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Increased blood urea nitrogen

MedGen UID:
760252
Concept ID:
C0151539
Finding
Synonyms: Increased blood urea nitrogen (BUN); Increased BUN
 
HPO: HP:0003138

Definition

An increased amount of nitrogen in the form of urea in the blood. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Increased blood urea nitrogen

Conditions with this feature

Familial dysautonomia
MedGen UID:
41678
Concept ID:
C0013364
Disease or Syndrome
Familial dysautonomia, which affects the development and survival of sensory, sympathetic, and parasympathetic neurons, is a debilitating disorder present from birth. Neuronal degeneration progresses throughout life. Affected individuals have gastrointestinal dysfunction, autonomic crises (i.e., hypertensive vomiting attacks), recurrent pneumonia, altered pain sensitivity, altered temperature perception, and blood pressure instability. Hypotonia contributes to delay in acquisition of motor milestones. Optic neuropathy results in progressive vision loss. Older individuals often have a broad-based and ataxic gait that deteriorates over time. Developmental delay / intellectual disability occur in about 21% of individuals. Life expectancy is decreased.
Anti-glomerular basement membrane disease
MedGen UID:
140788
Concept ID:
C0403529
Disease or Syndrome
A rare, fulminant small vessel vasculitis that affects the capillary beds of the kidneys and lungs and characterized by the presence of anti-glomerular basement membrane (GBM) and, in its full-blown form, anti-alveolar basement membrane (ABM) antibodies. Consequently, it may manifest as a rapidly progressive, isolated glomerulonephritis (anti-GBM nephritis) or as a pulmonary-renal syndrome with severe lung hemorrhage.
Upshaw-Schulman syndrome
MedGen UID:
224783
Concept ID:
C1268935
Disease or Syndrome
Hereditary thrombotic thrombocytopenic purpura (TTP), also known as Upshaw-Schulman syndrome (USS), is a rare autosomal recessive thrombotic microangiopathy (TMA). Clinically, acute phases of TTP are defined by microangiopathic mechanical hemolytic anemia, severe thrombocytopenia, and visceral ischemia. Hereditary TTP makes up 5% of TTP cases and is caused mostly by biallelic mutation in the ADAMTS13 gene, or in very rare cases, by monoallelic ADAMTS13 mutation associated with a cluster of single-nucleotide polymorphisms (SNPs); most cases of all TTP (95%) are acquired via an autoimmune mechanism (see 188030). Hereditary TTP is more frequent among child-onset TTP compared with adult-onset TTP, and its clinical presentation is significantly different as a function of its age of onset. Child-onset TTP usually starts in the neonatal period with hematological features and severe jaundice. In contrast, almost all cases of adult-onset hereditary TTP are unmasked during the first pregnancy of a woman whose disease was silent during childhood (summary by Joly et al., 2018).
Hemolytic uremic syndrome, atypical, susceptibility to, 1
MedGen UID:
412743
Concept ID:
C2749604
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
Atypical hemolytic-uremic syndrome with thrombomodulin anomaly
MedGen UID:
414541
Concept ID:
C2752036
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
Atypical hemolytic-uremic syndrome with C3 anomaly
MedGen UID:
442875
Concept ID:
C2752037
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
Atypical hemolytic-uremic syndrome with B factor anomaly
MedGen UID:
416691
Concept ID:
C2752038
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
Atypical hemolytic-uremic syndrome with I factor anomaly
MedGen UID:
414542
Concept ID:
C2752039
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
Atypical hemolytic-uremic syndrome with MCP/CD46 anomaly
MedGen UID:
414167
Concept ID:
C2752040
Finding
