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## [[Bartter syndrome]]<ref>Jeck N, Schlingmann KP, Reinalter SC, Komhoff M, Peters M, Waldegger S, Seyberth HW: Salt handling in the distal nephron: lessons learned from inherited human disorders. American journal of physiology Regulatory, integrative and comparative physiology 2005, 288(4):R782-795.</ref>
## [[Bartter syndrome]]<ref>Jeck N, Schlingmann KP, Reinalter SC, Komhoff M, Peters M, Waldegger S, Seyberth HW: Salt handling in the distal nephron: lessons learned from inherited human disorders. American journal of physiology Regulatory, integrative and comparative physiology 2005, 288(4):R782-795.</ref>
## [[Cystinosis]]<ref>Knoepfelmacher M1, Rocha R, Salgado LR, et al. [Nephropathic cystinosis: report of 2 cases and review of the literature]. Rev Assoc Med Bras 1994; 40:43.
## [[Cystinosis]]<ref>Knoepfelmacher M1, Rocha R, Salgado LR, et al. [Nephropathic cystinosis: report of 2 cases and review of the literature]. Rev Assoc Med Bras 1994; 40:43.
# '''[[Primary Polydipsia]]'''


===Causes by Organ System===
===Causes by Organ System===

Revision as of 23:43, 5 June 2018

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Resident
Survival
Guide
Polyuria
ICD-10 R35
ICD-9 788.42

Template:Search infobox Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1] Phone:617-632-7753;

To view a comprehensive algorithm of common findings of urine composition and urine output, click here
Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Overview

Polyuria is the passage of a large volume of urine in a given period (>= 2.5L/24 hours in adult humans) [2] It often appears with increased thrist (polydipsia), though it is possible to have one without the other.

Causes

  1. Central diabetes inspidous (CDI)
    1. Idiopathic CDI: the most common cause of CDI[1][2]
    2. Familial CDI[3]
    3. Wolfram syndrome ( DIDOMAD syndrome)[4]
    4. Congenital hypopituitarism[5]
    5. Septo-optic dysplasia[6]
    6. Surgery/trauma[7]
    7. Cancer (lung cancer, leukemia, lymphoma)[1]
    8. Hypoxic encephalopathy[8]
    9. Infiltrative disorders ( histiocytosis X, sarcoidosis, granulomatosis with polyangiitis)[9][10]
    10. Post-supraventricular tachycardia[11][12]
    11. Anorexia nervosa[13]
  2. Nephrogenic diabetes inspidous (NDI)
    1. Hereditary NDI[14][15]
    2. Lithium[16]
    3. Hypercalcemia[17][18]
    4. Hypokalemia[19][20]
    5. Renal disease:
      1. Bilateral urinary tract obstruction[21]
      2. Medullary cystic kidney disease[22]
      3. Amyloidosis[23]
      4. Sjogren's syndrome[24]
      5. Autosomal dominant polycystic kidney disease[22]
      6. Sickle cell disease[25]
    6. Medications:
      1. Cidofovir[26]
      2. Foscarnet[27]
      3. Amphotericin B
      4. Demeclocycline
      5. Ifosfamide
      6. Ofloxacin
      7. Orlistat
      8. Didanosine[28]
      9. V2 receptor antagonists[29]
    7. Gestational diabetes inspidous[30][31]
    8. Craniopharyngioma surgery[32]
    9. Bardet-biedl syndrome[33]
    10. Bartter syndrome[34]
    11. Cystinosis [35]

Abbreviations: Na= Natrium/ Sodium, ADH= Antidiuretic hormone


POLYURIA[36]

