Polyuria

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Resident
Survival
Guide

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Amandeep Singh M.D.[2] Luke Rusowicz-Orazem, B.S., Roshan Dinparasti Saleh M.D.

To view a comprehensive algorithm of common findings of urine composition and urine output, click here

Overview

Polyuria is the passage of a large volume of urine in a given period (>= 2.5L/24 hours in adult humans). It often appears with increased thirst (polydipsia). Various causes of polyuria include

Causes

  1. Central diabetes inispidus (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 insipidus[30][31]
    8. Craniopharyngioma surgery[32]
    9. Bardet-biedl syndrome[33]
    10. Bartter syndrome[34]
    11. Cystinosis[35]
  3. Primary Polydipsia
  4. Osmotic diuresis: Diabetes mellitus

Causes by Organ System

Cardiovascular Cardiorespiratory disease, Circulation, Congestive heart failure, Paroxysmal tachycardia
Chemical/Poisoning 3,3-dichlorobenzidine, Caffeine poisoning, Foscarnet sodium, Frusemide, Juniper tar poisoning, Oak poisoning, Silicon dioxide, Sodium ferrocyanide, Sorbitol
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Amitraz  , BCG vaccine, Bendrofluazide, Bumetanide, Canagliflozin, Conivaptan, Dapagliflozin, Diuretic therapy, Empagliflozin, Goserelin, Hydrochlorothiazide, Isosorbide, Lithium, Mannitol, Nabilone, Phendimetrazine, Probenecid, Tiagabine, Tolvaptan, corticosteroid
Ear Nose Throat Sicca syndrome
Endocrine Adrenal adenoma, Adrenal cancer, Adrenal cortex neoplasms, Adrenal gland hyperfunction, Aldosteronism, Conn's disease, Cushing syndrome, Cystinosis, DKA, Ectopic ACTH syndrome, Electrolyte abnormality, Familial hypopituitarism, Fanconi syndrome, Froelich's syndrome, Hair-an syndrome, Hormonal, Hyperadrenalism, Hypercalcemia, Hypercalcuria, Hyperglycemia, Hyperosmolar hyperglycemic nonketotic syndrome, Hyperparathyroidism, Hyperthyroidism, Hypokalemia, Hypokalemic periodic paralysis, Hypopituitarism, Hypothalamic dysfunction, Intermediate cystinosis, Multiple endocrine neoplasia, Panhypopituitarism, Parathyroid cancer, Pheochromocytoma, Pituitary tumors, Postural orthostatic tachycardia syndrome, Primary hyperaldosteronism, Syndrome of inappropriate antidiuretic hormone
Environmental Postobstructive uropathy
Gastroenterologic Gestational diabetes, Rib tumor, Wandering spleen
Genetic Aceruloplasminemia, Amelogenesis imperfeca, Apparent mineralocorticoid excess, Bartter syndrome, Boichis syndrome, Conn's disease, Dend syndrome, East syndrome, Gitelman syndrome, Hair-an syndrome, Hereditary primary fanconi disease, Machado-joseph disease, Senior-loken syndrome, Wolfram's disease
Hematologic Diabetes insipidus  , Diabetes mellitus, Excessive riboflavin, Excessive vitamin d, Hemochromatosis  , Hhns, Hypercalcemia, Hypercalcuria  , Hyperglycemia  , Hyperosmolar hyperglycemic nonketotic syndrome  , Hypervitaminosis a, Hypervitaminosis d, Hypokalemia, Hypokalemic periodic paralysis  , Langerhans cell histiocytosis  , Leukemia, Neurosarcoidosis  , Proximal renal tubular acidosis  , Resolving hematoma, Sickle-cell anemia
Iatrogenic Bcg vaccine, Chemotherapy-induced cystitis, Diuretic therapy, Pelvic lipomatosis  , Radiation cystitis, Radiographic contrast media
Infectious Disease Gonococcal urethritis  , Serratia urinary tract infection  , Streptococcal group b invasive disease  , Urinary tract infection
