Polyuria
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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.
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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
- Central diabetes inispidus (CDI)
- Idiopathic CDI: the most common cause of CDI[1][2]
- Familial CDI[3]
- Wolfram syndrome ( DIDOMAD syndrome)[4]
- Congenital hypopituitarism[5]
- Septo-optic dysplasia[6]
- Surgery/trauma[7]
- Cancer (lung cancer, leukemia, lymphoma)[1]
- Hypoxic encephalopathy[8]
- Infiltrative disorders ( histiocytosis X, sarcoidosis, granulomatosis with polyangiitis)[9][10]
- Post-supraventricular tachycardia[11][12]
- Anorexia nervosa[13]
- Nephrogenic diabetes inspidous (NDI)
- Hereditary NDI[14][15]
- Lithium[16]
- Hypercalcemia[17][18]
- Hypokalemia[19][20]
- Renal disease:
- Medications:
- Cidofovir[26]
- Foscarnet[27]
- Amphotericin B
- Demeclocycline
- Ifosfamide
- Ofloxacin
- Orlistat
- Didanosine[28]
- V2 receptor antagonists[29]
- Gestational diabetes insipidus[30][31]
- Craniopharyngioma surgery[32]
- Bardet-biedl syndrome[33]
- Bartter syndrome[34]
- Cystinosis[35]
- Primary Polydipsia
- Osmotic diuresis: Diabetes mellitus
Causes by Organ System
Causes in Alphabetical Order
- 3,3-dichlorobenzidine
- Aceruloplasminemia
- Acid-base imbalance
- Acute tubular necrosis
- Adrenal adenoma
- Adrenal cancer
- Adrenal cortex neoplasms
- Adrenal gland hyperfunction
- Adrenal incidentaloma
- Adrenocortical carcinoma
- Aldosteronism
- Alsing syndrome
- Altitude diuresis
- Amelogenesis imperfeca
- Amitraz
- Anorexia nervosa
- Apparent mineralocorticoid excess
- Back tumor
- Bartter syndrome
- BCG vaccine
- Bendrofluazide
- Benign prostatic hyperplasia
- Bladder cancer
- Bladder compression
- Bladder diverticulum
- Boichis syndrome
- Bumetanide
- Caffeine poisoning
- Canagliflozin
- Cardiorespiratory disease
- Cerebral salt-wasting syndrome
- Chemotherapy-induced cystitis
- Chronic glomerulonephritis
- Chronic interstitial nephritis
- Chronic kidney disease
- Chronic renal failure
- Chronic wasting disease
- Combat stress reaction
- Congestive heart failure
- Conivaptan
- Conn-louis carcinoma
- Conn's adenoma
- Conn's syndrome
- Cushing syndrome
- Cushing's syndrome
- Cystinosis
- Cystitis
- Danubian endemic familial nephropathy
- Dapagliflozin
- Dend syndrome
- Diabetes insipidus
- Diabetes mellitus
- Diabetic nephropathy
- Diencephalic syndrome
- Diuretic therapY
- DKA
- Early chronic pyelonephritis
- East syndrome
- Ectopic ACTH syndrome
- Electrolyte abnormality
- Empagliflozin
- Eosinophilic cystitis
- Erdheim-chester syndrome
- Excessive riboflavin
- Excessive vitamin d
- Familial hypopituitarism
- Fanconi syndrome
- Foscarnet sodium
- Froelich's syndrome
- Frusemide
- Generalized anxiety disorder
- Gestational diabetes
- Gitelman syndrome
- Glomerulonephritis
- Gonococcal urethritis
- Goserelin
- Hair-an syndrome
- Heerfordt syndrome
- Hemochromatosis
- Hereditary primary fanconi disease
- Hhns
- Hip cancer
- Hormonal
- Hydrochlorothiazide
- Hyperadrenalism
- Hypercalcemia
- Hypercalcuria
- Hyperglycemia
- Hyperosmolar hyperglycemic nonketotic syndrome
- Hyperosmolarity
- Hyperparathyroidism
- Hyperthyroidism
- Hypervitaminosis a
- Hypervitaminosis d
- Hypokalemia
- Hypokalemic periodic paralysis
- Hypopituitarism
- Hypothalamic dysfunction
- Intermediate cystinosis
- Interstitial cystitis
- Isosorbide
- Juniper tar poisoning
- Juvenile nephronophthisis
- Langerhans cell histiocytosis
- Leukemia
- Lithium
- Machado-joseph disease
- Mannitol
- Medullary cystic kidney disease
- Megalocytic interstitial nephritis
- Membranoproliferative glomerulonephritis
- Migraine
- Multiple endocrine neoplasia
- Nabilone
- Nephrocalcinosis
- Nephrogenic diabetes insipidus
- Nephrolithiasis
- Nephronophthisis
- Nephronophthisis type 1
- Nephropathic cystinosis
- Neurologic damage
- Neurosarcoidosis
- Noctural polyuria syndrome
- Oak poisoning
- Oligomeganephronic renal hypoplasia
- Olivopontocerebellar atrophy type 3
- Osmotic diuresis
- Ovarian cysts
- Overactive bladder
- Panhypopituitarism
- Parathyroid cancer
- Paroxysmal tachycardia
- Pathological water intake
- Pelvic lipomatosis
- Phendimetrazine
- Pheochromocytoma
- Pituitary tumors
