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Decreased circulating renin level

MedGen UID:
337182
Concept ID:
C1845206
Finding
Synonyms: Decreased plasma renin activity; Low plasma renin activity
 
HPO: HP:0003351

Definition

An decreased level of renin in the blood. [from HPO]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • CROGVDecreased circulating renin level

Conditions with this feature

Liddle syndrome
MedGen UID:
67439
Concept ID:
C0221043
Disease or Syndrome
Liddle syndrome is an inherited form of high blood pressure (hypertension). This condition is characterized by severe hypertension that begins unusually early in life, often in childhood, although some affected individuals are not diagnosed until adulthood. Some people with Liddle syndrome have no additional signs or symptoms, especially in childhood. Over time, however, untreated hypertension can lead to heart disease or stroke, which may be fatal.\n\nIn addition to hypertension, affected individuals can have low levels of potassium in the blood (hypokalemia). Signs and symptoms of hypokalemia include muscle weakness or pain, fatigue, constipation, or heart palpitations. The shortage of potassium can also raise the pH of the blood, a condition known as metabolic alkalosis.
Deficiency of steroid 11-beta-monooxygenase
MedGen UID:
82783
Concept ID:
C0268292
Disease or Syndrome
Congenital adrenal hyperplasia due to 11-beta-hydroxylase deficiency is an autosomal recessive disorder of corticosteroid biosynthesis resulting in androgen excess, virilization, and hypertension. The defect causes decreased synthesis of cortisol and corticosterone in the zona fasciculata of the adrenal gland, resulting in accumulation of the precursors 11-deoxycortisol and 11-deoxycorticosterone; the latter is a potent salt-retaining mineralocorticoid that leads to arterial hypertension (White et al., 1991). CAH due to 11-beta-hydroxylase deficiency accounts for approximately 5 to 8% of all CAH cases; approximately 90% of cases are caused by 21-hydroxylase deficiency (201910) (White et al., 1991).
Apparent mineralocorticoid excess
MedGen UID:
90983
Concept ID:
C0342488
Disease or Syndrome
Apparent mineralocorticoid excess (AME) is an autosomal recessive form of low-renin hypertension associated with low aldosterone, metabolic alkalosis, hypernatremia, and hypokalemia. The disorder is due to a congenital defect in 11-beta-hydroxysteroid dehydrogenase type II (HSD11B2) activity, resulting in decreased conversion of biologically active cortisol to inactive cortisone; this defect allows cortisol to act as a ligand for the mineralocorticoid receptor, resulting in sodium retention and volume expansion. There is a favorable therapeutic response to spironolactone (review by Ferrari, 2010).
Pseudohypoaldosteronism type 2C
MedGen UID:
327089
Concept ID:
C1840391
Disease or Syndrome
Pseudohypoaldosteronism type II (PHAII) is characterized by hyperkalemia despite normal glomerular filtration rate (GFR) and frequently by hypertension. Other associated findings in both children and adults include hyperchloremia, metabolic acidosis, and suppressed plasma renin levels. Aldosterone levels are variable, but are relatively low given the degree of hyperkalemia (elevated serum potassium is a potent stimulus for aldosterone secretion). Hypercalciuria is well described.
Nephrogenic syndrome of inappropriate antidiuresis
MedGen UID:
336877
Concept ID:
C1845202
Disease or Syndrome
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common cause of hyponatremia. The syndrome manifests as an inability to excrete a free water load, with inappropriately concentrated urine and resultant hyponatremia, hypoosmolality, and natriuresis. SIADH occurs in a setting of normal blood volume, without evidence of renal disease or deficiency of thyroxine or cortisol. Although usually transient, SIADH may be chronic; it is often associated with drug use or a lesion in the central nervous system or lung. When the cardinal features of SIADH were defined by Bartter and Schwartz (1967), levels of AVP could not be measured. Subsequently, radioimmunoassays revealed that SIADH is usually associated with measurably elevated serum levels of AVP. Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is characterized by a clinical picture similar to SIADH, but is associated with undetectable levels of AVP (Feldman et al., 2005).
Pseudohyperaldosteronism type 2
MedGen UID:
343170
Concept ID:
C1854631
Disease or Syndrome
