intranasal route|Intranasal]] (100 mcg/mL nasal solution): Usual dose range: 10 to 40 mcg daily (0.1 to 0.4 mL) as a single dose or divided 2 to 3 times daily. | ||
**Oral | **[[Oral]] | ||
***US labeling: Initial: 0.05 mg twice daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis (range: 0.1 to 1.2 mg divided 2 to 3 times daily). | ***US labeling: Initial: 0.05 mg twice daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis (range: 0.1 to 1.2 mg divided 2 to 3 times daily). | ||
***Canadian labeling: Initial: 0.1 mg 3 times daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis (maximum: 1.2 mg/day in 3 divided doses) | ***Canadian labeling: Initial: 0.1 mg 3 times daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis (maximum: 1.2 mg/day in 3 divided doses) | ||
**Sublingual formulation | **[[Sublingual]] formulation | ||
***[Canadian product]: DDAVP Melt: Initial: 60 mcg 3 times daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis. Usual maintenance: 120 to 720 mcg equally divided 2 or 3 times daily. | ***[Canadian product]: [[DDAVP]] Melt: Initial: 60 mcg 3 times daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis. Usual maintenance: 120 to 720 mcg equally divided 2 or 3 times daily. | ||
*Chlorpropamide | *[[Chlorpropamide]] | ||
*Carbamazepine or clofibrate | *[[Carbamazepine]] or [[clofibrate]] | ||
*Thiazide diuretics | *[[Thiazide diuretics]] | ||
*NSAIDs | *[[NSAIDs]] | ||
===Nephrogenic diabetes insipidus=== | ===[[Nephrogenic diabetes insipidus]]=== | ||
Early diagnosis is helpful in decreasing the long term side effects of nephrogenic diabetes insipidus such as mental retardation that results from repeated episodes of dehydration and hypernatremia. | Early diagnosis is helpful in decreasing the long term side effects of [[nephrogenic diabetes insipidus]] such as [[mental retardation]] that results from repeated episodes of [[dehydration]] and [[hypernatremia]]. | ||
*Decreased dietary solute<ref name="pmid22427315">{{cite journal |vauthors=Wesche D, Deen PM, Knoers NV |title=Congenital nephrogenic diabetes insipidus: the current state of affairs |journal=Pediatr. Nephrol. |volume=27 |issue=12 |pages=2183–204 |year=2012 |pmid=22427315 |doi=10.1007/s00467-012-2118-8 |url=}}</ref> | *Decreased dietary [[solute]]<ref name="pmid22427315">{{cite journal |vauthors=Wesche D, Deen PM, Knoers NV |title=Congenital nephrogenic diabetes insipidus: the current state of affairs |journal=Pediatr. Nephrol. |volume=27 |issue=12 |pages=2183–204 |year=2012 |pmid=22427315 |doi=10.1007/s00467-012-2118-8 |url=}}</ref> | ||
*Diuretics | *[[Diuretics]] | ||
**Thiazide diuretics 25 mg once or twice daily<ref name="pmid16695887">{{cite journal |vauthors=Earley LE, Orloff J |title=THE MECHANISM OF ANTIDIURESIS ASSOCIATED WITH THE ADMINISTRATION OF HYDROCHLOROTHIAZIDE TO PATIENTS WITH VASOPRESSIN-RESISTANT DIABETES INSIPIDUS |journal=J. Clin. Invest. |volume=41 |issue=11 |pages=1988–97 |year=1962 |pmid=16695887 |pmc=291129 |doi=10.1172/JCI104657 |url=}}</ref><ref name="pmid3969096">{{cite journal |vauthors=Batlle DC, von Riotte AB, Gaviria M, Grupp M |title=Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy |journal=N. Engl. J. Med. |volume=312 |issue=7 |pages=408–14 |year=1985 |pmid=3969096 |doi=10.1056/NEJM198502143120705 |url=}}</ref> | **[[Thiazide diuretics]] 25 mg once or twice daily<ref name="pmid16695887">{{cite journal |vauthors=Earley LE, Orloff J |title=THE MECHANISM OF ANTIDIURESIS ASSOCIATED WITH THE ADMINISTRATION OF HYDROCHLOROTHIAZIDE TO PATIENTS WITH VASOPRESSIN-RESISTANT DIABETES INSIPIDUS |journal=J. Clin. Invest. |volume=41 |issue=11 |pages=1988–97 |year=1962 |pmid=16695887 |pmc=291129 |doi=10.1172/JCI104657 |url=}}</ref><ref name="pmid3969096">{{cite journal |vauthors=Batlle DC, von Riotte AB, Gaviria M, Grupp M |title=Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy |journal=N. Engl. J. Med. |volume=312 |issue=7 |pages=408–14 |year=1985 |pmid=3969096 |doi=10.1056/NEJM198502143120705 |url=}}</ref> | ||
**Amiloride<ref name="pmid18596116">{{cite journal |vauthors=Bedford JJ, Weggery S, Ellis G, McDonald FJ, Joyce PR, Leader JP, Walker RJ |title=Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride |journal=Clin J Am Soc Nephrol |volume=3 |issue=5 |pages=1324–31 |year=2008 |pmid=18596116 |pmc=2518801 |doi=10.2215/CJN.01640408 |url=}}</ref> | **[[Amiloride]]<ref name="pmid18596116">{{cite journal |vauthors=Bedford JJ, Weggery S, Ellis G, McDonald FJ, Joyce PR, Leader JP, Walker RJ |title=Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride |journal=Clin J Am Soc Nephrol |volume=3 |issue=5 |pages=1324–31 |year=2008 |pmid=18596116 |pmc=2518801 |doi=10.2215/CJN.01640408 |url=}}</ref> | ||
*Nonsteroidal anti-inflammatory drugs<ref name="pmid7018256">{{cite journal |vauthors=Stokes JB |title=Integrated actions of renal medullary prostaglandins in the control of water excretion |journal=Am. J. Physiol. |volume=240 |issue=6 |pages=F471–80 |year=1981 |pmid=7018256 |doi= |url=}}</ref> | *[[Nonsteroidal anti-inflammatory drugs]]<ref name="pmid7018256">{{cite journal |vauthors=Stokes JB |title=Integrated actions of renal medullary prostaglandins in the control of water excretion |journal=Am. J. Physiol. |volume=240 |issue=6 |pages=F471–80 |year=1981 |pmid=7018256 |doi= |url=}}</ref> | ||
*Exogenous ADH<ref name="pmid18596116">{{cite journal |vauthors=Bedford JJ, Weggery S, Ellis G, McDonald FJ, Joyce PR, Leader JP, Walker RJ |title=Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride |journal=Clin J Am Soc Nephrol |volume=3 |issue=5 |pages=1324–31 |year=2008 |pmid=18596116 |pmc=2518801 |doi=10.2215/CJN.01640408 |url=}}</ref> | *Exogenous [[ADH]]<ref name="pmid18596116">{{cite journal |vauthors=Bedford JJ, Weggery S, Ellis G, McDonald FJ, Joyce PR, Leader JP, Walker RJ |title=Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride |journal=Clin J Am Soc Nephrol |volume=3 |issue=5 |pages=1324–31 |year=2008 |pmid=18596116 |pmc=2518801 |doi=10.2215/CJN.01640408 |url=}}</ref> | ||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The hallmark symptoms of both central and nephrogenic diabetes insipidus (DI) are polyuria, nocturia, and polydipsia due to the concentrating defect. Treatment of central diabetes insipidus is primarily aimed at decreasing the urine output, usually by increasing the activity of antidiuretic hormone (ADH, also called arginine vasopressin or AVP). However, nephrogenic diabetes insipidus (DI) results from resistance of the kidney to the actions of antidiuretic hormone(ADH). As a result, patients with this disorder are not likely to have a good response to hormone administration (as DDAVP) or to drugs that increase either the renal response to ADH or ADH secretion and so other treatment options must be explored.