Mechanism Etiology Clinical manifestations Paraclinical findings Comments
Symptoms and signs Lab findings/Urine exam
Dysuria Nocturia Hesitancy Dribbling Hematuria Proteinuria Serum osmolarity S. ADH Urine osmolarity Water deprivation test ADH administration
Increased intake of fluid Psychogenic polydipsia[37] – – – – – – Normal Normal Low Improves urine osmolarity No improvement Increased thirst
Increased solute excretion Osmotic causes Diabetes mellitus[38] – ± – – – Late stage High in Type 2 Normal Normal No effect No effect Hyperosmolar hyperglycemic state
Salt loss Diuretics – + – + – ± Normal Raised[39] Normal, increased with thiazides[40] No effect No effect
Cerebral salt-wasting syndrome[41] – – – – – – Normal Normal Low Improves urine osmolarity No effect
Impaired urinary concentration Low ADH Central diabetes insipidus – + – – ± ± Increased Low Low No improvement Urine osmolarity improves
Nephrogenic diabetes insipidus – + – – ± ± Increased Normal Low No improvement No improvement
Renal disease Renal tubular acidosis[42] ± ±[43] – – ± + Increased
Bartter syndrome
Miscellaneous Benign Prostatic Hyperplasia (BPH)[44] + + + + ± – Normal