Musculoskeletal/Orthopedic Back tumor  , Hip cancer  , Pyelonephritis, Secondary bone cancer 
Neurologic Adrenocortical carcinoma, Anorexia nervosa, Cerebral salt-wasting syndrome, Diencephalic syndrome, Migraine, Neurologic damage, Neurosarcoidosis, Olivopontocerebellar atrophy type 3, Postural orthostatic tachycardia syndrome, Psychogenic polydipsia, Seizures
Nutritional/Metabolic Aceruloplasminemia, Dend syndrome, Diabetes insipidus, Diabetes mellitus, Diabetic nephropathy, Excessive riboflavin, Excessive vitamin d, Gestational diabetes, Hhns, Hypervitaminosis a, Hypervitaminosis d, Nephrogenic diabetes insipidus, [Renal tubular transport disorders]], Renal tubulopathy
Obstetric/Gynecologic Ovarian cysts, Premenstrual syndrome, Vagina cancer
Oncologic Adrenal adenoma, Adrenal cancer, Adrenal cortex neoplasms, Adrenal incidentaloma, Adrenocortical carcinoma, Back tumor, Bladder cancer, Chemotherapy-induced cystitis, Conn-louis carcinoma, Conn's adenoma, Ectopic ACTHsyndrome, Erdheim-chester disease, Hip cancer, Leukemia, Parathyroid cancer, Pituitary tumors, Prostate cancer, Prostate conditions, Renal cell cancer, Rib tumor, Secondary bone cancer, Urethral cancer, Uterine leiomyoma, Vagina cancer
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric Anorexia nervosa  , Combat stress reaction  , Generalized anxiety disorder, Seizures
Pulmonary Cardiorespiratory disease, East syndrome  , Heerfordt syndrome 
Renal/Electrolyte Acid-base imbalance, Acute tubular necrosis, Aldosteronism, Alsing syndrome  , Altitude diuresis, Apparent mineralocorticoid excess  , Bartter syndrome  , Boichis syndrome  , Cerebral salt-wasting syndrome, Chronic glomerulonephritis, Chronic interstitial nephritis, Chronic kidney disease  , Chronic renal failure, Chronic wasting disease , Cystitis  , Danubian endemic familial nephropathy, Diabetic nephropathy  , Early chronic pyelonephritis, Electrolyte abnormality  , Eosinophilic cystitis, Gitelman syndrome  , Glomerulonephritis  , Interstitial cystitis, Juvenile nephronophthisis  , Medullary cystic kidney disease  , Megalocytic interstitial nephritis  , Membranoproliferative glomerulonephritis , Nephrocalcinosis  , Nephrogenic diabetes insipidus  , Nephrolithiasis , Nephronophthisis, Nephropathic cystinosis  , Oligomeganephronic renal hypoplasia  , Osmotic diuresis, Polycystic kidney disease  , Polydipsia, Primary tubular proximal acidosis  , Proximal renal tubular acidosis  , Proximal tubulopathy, Psychogenic polydipsia, Pyelonephritis, Radiation cystitis, Reflux nephropathy  , Renal cell cancer  , Renal failure, Renal tubular acidosis, Renal tubular transport disorders, Renal tubulopathy , Toni-fanconi syndrome type 1 
Rheumatology/Immunology/Allergy Heerfordt syndrome  , Neurosarcoidosis  , Reiter’s syndrome  , Uterine fibroids 
Sexual No underlying causes
Trauma No underlying causes
Urologic Benign prostatic hyperplasia, Bladder cancer  , Bladder compression, Bladder conditions, Bladder diverticulum, Enlarged prostate  , Noctural polyuria syndrome, Overactive bladder, Pathological water intake, ostobstructive uropathy, rostate cancer, rostate conditions, Sassoon hospital syndrome, Serratia urinary tract infection  rethral cancer , Urethritis  , rinary outflow obstruction, Urinary stones  Urinary tract infection, Uterine fibroids, Uterine leiomyoma 
Miscellaneous No underlying causes

Causes in Alphabetical Order

Differential Diagnosis of Polyuria








 
 
 
 
 
 
