nephrogenic diabetes insipidus (NDI)
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Etiology
- acquired tubulointerstitial disease
- drugs or toxins
- congenital anomalies
- 3rd trimester of pregnancy (rare)
- vasopressinase production by placenta resulting in catabolism of vasopressin[2]
Pathology
- complete or partial resistance of antidiuretic hormone (ADH) or vasopressin &/or impairment of the counter-current mechanism in the loop of Henle
Genetics
Clinical manifestations
Laboratory
- urine concentrating deficit is not severe
- urine osmolality - may reach 300 mosm/kg
- 24 hour urine - volumes of 2-3 L/day, as high as 6 liters/day
- urine concentrating test
- urine osmolality does not increase after water deprivation
- urine osmolality does NOT increase 60 minutes after administration of 5 units subcutaneous arginine vasopressin
- ADH in plasma is normal or high
- serum sodium generally normal
Radiology
Differential diagnosis
psychogenic polydipsea: low normal serum sodium to hyponatremia
Management
- unresponsive to vasopressin (dDAVP)
- most cases have treatable cause
- general measures (see diabetes insipidus)
- thiazide diuretics & dietary salt restriction (not drug induced)
- indomethacin may be used in combination[5]
- thiazide diuretics & dietary salt restriction (not drug induced)
- discontinue offending medications
- Li+
- if Li+ must be continued, use with amiloride
- amiloride blocks uptake of Li+ by the distal tubule
- mild extracellular fluid volume contraction
- increased Na+ & H2O absorption at the proximal tubule
- decreased urine volume
- volume depletion induced by diuretics may increase proximal tubule resorption of Na+ & Li+, & increase Li+ concentration
- if Li+ must be continued, use with amiloride
- Li+
- correct hypokalemia
- correct hypercalcemia
More general terms
Additional terms
- amyloidosis
- chronic interstitial nephritis (analgesic nephropathy, drug-induced chronic interstitial nephritis)
- hypercalcemia
- hypokalemia
- multiple myeloma; plasmacytoma/plasma cell myeloma
- postrenal azotemia; obstructive uropathy
- pyelonephritis
- renal transplantation
- sarcoidosis
- sickle cell (hemoglobin SS) disease
- Sjogren's syndrome (autoimmune epitheliitis)
References
- ↑ Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995, pg 50-51
- ↑ 2.0 2.1 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 15, 16, 17. American College of Physicians, Philadelphia 1998, 2006, 2009, 2012, 2015
- ↑ Harrison's Principles of Internal Medicine, 13th ed. Isselbacher et al (eds), McGraw-Hill Inc. NY, 1994, pg 239, 1324
- ↑ Grunfeld JP, Rossier BC. Lithium nephrotoxicity revisited. Nat Rev Nephrol. 2009 May;5(5):270-6 PMID: https://www.ncbi.nlm.nih.gov/pubmed/19384328
- ↑ 5.0 5.1 Bedford JJ, Weggery S, Ellis G et al Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride. Clin J Am Soc Nephrol. 2008 Sep;3(5):1324-31. PMID: https://www.ncbi.nlm.nih.gov/pubmed/18596116 Free PMC Article
- ↑ Christensen BM, Zuber AM, Loffing J et al alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus. J Am Soc Nephrol. 2011 Feb;22(2):253-61. PMID: https://www.ncbi.nlm.nih.gov/pubmed/21051735 Free PMC Article
- ↑ Feldman BJ, Rosenthal SM, Vargas GA et al Nephrogenic syndrome of inappropriate antidiuresis. N Engl J Med. 2005 May 5;352(18):1884-90. PMID: https://www.ncbi.nlm.nih.gov/pubmed/15872203 Free Article
- ↑ Devuyst O. Physiopathology and diagnosis of nephrogenic diabetes insipidus. Ann Endocrinol (Paris). 2012 Apr;73(2):128-9. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/22503803
- ↑ NEJM Knowledge+
Sands JM, Bichet DG; Nephrogenic diabetes insipidus. Ann Intern Med. 2006 Feb 7;144(3):186-94. PMID: https://www.ncbi.nlm.nih.gov/pubmed/16461963 Review. - ↑ MedlinePlus: Diabetes insipidus - neprogenic http://www.nlm.nih.gov/medlineplus/ency/article/000511.htm