References

  1. ↑ 1.0 1.1 Kimmel DW, O'Neill BP: Systemic cancer presenting as diabetes insipidus. Clinical and radiographic features of 11 patients with a review of metastatic-induced diabetes insipidus. Cancer 1983, 52(12):2355-2358.
  2. ↑ Maghnie M, Cosi G, Genovese E, Manca-Bitti ML, Cohen A, Zecca S, Tinelli C, Gallucci M, Bernasconi S, Boscherini B et al: Central diabetes insipidus in children and young adults. The New England journal of medicine 2000, 343(14):998-1007.
  3. ↑ Christensen JH, Rittig S: Familial neurohypophyseal diabetes insipidus--an update. Seminars in nephrology 2006, 26(3):209-223.
  4. ↑ Bischoff AN, Reiersen AM, Buttlaire A, Al-Lozi A, Doty T, Marshall BA, Hershey T: Selective cognitive and psychiatric manifestations in Wolfram Syndrome. Orphanet journal of rare diseases 2015, 10:66.
  5. ↑ Lukezic M, Righini V, Di Natale B, De Angelis R, Norbiato G, Bevilacqua M, Chiumello G: Vasopressin and thirst in patients with posterior pituitary ectopia and hypopituitarism. Clinical endocrinology 2000, 53(1):77-83.
  6. ↑ Hoyt WF, Kaplan SL, Grumbach MM, Glaser JS: Septo-optic dysplasia and pituitary dwarfism. Lancet (London, England) 1970, 1(7652):893-894.
  7. ↑ Nemergut EC, Zuo Z, Jane JA, Jr., Laws ER, Jr.: Predictors of diabetes insipidus after transsphenoidal surgery: a review of 881 patients. Journal of neurosurgery 2005, 103(3):448-454.
  8. ↑ Wickramasinghe LS, Chazan BI, Mandal AR, Baylis PH, Russell I: Cranial diabetes insipidus after upper gastrointestinal hemorrhage. British medical journal (Clinical research ed) 1988, 296(6627):969.
  9. ↑ Dunger DB, Broadbent V, Yeoman E, Seckl JR, Lightman SL, Grant DB, Pritchard J: The frequency and natural history of diabetes insipidus in children with Langerhans-cell histiocytosis. The New England journal of medicine 1989, 321(17):1157-1162.
  10. ↑ Garovic VD, Clarke BL, Chilson TS, Specks U: Diabetes insipidus and anterior pituitary insufficiency as presenting features of Wegener's granulomatosis. American journal of kidney diseases : the official journal of the National Kidney Foundation 2001, 37(1):E5.
  11. ↑ Canepa-Anson R, Williams M, Marshall J, Mitsuoka T, Lightman S, Sutton R: Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia. British medical journal (Clinical research ed) 1984, 289(6449):866-868.
  12. ↑ Fujii T, Kojima S, Imanishi M, Ohe T, Omae T: Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia. The American journal of cardiology 1991, 68(4):343-348.
  13. ↑ Gold PW, Kaye W, Robertson GL, Ebert M: Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa. The New England journal of medicine 1983, 308(19):1117-1123.
  14. ↑ van Lieburg AF, Knoers NV, Monnens LA: Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus. Journal of the American Society of Nephrology : JASN 1999, 10(9):1958-1964.
  15. ↑ van Lieburg AF, Knoers NV, Monnens LA: Clinical presentation and follow-up of 30 patients with congenital nephrogenic diabetes insipidus. Journal of the American Society of Nephrology : JASN 1999, 10(9):1958-1964.
  16. ↑ Grunfeld JP, Rossier BC: Lithium nephrotoxicity revisited. Nature reviews Nephrology 2009, 5(5):270-276.
  17. ↑ Berl T: The cAMP system in vasopressin-sensitive nephron segments of the vitamin D-treated rat. Kidney international 1987, 31(5):1065-1071.
  18. ↑ Peterson LN, McKay AJ, Borzecki JS: Endogenous prostaglandin E2 mediates inhibition of rat thick ascending limb Cl reabsorption in chronic hypercalcemia. The Journal of clinical investigation 1993, 91(6):2399-2407.
  19. ↑ Marples D, Frokiaer J, Dorup J, Knepper MA, Nielsen S: Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex. The Journal of clinical investigation 1996, 97(8):1960-1968.
  20. ↑ Jung JY, Madsen KM, Han KH, Yang CW, Knepper MA, Sands JM, Kim J: Expression of urea transporters in potassium-depleted mouse kidney. American journal of physiology Renal physiology 2003, 285(6):F1210-1224.
  21. ↑ Frokiaer J, Marples D, Knepper MA, Nielsen S: Bilateral ureteral obstruction downregulates expression of vasopressin-sensitive AQP-2 water channel in rat kidney. The American journal of physiology 1996, 270(4 Pt 2):F657-668.
  22. ↑ 22.0 22.1 Gabow PA, Kaehny WD, Johnson AM, Duley IT, Manco-Johnson M, Lezotte DC, Schrier RW: The clinical utility of renal concentrating capacity in polycystic kidney disease. Kidney international 1989, 35(2):675-680.
  23. ↑ Carone FA, Epstein FH: Nephrogenic diabetes insipidus caused by amyloid disease. Evidence in man of the role of the collecting ducts in concentrating urine. The American journal of medicine 1960, 29:539-544.