Medical Therapy
Central Diabetes Insipidus
- The mainstay of therapy for central diabetes insipidus is desmopressin. Fluid restriction should be observed. Dosing should be individualized to response.[1][2]
- IV, SubQ: US labeling: 2 to 4 mcg daily (0.5 to 1 mL) in 2 divided doses or one-tenth (1/10) of the maintenance intranasal dose.
- IM, IV, SubQ: Canadian labeling (DDAVP Injection only): 1 to 4 mcg (0.25 to 1 mL) once daily or one-tenth (1/10) of the maintenance intranasal dose.
- Intranasal (100 mcg/mL nasal solution): Usual dose range: 10 to 40 mcg daily (0.1 to 0.4 mL) as a single dose or divided 2 to 3 times daily.
- Oral
- US labeling: Initial: 0.05 mg twice daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis (range: 0.1 to 1.2 mg divided 2 to 3 times daily).
- Canadian labeling: Initial: 0.1 mg 3 times daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis (maximum: 1.2 mg/day in 3 divided doses)
- Sublingual formulation
- [Canadian product]: DDAVP Melt: Initial: 60 mcg 3 times daily; total daily dose should be increased or decreased as needed to obtain adequate antidiuresis. Usual maintenance: 120 to 720 mcg equally divided 2 or 3 times daily.
- Chlorpropamide
- Carbamazepine or clofibrate
- Thiazide diuretics
- NSAIDs
Nephrogenic diabetes insipidus
Early diagnosis is helpful in decreasing the long term side effects of nephrogenic diabetes insipidus such as mental retardation that results from repeated episodes of dehydration and hypernatremia.
- Decreased dietary solute[3]
- Diuretics
- Thiazide diuretics 25 mg once or twice daily[4][5]
- Amiloride[6]
- Nonsteroidal anti-inflammatory drugs[7]
- Exogenous ADH[6]
References
- ↑ Lam KS, Wat MS, Choi KL, Ip TP, Pang RW, Kumana CR (1996). "Pharmacokinetics, pharmacodynamics, long-term efficacy and safety of oral 1-deamino-8-D-arginine vasopressin in adult patients with central diabetes insipidus". Br J Clin Pharmacol. 42 (3): 379–85. PMC 2042683. PMID 8877030.
- ↑ Fjellestad-Paulsen A, Laborde K, Kindermans C, Czernichow P (1993). "Water-balance hormones during long-term follow-up of oral dDAVP treatment in diabetes insipidus". Acta Paediatr. 82 (9): 752–7. PMID 8241672.
- ↑ Wesche D, Deen PM, Knoers NV (2012). "Congenital nephrogenic diabetes insipidus: the current state of affairs". Pediatr. Nephrol. 27 (12): 2183–204. doi:10.1007/s00467-012-2118-8. PMID 22427315.
- ↑ Earley LE, Orloff J (1962). "THE MECHANISM OF ANTIDIURESIS ASSOCIATED WITH THE ADMINISTRATION OF HYDROCHLOROTHIAZIDE TO PATIENTS WITH VASOPRESSIN-RESISTANT DIABETES INSIPIDUS". J. Clin. Invest. 41 (11): 1988–97. doi:10.1172/JCI104657. PMC 291129. PMID 16695887.
- ↑ Batlle DC, von Riotte AB, Gaviria M, Grupp M (1985). "Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy". N. Engl. J. Med. 312 (7): 408–14. doi:10.1056/NEJM198502143120705. PMID 3969096.
- ↑ 6.0 6.1 Bedford JJ, Weggery S, Ellis G, McDonald FJ, Joyce PR, Leader JP, Walker RJ (2008). "Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride". Clin J Am Soc Nephrol. 3 (5): 1324–31. doi:10.2215/CJN.01640408. PMC 2518801. PMID 18596116.
- ↑ Stokes JB (1981). "Integrated actions of renal medullary prostaglandins in the control of water excretion". Am. J. Physiol. 240 (6): F471–80. PMID 7018256.