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Urinary retention

MedGen UID:
Concept ID:
Functional Concept
Synonyms: Retention, Urinary; Urinary Retention
SNOMED CT: Not passing urine (267064002); Retention of urine (267064002); Unable to pass urine (267064002); Urinary retention (267064002); Cannot pass urine - retention (267064002); Unable to empty bladder (267064002); Urine retention (1251594002); Unable to void urine (449491000124101); Unable to pass urine (449491000124101)
HPO: HP:0000016


Inability to completely empty the urinary bladder during the process of urination. [from HPO]

Conditions with this feature

Acute intermittent porphyria
MedGen UID:
Concept ID:
Disease or Syndrome
Acute intermittent porphyria (AIP), an autosomal dominant disorder, occurs in heterozygotes for an HMBS pathogenic variant that causes reduced activity of the enzyme porphobilinogen deaminase. AIP is considered "overt" in a heterozygote who was previously or is currently symptomatic; AIP is considered "latent" in a heterozygote who has never had symptoms, and typically has been identified during molecular genetic testing of at-risk family members. Note that GeneReviews does not use the term "carrier" for an individual who is heterozygous for an autosomal dominant pathogenic variant; GeneReviews reserves the term "carrier" for an individual who is heterozygous for an autosomal recessive disorder and thus is not expected to ever develop manifestations of the disorder. Overt AIP is characterized clinically by life-threatening acute neurovisceral attacks of severe abdominal pain without peritoneal signs, often accompanied by nausea, vomiting, tachycardia, and hypertension. Attacks may be complicated by neurologic findings (mental changes, convulsions, and peripheral neuropathy that may progress to respiratory paralysis), and hyponatremia. Acute attacks, which may be provoked by certain drugs, alcoholic beverages, endocrine factors, calorie restriction, stress, and infections, usually resolve within two weeks. Most individuals with AIP have one or a few attacks; about 3%-8% (mainly women) have recurrent attacks (defined as >3 attacks/year) that may persist for years. Other long-term complications are chronic renal failure, hepatocellular carcinoma (HCC), and hypertension. Attacks, which are very rare before puberty, are more common in women than men. Latent AIP. While all individuals heterozygous for an HMBS pathogenic variant that predisposes to AIP are at risk of developing overt AIP, most have latent AIP and never have symptoms.
Fatal familial insomnia
MedGen UID:
Concept ID:
Disease or Syndrome
Genetic prion disease generally manifests with cognitive difficulties, ataxia, and myoclonus (abrupt jerking movements of muscle groups and/or entire limbs). The order of appearance and/or predominance of these features and other associated neurologic and psychiatric findings vary. The three major phenotypes of genetic prion disease are genetic Creutzfeldt-Jakob disease (gCJD), fatal familial insomnia (FFI), and Gerstmann-Sträussler-Scheinker (GSS) syndrome. Although these phenotypes display overlapping clinical and pathologic features, recognition of these phenotypes can be useful when providing affected individuals and their families with information about the expected clinical course. The age at onset typically ranges from 50 to 60 years. The disease course ranges from a few months in gCJD and FFI to a few (up to 4, and in rare cases up to 10) years in GSS syndrome.
Sacral defect with anterior meningocele
MedGen UID:
Concept ID:
Disease or Syndrome
Sacral defect with anterior meningocele (SDAM) is a form of caudal dysgenesis. It is present at birth and becomes symptomatic later in life, usually because of obstructive labor in females, chronic constipation, or meningitis. Inheritance is autosomal dominant (Chatkupt et al., 1994). Welch and Aterman (1984) gave a population frequency of 0.14%. Caudal dysgenesis syndrome and caudal regression syndrome are broad terms that refer to a heterogeneous constellation of congenital caudal anomalies affecting the caudal spine and spinal cord, the hindgut, the urogenital system, and the lower limbs. Approximately 15 to 25% of mothers of children with caudal dysgenesis have insulin-dependent diabetes mellitus (222100) (Lynch et al., 2000). See also Currarino syndrome (176450), a similar disorder caused by mutation in the HLXB9 gene (142994) on chromosome 7q36. Currarino syndrome classically comprises the triad of hemisacrum, anorectal malformation, and presacral mass. However, Currarino syndrome also shows phenotypic variability: Lynch et al. (2000) stated that there is variable expressivity of clinical features and that some patients with Currarino syndrome are asymptomatic. Kochling et al. (2001) found the complete triad of Currarino syndrome in only 8 of 23 patients with mutations in the HLXB9 gene, These reports suggest that some patients previously reported as having forms of sacral agenesis, including SDAM, may have had Currarino syndrome and vice versa. See also spina bifida (182940), which can be seen in some patients with sacral agenesis or caudal regression syndrome and may be etiologically related.
Intellectual disability, autosomal dominant 54
MedGen UID:
Concept ID:
Mental or Behavioral Dysfunction
Visceral myopathy 1
MedGen UID:
Concept ID:
Disease or Syndrome
ACTG2 visceral myopathy is a disorder of smooth muscle dysfunction of the bladder and gastrointestinal system with phenotypic spectrum that ranges from mild to severe. Bladder involvement can range from neonatal megacystis and megaureter (with its most extreme form of prune belly syndrome) at the more severe end, to recurrent urinary tract infections and bladder dysfunction at the milder end. Intestinal involvement can range from malrotation, neonatal manifestations of microcolon, megacystis microcolon intestinal hypoperistalsis syndrome, and chronic intestinal pseudoobstruction (CIPO) in neonates at the more severe end to intermittent abdominal distention and functional intestinal obstruction at the milder end. Affected infants (with or without evidence of intestinal malrotation) often present with feeding intolerance and findings of non-mechanical bowel obstruction that persist after successful surgical correction of malrotation. Individuals who develop manifestations of CIPO in later childhood or adulthood often experience episodic waxing and waning of bowel motility. They may undergo frequent abdominal surgeries (perhaps related to malrotation or adhesions causing mechanical obstruction) resulting in resection of dilated segments of bowel, often becoming dependent on total parenteral nutrition (TPN).
Autosomal recessive complex spastic paraplegia type 9B
MedGen UID:
Concept ID:
Disease or Syndrome
Autosomal recessive SPG9B is a neurologic disorder characterized by early-onset complex spastic paraplegia. Affected individuals had delayed psychomotor development, intellectual disability, and severe motor impairment. More variable features include dysmorphic facial features, tremor, and urinary incontinence (summary by Coutelier et al., 2015). For a discussion of genetic heterogeneity of autosomal recessive SPG, see SPG5A (270800).