Hemolytic-uremic syndrome (HUS) is characterized by hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney and other organs. The onset of atypical HUS (aHUS) ranges from the neonatal period to adulthood. Genetic aHUS accounts for an estimated 60% of all aHUS. Individuals with genetic aHUS frequently experience relapse even after complete recovery following the presenting episode; 60% of genetic aHUS progresses to end-stage renal disease (ESRD).
46,XY sex reversal 4
MedGen UID:
416704
Concept ID:
C2752149
Congenital Abnormality
Sex reversal in an individual associated with a 9p24.3 deletion.
Hyperuricemia, pulmonary hypertension, renal failure, alkalosis syndrome
MedGen UID:
462559
Concept ID:
C3151209
Disease or Syndrome
HUPRA syndrome is a severe autosomal recessive multisystem disorder characterized by onset in infancy of progressive renal failure leading to electrolyte imbalances, metabolic alkalosis, pulmonary hypertension, hypotonia, and delayed development. Affected individuals are born prematurely (summary by Belostotsky et al., 2011).
Karyomegalic interstitial nephritis
MedGen UID:
766688
Concept ID:
C3553774
Disease or Syndrome
Karyomegalic tubulointerstitial nephritis (KMIN) is a rare kidney disease characterized clinically by onset in the third decade of progressive renal failure. Renal biopsy shows chronic tubulointerstitial nephritis and interstitial fibrosis associated with enlarged and atypical tubular epithelial cell nuclei (summary by Baba et al., 2006).
Combined oxidative phosphorylation deficiency 34
MedGen UID:
1631307
Concept ID:
C4693450
Disease or Syndrome
COXPD34 is an autosomal recessive disorder resulting from a defect in mitochondrial function. The phenotype is variable, but may include congenital sensorineural deafness, increased serum lactate, and hepatic and renal dysfunction. Neurologic function is relatively preserved (summary by Menezes et al., 2015). For a discussion of genetic heterogeneity of combined oxidative phosphorylation deficiency, see COXPD1 (609060).
Orthostatic hypotension 1
MedGen UID:
1648402
Concept ID:
C4746777
Disease or Syndrome
Dopamine beta-hydroxylase (DBH) deficiency is characterized by lack of sympathetic noradrenergic function but normal parasympathetic and sympathetic cholinergic function. Affected individuals exhibit profound deficits in autonomic regulation of cardiovascular function that predispose to orthostatic hypotension. Although DBH deficiency appears to be present from birth, the diagnosis is not generally recognized until late childhood. The combination of ptosis of the eyelids in infants and children, together with hypotension, is suggestive of the disease. In the perinatal period, DBH deficiency has been complicated by vomiting, dehydration, hypotension, hypothermia, and hypoglycemia requiring repeated hospitalization; children have reduced exercise capacity. By early adulthood, individuals have profound orthostatic hypotension, greatly reduced exercise tolerance, ptosis of the eyelids, and nasal stuffiness. Presyncopal symptoms include dizziness, blurred vision, dyspnea, nuchal discomfort, and chest pain; symptoms may worsen in hot environments or after heavy meals or alcohol ingestion. Life expectancy is unknown, but some affected individuals have lived beyond age 60 years.
Hypermetabolism due to uncoupled mitochondrial oxidative phosphorylation 2
MedGen UID:
1824010
Concept ID:
C5774237
Disease or Syndrome
Hypermetabolism due to uncoupled mitochondrial oxidative phosphorylation-2 (HUMOP2) is characterized by failure to thrive apparent in infancy despite adequate caloric intake. Affected individuals show normal thyroid function, hyperphagia, tachypnea, increased basal temperature, and increased sweating. Biochemical studies demonstrate increased mitochondrial oxygen consumption with inefficient production of ATP in the final steps of oxidative phosphorylation due to an uncoupling defect (Ganetzky et al., 2022). Genetic Heterogeneity of Hypermetabolism due to Uncoupled Mitochondrial Oxidative Phosphorylation See also HUMOP1 (238800).