Hypertension due to gain-of-function mutations in the mineralocorticoid receptor is a rare genetic hypertension characterized by a familial severe hypertension with an onset before age 20 years, associated with suppressed plasma renin and low aldosterone levels in the presence of low or normal levels of the mineralocorticoid aldosterone, that is highly resistant to antihypertensive medication. During pregnancy, there is a marked exacerbation of hypertension, accompanied by low serum potassium levels and undetectable aldosterone levels, but without signs of preeclampsia, requiring early delivery.
Antley-Bixler syndrome with genital anomalies and disordered steroidogenesis
MedGen UID:
461449
Concept ID:
C3150099
Disease or Syndrome
Cytochrome P450 oxidoreductase deficiency (PORD) is a disorder of steroidogenesis with a broad phenotypic spectrum including cortisol deficiency, altered sex steroid synthesis, disorders of sex development (DSD), and skeletal malformations of the Antley-Bixler syndrome (ABS) phenotype. Cortisol deficiency is usually partial, with some baseline cortisol production but failure to mount an adequate cortisol response in stress. Mild mineralocorticoid excess can be present and causes arterial hypertension, usually presenting in young adulthood. Manifestations of altered sex steroid synthesis include ambiguous genitalia/DSD in both males and females, large ovarian cysts in females, poor masculinization and delayed puberty in males, and maternal virilization during pregnancy with an affected fetus. Skeletal malformations can manifest as craniosynostosis, mid-face retrusion with proptosis and choanal stenosis or atresia, low-set dysplastic ears with stenotic external auditory canals, hydrocephalus, radiohumeral synostosis, neonatal fractures, congenital bowing of the long bones, joint contractures, arachnodactyly, and clubfeet; other anomalies observed include urinary tract anomalies (renal pelvic dilatation, vesicoureteral reflux). Cognitive impairment is of minor concern and likely associated with the severity of malformations; studies of developmental outcomes are lacking.
Aldosterone-producing adenoma with seizures and neurological abnormalities
MedGen UID:
815939
Concept ID:
C3809609
Disease or Syndrome
A rare, genetic, neurologic disease characterized by primary hyperaldosteronism presenting with early-onset, severe hypertension, hypokalemia and neurological manifestations (including seizures, severe hypotonia, spasticity, cerebral palsy and profound developmental delay/intellectual disability).
Glucocorticoid-remediable aldosteronism
MedGen UID:
824577
Concept ID:
C3838731
Disease or Syndrome
Familial hyperaldosteronism type I (HALD1), also referred to as glucocorticoid-remediable aldosteronism (GRA), is an autosomal dominant disorder characterized by hypertension, variable hyperaldosteronism, and abnormal adrenal steroid production, including 18-oxocortisol and 18-hydroxycortisol (Lifton et al., 1992). There is significant phenotypic heterogeneity, and some individuals never develop hypertension (Stowasser et al., 2000). Genetic Heterogeneity of Familial Hyperaldosteronism Familial hyperaldosteronism type II (HALD2; 605635) is caused by mutation in the CLCN2 gene (600570) on chromosome 3q27. Familial hyperaldosteronism type III (HALD3; 613677) is caused by mutation in the KCNJ5 gene (600734) on chromosome 11q24. Familial hyperaldosteronism type IV (HALD4; 617027) is caused by mutation in the CACNA1H gene (607904) on chromosome 16p13.
Familial hyperaldosteronism type III
MedGen UID:
824604
Concept ID:
C3838758
Disease or Syndrome
Hyperaldosteronism type III (HALD3) is characterized by hypertension secondary to massive adrenal mineralocorticoid production. Like patients with glucocorticoid-remediable aldosteronism (GRA, or HALD1; 103900), patients with HALD3 present with childhood hypertension, elevated aldosteronism levels, and high levels of the hybrid steroids 18-oxocortisol and 18-hydroxycortisol. However, hypertension and aldosteronism in HALD3 are not reversed by administration of exogenous glucocorticoids and patients require adrenalectomy to control hypertension (Geller et al., 2008).
Liddle syndrome 2
MedGen UID:
1648476
Concept ID:
C4748251
Disease or Syndrome
Liddle syndrome is an autosomal dominant form of hypertension characterized by early onset of hypertension associated with hypokalemia, suppressed plasma renin activity, and suppressed secretion of the mineralocorticoid hormone aldosterone (summary by Hansson et al., 1995). For a general phenotypic description and a discussion of genetic heterogeneity of Liddle syndrome, see 177200.
Liddle syndrome 3
MedGen UID:
1648443
Concept ID:
C4748292
Disease or Syndrome
Liddle syndrome, or pseudoaldosteronism, is an autosomal dominant form of salt-sensitive hypertension characterized by suppressed plasma renin and aldosterone, hypokalemia, and metabolic alkalosis (summary by Salih et al., 2017). For a discussion of genetic heterogeneity of Liddle syndrome, see 177200.