Professional guidelines


De La Cruz MS, Buchanan EM
Am Fam Physician 2017 Jan 15;95(2):100-107. PMID: 28084714
Coker TJ, Dierfeldt DM
Am Fam Physician 2016 Jan 15;93(2):114-20. PMID: 26926407
Casazza BA
Am Fam Physician 2012 Feb 15;85(4):343-50. PMID: 22335313

Recent systematic reviews

Memtsoudis SG, Cozowicz C, Bekeris J, Bekere D, Liu J, Soffin EM, Mariano ER, Johnson RL, Hargett MJ, Lee BH, Wendel P, Brouillette M, Go G, Kim SJ, Baaklini L, Wetmore D, Hong G, Goto R, Jivanelli B, Argyra E, Barrington MJ, Borgeat A, De Andres J, Elkassabany NM, Gautier PE, Gerner P, Gonzalez Della Valle A, Goytizolo E, Kessler P, Kopp SL, Lavand'Homme P, MacLean CH, Mantilla CB, MacIsaac D, McLawhorn A, Neal JM, Parks M, Parvizi J, Pichler L, Poeran J, Poultsides LA, Sites BD, Stundner O, Sun EC, Viscusi ER, Votta-Velis EG, Wu CL, Ya Deau JT, Sharrock NE
Br J Anaesth 2019 Sep;123(3):269-287. Epub 2019 Jul 24 doi: 10.1016/j.bja.2019.05.042. PMID: 31351590Free PMC Article
Jackson J, Davies P, Leggett N, Nugawela MD, Scott LJ, Leach V, Richards A, Blacker A, Abrams P, Sharma J, Donovan J, Whiting P
BJS Open 2019 Feb;3(1):11-23. Epub 2018 Nov 19 doi: 10.1002/bjs5.50114. PMID: 30734011Free PMC Article
Anim-Somuah M, Smyth RM, Cyna AM, Cuthbert A
Cochrane Database Syst Rev 2018 May 21;5(5):CD000331. doi: 10.1002/14651858.CD000331.pub4. PMID: 29781504Free PMC Article
Simmons SW, Taghizadeh N, Dennis AT, Hughes D, Cyna AM
Cochrane Database Syst Rev 2012 Oct 17;10(10):CD003401. doi: 10.1002/14651858.CD003401.pub3. PMID: 23076897Free PMC Article
Jones L, Othman M, Dowswell T, Alfirevic Z, Gates S, Newburn M, Jordan S, Lavender T, Neilson JP
Cochrane Database Syst Rev 2012 Mar 14;2012(3):CD009234. doi: 10.1002/14651858.CD009234.pub2. PMID: 22419342Free PMC Article

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