Professional guidelines

PubMed

Ricci PP, Gregory OJ
Sci Rep 2021 Mar 30;11(1):7185. doi: 10.1038/s41598-021-86686-1. PMID: 33785837Free PMC Article
Siribamrungwong M, Yothasamutr K, Puangpanngam K
Ther Apher Dial 2014 Jun;18(3):305-8. Epub 2013 Sep 30 doi: 10.1111/1744-9987.12105. PMID: 24118730
Ng TM, Ackerbauer KA, Hyderi AF, Hshieh S, Elkayam U
J Cardiovasc Pharmacol Ther 2012 Mar;17(1):79-85. Epub 2011 May 2 doi: 10.1177/1074248411406441. PMID: 21536855

Recent clinical studies

Etiology

Yang H, Cui Z, Quan Z
Metab Syndr Relat Disord 2024 Mar;22(2):114-122. Epub 2023 Nov 10 doi: 10.1089/met.2023.0161. PMID: 37944108
Fu S, Zhang L, Ma F, Xue S, Sun T, Xu Z
Nutrients 2022 Oct 23;14(21) doi: 10.3390/nu14214458. PMID: 36364721Free PMC Article
Kameda T, Shide K, Tahira Y, Sekine M, Sato S, Ishizaki J, Takeuchi M, Akizuki K, Kamiunten A, Shimoda H, Toyama T, Maeda K, Yamashita K, Kawano N, Kawano H, Hidaka T, Yamaguchi H, Kubuki Y, Kitanaka A, Matsuoka H, Shimoda K
Viruses 2022 Mar 29;14(4) doi: 10.3390/v14040710. PMID: 35458440Free PMC Article
Kjaergaard AD, Teumer A, Witte DR, Stanzick KJ, Winkler TW, Burgess S, Ellervik C
Clin Chem 2022 Mar 4;68(3):461-472. doi: 10.1093/clinchem/hvab249. PMID: 34922334Free PMC Article
Li M, Liu X, Zhang Z
Toxicol Ind Health 2021 Sep;37(9):555-563. Epub 2021 Aug 27 doi: 10.1177/07482337211037880. PMID: 34452584

Diagnosis

Yang H, Cui Z, Quan Z
Metab Syndr Relat Disord 2024 Mar;22(2):114-122. Epub 2023 Nov 10 doi: 10.1089/met.2023.0161. PMID: 37944108
Fu S, Zhang L, Ma F, Xue S, Sun T, Xu Z
Nutrients 2022 Oct 23;14(21) doi: 10.3390/nu14214458. PMID: 36364721Free PMC Article
Kameda T, Shide K, Tahira Y, Sekine M, Sato S, Ishizaki J, Takeuchi M, Akizuki K, Kamiunten A, Shimoda H, Toyama T, Maeda K, Yamashita K, Kawano N, Kawano H, Hidaka T, Yamaguchi H, Kubuki Y, Kitanaka A, Matsuoka H, Shimoda K
Viruses 2022 Mar 29;14(4) doi: 10.3390/v14040710. PMID: 35458440Free PMC Article
Kjaergaard AD, Teumer A, Witte DR, Stanzick KJ, Winkler TW, Burgess S, Ellervik C
Clin Chem 2022 Mar 4;68(3):461-472. doi: 10.1093/clinchem/hvab249. PMID: 34922334Free PMC Article
Bae SJ, Kim K, Yun SJ, Lee SH
Am J Emerg Med 2021 Mar;41:152-157. Epub 2020 Dec 23 doi: 10.1016/j.ajem.2020.12.022. PMID: 33465709

Therapy

Yang H, Cui Z, Quan Z
Metab Syndr Relat Disord 2024 Mar;22(2):114-122. Epub 2023 Nov 10 doi: 10.1089/met.2023.0161. PMID: 37944108
Fu S, Zhang L, Ma F, Xue S, Sun T, Xu Z
Nutrients 2022 Oct 23;14(21) doi: 10.3390/nu14214458. PMID: 36364721Free PMC Article
Kim DH, Choi HI, Park JS, Kim CS, Bae EH, Ma SK, Kim SW
Redox Biol 2022 Aug;54:102382. Epub 2022 Jun 23 doi: 10.1016/j.redox.2022.102382. PMID: 35767918Free PMC Article
Kjaergaard AD, Teumer A, Witte DR, Stanzick KJ, Winkler TW, Burgess S, Ellervik C
Clin Chem 2022 Mar 4;68(3):461-472. doi: 10.1093/clinchem/hvab249. PMID: 34922334Free PMC Article
Elfar A, Sambandam KK
Curr Heart Fail Rep 2017 Aug;14(4):311-320. doi: 10.1007/s11897-017-0344-x. PMID: 28674911