  24. ↑ Shearn MA, Tu WH: NEPHROGENIC DIABETIC INSIPIDUS AND OTHER DEFECTS OF RENAL TUBULAR FUNCTION IN SJOERGREN'S SYNDROME. The American journal of medicine 1965, 39:312-318.
  25. ↑ Scolari F, Caridi G, Rampoldi L, Tardanico R, Izzi C, Pirulli D, Amoroso A, Casari G, Ghiggeri GM: Uromodulin storage diseases: clinical aspects and mechanisms. American journal of kidney diseases : the official journal of the National Kidney Foundation 2004, 44(6):987-999.
  26. ↑ Schliefer K, Rockstroh JK, Spengler U, Sauerbruch T: Nephrogenic diabetes insipidus in a patient taking cidofovir. Lancet (London, England) 1997, 350(9075):413-414.
  27. ↑ Navarro JF, Quereda C, Quereda C, Gallego N, Antela A, Mora C, Ortuno J: Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy. American journal of kidney diseases : the official journal of the National Kidney Foundation 1996, 27(3):431-434.
  28. ↑ D'Ythurbide G, Goujard C, Mechai F, Blanc A, Charpentier B, Snanoudj R: Fanconi syndrome and nephrogenic diabetes insipidus associated with didanosine therapy in HIV infection: a case report and literature review. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2007, 22(12):3656-3659.
  29. ↑ Schrier RW, Gross P, Gheorghiade M, Berl T, Verbalis JG, Czerwiec FS, Orlandi C: Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. The New England journal of medicine 2006, 355(20):2099-2112.
  30. ↑ Brewster UC, Hayslett JP: Diabetes insipidus in the third trimester of pregnancy. Obstetrics and gynecology 2005, 105(5 Pt 2):1173-1176.
  31. ↑ Aleksandrov N, Audibert F, Bedard MJ, Mahone M, Goffinet F, Kadoch IJ: Gestational diabetes insipidus: a review of an underdiagnosed condition. Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstetrique et gynecologie du Canada : JOGC 2010, 32(3):225-231.
  32. ↑ Ghirardello S, Hopper N, Albanese A, Maghnie M: Diabetes insipidus in craniopharyngioma: postoperative management of water and electrolyte disorders. Journal of pediatric endocrinology & metabolism : JPEM 2006, 19 Suppl 1:413-421.
  33. ↑ Anadoliiska A, Roussinov D: Clinical aspects of renal involvement in Bardet-Biedl syndrome. International urology and nephrology 1993, 25(5):509-514.
  34. ↑ Jeck N, Schlingmann KP, Reinalter SC, Komhoff M, Peters M, Waldegger S, Seyberth HW: Salt handling in the distal nephron: lessons learned from inherited human disorders. American journal of physiology Regulatory, integrative and comparative physiology 2005, 288(4):R782-795.
  35. ↑ Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X
  36. ↑ Bhasin, Bhavna; Velez, Juan Carlos Q. (2016). "Evaluation of Polyuria: The Roles of Solute Loading and Water Diuresis". American Journal of Kidney Diseases. 67 (3): 507–511. doi:10.1053/j.ajkd.2015.10.021. ISSN 0272-6386.
  37. ↑ Mellinger RC, Zafar MS (1983). "Primary polydipsia. Syndrome of inappropriate thirst". Arch Intern Med. 143 (6): 1249–51. PMID 6860053.
  38. ↑ Ahloulay M, Schmitt F, Déchaux M, Bankir L (1999). "Vasopressin and urinary concentrating activity in diabetes mellitus". Diabetes Metab. 25 (3): 213–22. PMID 10499190.
  39. ↑ Hwang KS, Kim GH (2010). "Thiazide-induced hyponatremia". Electrolyte Blood Press. 8 (1): 51–7. doi:10.5049/EBP.2010.8.1.51. PMC 3041494. PMID 21468197.
  40. ↑ Loffing, J. (2004). "Paradoxical Antidiuretic Effect of Thiazides in Diabetes Insipidus: Another Piece in the Puzzle". Journal of the American Society of Nephrology. 15 (11): 2948–2950. doi:10.1097/01.ASN.0000146568.82353.04. ISSN 1046-6673.
  41. ↑ Ozdemir H, Aycan Z, Degerliyurt A, Metin A (2010). "The treatment of cerebral salt wasting with fludrocortisone in a child with lissencephaly". Turk Neurosurg. 20 (1): 100–2. PMID 20066633.
  42. ↑ Pereira PC, Miranda DM, Oliveira EA, Silva AC (2009). "Molecular pathophysiology of renal tubular acidosis". Curr Genomics. 10 (1): 51–9. doi:10.2174/138920209787581262. PMC 2699831. PMID 19721811.
  43. ↑ Ranawaka R, Dayasiri K, Gamage M (2017). "A child with distal (type 1) renal tubular acidosis presenting with progressive gross motor developmental regression and acute paralysis". BMC Res Notes. 10 (1): 618. doi:10.1186/s13104-017-2949-2. PMC 5702097. PMID 29178965.
  44. ↑ Yoong HF, Sundaram MB, Aida Z (2005). "Prevalence of nocturnal polyuria in patients with benign prostatic hyperplasia". Med J Malaysia. 60 (3): 294–6. PMID 16379182.


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