 
Polyuria
❑ 24-hour urine volume >3L
❑ 24-hour urine volume >50 ml/kg
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Urine Osmolality >300mosmol
 
 
 
 
 
 
 
Urine Osmolality <300[36]mosmol
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Solute diuresis
❑ Glucose
❑ Mannitol
❑ Contrast media
❑ High protein intake
❑ Diuretics
❑ Medullary cystic disease
❑ Resolving ATN
❑ Resolving obstruction
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Water diuresis
❑ Primary polydipsia
❑ Diabetes inspidous
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Water restriction test OR administration of hypertonic saline 0.05 mL/kg/min for 2 h
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Water restriction test
❑ Overnight fluid restriction should be avoided
❑ Recommend the patient to stop drinking 2-3 hours before coming to clinic
❑ Meaure urine volume every hour
❑ Measure urine osmolality every hour
❑ Measure plasma sodium concentration every 2 hours
❑ Measure plasma osmolality every 2 hours
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Test endpoints in adults:
❑ Urine osmolality reaches normal value (above 600 mosmol/kg)[means that ADH release and effect are intact]
❑ The urine osmolality is stable for 2 or 3 successive hourly measurements despite a rising plasma osmolality
❑ Plasma osmolality >295-300 mosmol/kg
❑ Plasma sodium is 145 or higher
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
In the last 3 settings desmopressin 10mcg intranasal, or 4mcg SC/IV is administered
❑ Measure urine volume and urine osmolality every 30 minutes over the next two hours
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
>100% rise in urine osmolality
 
15-50% rise in urine osmolality after administration of exogenous desmopressin
 
 
<15% rise in urine osmolality
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Complete central diabetes inspidous[37]
 
Partial central DI or partial nephrogenic DI[38]
 
 
complete nephrogenic DI or '''primary polydipsia'''
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check plasma and urine ADH[39]and copeptin prior to administration of exogenous ADH
❑ Increase in plasma/urine ADH in response to rising plasma osmolality excludes central DI
❑ Appropriate elevation in urine osmolality as ADH secretion is increased excludes nephrogenic DI
❑ Copeptin > 21.4 picomol/L differentiates Nephrogenic DI from other etiologies with 100% sensivity and specifity[40]
POLYURIA[41]
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[42] – – – – – – Normal Normal Low Improves urine osmolarity No improvement Increased thirst
Increased solute excretion Osmotic causes Diabetes mellitus[43] – ± – – – Late stage High in type 2 Normal Normal No effect No effect Hyperosmolar hyperglycemic state
Salt loss Diuretics[44][45] – + – + – ± Normal Raised Normal, increased with thiazides No effect No effect –
Cerebral salt-wasting syndrome[46] – – – – – – 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[47][48][49][50] ± ± – – ± + Increased Raised Normal No effect Increases acidification –
Miscellaneous Benign Prostatic Hyperplasia (BPH)[51][52] + + + + ± – Normal Normal Normal No effect Improvement –

Pathophysiology

Central diabetes inspidus (CDI)

  • Results from a deficiency in production, and release of functional AVP, hence respond to administration of exogenous AVP.[53][54]
  • CDI can be acquired or hereditary. ADH-producing cells' injury in hypothalamus/pituitary can be idiopathic, or due to trauma or infection.
  • Hereditary forms of familial CDI can occur secondary to 66 different mutations of the genes encoding AVP-neurophysin II precursor.[55]

Nephrogenic diabetes insipidus (NDI)

  • It results from an inappropriate renal response to AVP and usually reflects a functional defect in V2R or AQP2 protein.[56]
  • Administration of AVP, therefore is not sufficient to rectify the concentration defect. It is more commonly an acquired disease.[57]
  • Over 225 different mutations in AVPR2 represent almost 90% of hereditary NDI cases.