Prognosis

Yang H, Cui Z, Quan Z
Metab Syndr Relat Disord 2024 Mar;22(2):114-122. Epub 2023 Nov 10 doi: 10.1089/met.2023.0161. PMID: 37944108
Fu S, Zhang L, Ma F, Xue S, Sun T, Xu Z
Nutrients 2022 Oct 23;14(21) doi: 10.3390/nu14214458. PMID: 36364721Free PMC Article
Kameda T, Shide K, Tahira Y, Sekine M, Sato S, Ishizaki J, Takeuchi M, Akizuki K, Kamiunten A, Shimoda H, Toyama T, Maeda K, Yamashita K, Kawano N, Kawano H, Hidaka T, Yamaguchi H, Kubuki Y, Kitanaka A, Matsuoka H, Shimoda K
Viruses 2022 Mar 29;14(4) doi: 10.3390/v14040710. PMID: 35458440Free PMC Article
Kjaergaard AD, Teumer A, Witte DR, Stanzick KJ, Winkler TW, Burgess S, Ellervik C
Clin Chem 2022 Mar 4;68(3):461-472. doi: 10.1093/clinchem/hvab249. PMID: 34922334Free PMC Article
Bae SJ, Kim K, Yun SJ, Lee SH
Am J Emerg Med 2021 Mar;41:152-157. Epub 2020 Dec 23 doi: 10.1016/j.ajem.2020.12.022. PMID: 33465709

Clinical prediction guides

Yang H, Cui Z, Quan Z
Metab Syndr Relat Disord 2024 Mar;22(2):114-122. Epub 2023 Nov 10 doi: 10.1089/met.2023.0161. PMID: 37944108
Mehri A, Sotoodeh Ghorbani S, Farhadi-Babadi K, Rahimi E, Barati Z, Taherpour N, Izadi N, Shahbazi F, Mokhayeri Y, Seifi A, Fallah S, Feyzi R, Etemed K, Hashemi Nazari SS
J Intensive Care Med 2023 Sep;38(9):825-837. Epub 2023 Mar 28 doi: 10.1177/08850666231166344. PMID: 36976873Free PMC Article
Fu S, Zhang L, Ma F, Xue S, Sun T, Xu Z
Nutrients 2022 Oct 23;14(21) doi: 10.3390/nu14214458. PMID: 36364721Free PMC Article
Kjaergaard AD, Teumer A, Witte DR, Stanzick KJ, Winkler TW, Burgess S, Ellervik C
Clin Chem 2022 Mar 4;68(3):461-472. doi: 10.1093/clinchem/hvab249. PMID: 34922334Free PMC Article
Bae SJ, Kim K, Yun SJ, Lee SH
Am J Emerg Med 2021 Mar;41:152-157. Epub 2020 Dec 23 doi: 10.1016/j.ajem.2020.12.022. PMID: 33465709

Recent systematic reviews

Mehri A, Sotoodeh Ghorbani S, Farhadi-Babadi K, Rahimi E, Barati Z, Taherpour N, Izadi N, Shahbazi F, Mokhayeri Y, Seifi A, Fallah S, Feyzi R, Etemed K, Hashemi Nazari SS
J Intensive Care Med 2023 Sep;38(9):825-837. Epub 2023 Mar 28 doi: 10.1177/08850666231166344. PMID: 36976873Free PMC Article
Novis BK, Roizen MF, Aronson S, Thisted RA
Anesth Analg 1994 Jan;78(1):143-9. doi: 10.1213/00000539-199401000-00023. PMID: 8267150

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