- Polycystic kidney disease
- Polydipsia
- Postobstructive uropathy
- Postural orthostatic tachycardia syndrome
- Premenstrual syndrome
- Primary hyperaldosteronism
- Primary tubular proximal acidosis
- Probenecid
- Prostate cancer
- Proximal renal tubular acidosis
- Proximal tubulopathy
- Psychogenic polydipsia
- Pyelonephritis
- Radiation cystitis
- Radiographic contrast media
- Reflux nephropathy
- Reiter’s syndrome
- Renal cell cancer
- Renal failure
- Renal tubular acidosis
- Renal tubular transport disorders
- Resolving hematoma
- Rib tumor
- Sassoon hospital syndrome
- Secondary bone cancer
- Seizures
- Senior-loken syndrome
- Serratia urinary tract infection
- Sicca syndrome
- Sickle-cell anemia
- Silicon dioxide
- Sodium ferrocyanide
- Sorbitol
- Streptococcal group b invasive disease
- Syndrome of inappropriate antidiuretic hormone
- Tiagabine
- Tolvaptan
- Toni-fanconi syndrome type 1
- Urethral cancer
- Urethritis
- Urinary outflow obstruction
- Urinary stones
- Urinary tract infection
- Uterine fibroids
- Uterine leiomyoma
- Vagina cancer
- Wandering spleen
- Wolfram's disease
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
- Glucose-induced osmotic diuresis is the major etiology of polyuria in patients with hyperglycemia.[58]
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
- Polyuria can result in dehydration, hypernatremia and electrolyte abnormalities if the etiology is solute diuresis.
References
- ↑ 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.
- ↑ 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.
- ↑ Christensen JH, Rittig S: Familial neurohypophyseal diabetes insipidus--an update. Seminars in nephrology 2006, 26(3):209-223.
- ↑ 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.
- ↑ 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.
- ↑ Hoyt WF, Kaplan SL, Grumbach MM, Glaser JS: Septo-optic dysplasia and pituitary dwarfism. Lancet (London, England) 1970, 1(7652):893-894.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Grunfeld JP, Rossier BC: Lithium nephrotoxicity revisited. Nature reviews Nephrology 2009, 5(5):270-276.
- ↑ Berl T: The cAMP system in vasopressin-sensitive nephron segments of the vitamin D-treated rat. Kidney international 1987, 31(5):1065-1071.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 22.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Schliefer K, Rockstroh JK, Spengler U, Sauerbruch T: Nephrogenic diabetes insipidus in a patient taking cidofovir. Lancet (London, England) 1997, 350(9075):413-414.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Brewster UC, Hayslett JP: Diabetes insipidus in the third trimester of pregnancy. Obstetrics and gynecology 2005, 105(5 Pt 2):1173-1176.
- ↑ 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.
- ↑ 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.
- ↑ Anadoliiska A, Roussinov D: Clinical aspects of renal involvement in Bardet-Biedl syndrome. International urology and nephrology 1993, 25(5):509-514.
- ↑ 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.
- ↑ 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.
- ↑ Robertson GL: Diabetes insipidus. Endocrinol Metab Clin North Am 24:549–572, 1995.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Mellinger RC, Zafar MS (1983). "Primary polydipsia. Syndrome of inappropriate thirst". Arch Intern Med. 143 (6): 1249–51. PMID 6860053.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Christensen JH, Siggaard C, Rittig S: Autosomal dominant familial neurohypophyseal diabetes insipidus. APMIS Suppl (109):92–95, 2003.
- ↑ Fujiwara TM, Bichet DG: Molecular biology of hereditary diabetes insipidus. J Am Soc Nephrol 16:2836–2846, 2005.
- ↑ Makaryus AN, McFarlane SI: Diabetes insipidus: diagnosis and treatment of a complex disease. Cleve Clin J Med 73:65–71, 2006.
- ↑ Bichet DG: Vasopressin receptor mutations in nephrogenic diabetes insipidus. Semin Nephrol 28:245–251, 2008.
- ↑ 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.
- ↑ 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.
- ↑ Illowsky BP, Kirch DG: Polydipsia and hyponatremia in psychiatric patients. The American journal of psychiatry 1988, 145(6):675-683.
- ↑ 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.