Diabetes mellitus

Primary polydipsia

  • It is presumed that a central defect in thirst regulation has an important role in pathophysiology of polydipsia.
  • In some polydipsia patients for example, the osmotic threshold for thirst is reduced below the threshold for release of AVP.[59]
  • AVP is suppressed by fall in plasma osmolality(because of excessive water intake), and causes rapid excretion of the excess water and continued stimulation of thirst.[60]

Complications

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. ↑ 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.
  36. ↑ Robertson GL: Diabetes insipidus. Endocrinol Metab Clin North Am 24:549–572, 1995.
  37. ↑ Zerbe RL, Robertson GL: A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria. The New England journal of medicine 1981, 305(26):1539-1546.
  38. ↑ Miller M, Dalakos T, Moses AM, Fellerman H, Streeten DH: Recognition of partial defects in antidiuretic hormone secretion. Annals of internal medicine 1970, 73(5):721-729.
  39. ↑ Diederich S, Eckmanns T, Exner P, Al-Saadi N, Bahr V, Oelkers W: Differential diagnosis of polyuric/polydipsic syndromes with the aid of urinary vasopressin measurement in adults. Clinical endocrinology 2001, 54(5):665-671.
  40. ↑ Timper K, Fenske W, Kuhn F, Frech N, Arici B, Rutishauser J, Kopp P, Allolio B, Stettler C, Muller B et al: Diagnostic Accuracy of Copeptin in the Differential Diagnosis of the Polyuria-polydipsia Syndrome: A Prospective Multicenter Study. The Journal of clinical endocrinology and metabolism 2015, 100(6):2268-2274.
  41. ↑ 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.
  42. ↑ Mellinger RC, Zafar MS (1983). "Primary polydipsia. Syndrome of inappropriate thirst". Arch Intern Med. 143 (6): 1249–51. PMID 6860053.
  43. ↑ 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.
  44. ↑ 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.
  45. ↑ 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.
  46. ↑ 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.
  47. ↑ 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.
  48. ↑ 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.
  49. ↑ Bichara M, Mercier O, Houillier P, Paillard M, Leviel F (September 1987). "Effects of antidiuretic hormone on urinary acidification and on tubular handling of bicarbonate in the rat". J. Clin. Invest. 80 (3): 621–30. doi:10.1172/JCI113114. PMC 442283. PMID 3624481.
  50. ↑ Sharman, Andrew; Low, James (2008). "Vasopressin and its role in critical care". Continuing Education in Anaesthesia Critical Care & Pain. 8 (4): 134–137. doi:10.1093/bjaceaccp/mkn021. ISSN 1743-1816.
  51. ↑ 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.
  52. ↑ Jin MH, Moon du G (July 2008). "Practical management of nocturia in urology". Indian J Urol. 24 (3): 289–94. doi:10.4103/0970-1591.42607. PMC 2684373. PMID 19468456.
  53. ↑ Christensen JH, Siggaard C, Rittig S: Autosomal dominant familial neurohypophyseal diabetes insipidus. APMIS Suppl (109):92–95, 2003.
  54. ↑ Fujiwara TM, Bichet DG: Molecular biology of hereditary diabetes insipidus. J Am Soc Nephrol 16:2836–2846, 2005.
  55. ↑ Makaryus AN, McFarlane SI: Diabetes insipidus: diagnosis and treatment of a complex disease. Cleve Clin J Med 73:65–71, 2006.
  56. ↑ Bichet DG: Vasopressin receptor mutations in nephrogenic diabetes insipidus. Semin Nephrol 28:245–251, 2008.
  57. ↑ Moeller HB, Rittig S, Fenton RA: Nephrogenic diabetes insipidus: essential insights into the molecular background and potential therapies for treatment. Endocr Rev 34:278–301, 2013.
  58. ↑ Spira A, Gowrishankar M, Halperin ML: Factors contributing to the degree of polyuria in a patient with poorly controlled diabetes mellitus. American journal of kidney diseases : the official journal of the National Kidney Foundation 1997, 30(6):829-835.
  59. ↑ Illowsky BP, Kirch DG: Polydipsia and hyponatremia in psychiatric patients. The American journal of psychiatry 1988, 145(6):675-683.
  60. ↑ Goldman MB, Luchins DJ, Robertson GL: Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia. The New England journal of medicine 1988, 318(7):397-403.
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