Professional guidelines

PubMed

Briasoulis A, Androulakis E, Christophides T, Tousoulis D
Heart Fail Rev 2016 Mar;21(2):169-76. doi: 10.1007/s10741-016-9533-z. PMID: 26872673
Roscioni SS, de Zeeuw D, Bakker SJ, Lambers Heerspink HJ
Nat Rev Nephrol 2012 Dec;8(12):691-9. Epub 2012 Oct 16 doi: 10.1038/nrneph.2012.217. PMID: 23070570
Simko F, Pechanova O
J Pineal Res 2009 Sep;47(2):127-133. Epub 2009 Jun 29 doi: 10.1111/j.1600-079X.2009.00697.x. PMID: 19570132

Recent clinical studies

Etiology

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Hubers SA, Brown NJ
Circulation 2016 Mar 15;133(11):1115-24. doi: 10.1161/CIRCULATIONAHA.115.018622. PMID: 26976916Free PMC Article

Diagnosis

Leal CRV, Costa LB, Ferreira GC, Ferreira AM, Reis FM, Simões E Silva AC
Pregnancy Hypertens 2022 Jun;28:15-20. Epub 2022 Feb 4 doi: 10.1016/j.preghy.2022.01.011. PMID: 35149272
Mohseni Z, Derksen E, Oben J, Al-Nasiry S, Spaanderman MEA, Ghossein-Doha C
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Gattoni A, Marotta F, Vangieri B, Pisani G, Cristiano F
Clin Ter 2004 Sep;155(9):375-89. PMID: 15700631
Strazzullo P, Galletti F
Curr Opin Nephrol Hypertens 2004 May;13(3):325-32. doi: 10.1097/00041552-200405000-00010. PMID: 15073492

Therapy

Lytvyn Y, Kimura K, Peter N, Lai V, Tse J, Cham L, Perkins BA, Soleymanlou N, Cherney DZI
Circulation 2022 Aug 9;146(6):450-462. Epub 2022 Jul 11 doi: 10.1161/CIRCULATIONAHA.122.059150. PMID: 35862082Free PMC Article
Gembillo G, Siligato R, Amatruda M, Conti G, Santoro D
Medicina (Kaunas) 2021 Feb 22;57(2) doi: 10.3390/medicina57020186. PMID: 33671780Free PMC Article
Hubers SA, Brown NJ
Circulation 2016 Mar 15;133(11):1115-24. doi: 10.1161/CIRCULATIONAHA.115.018622. PMID: 26976916Free PMC Article
Hajjar I, Hart M, Mack W, Lipsitz LA
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Gattoni A, Marotta F, Vangieri B, Pisani G, Cristiano F
Clin Ter 2004 Sep;155(9):375-89. PMID: 15700631

Prognosis

Busse LW, Schaich CL, Chappell MC, McCurdy MT, Staples EM, Ten Lohuis CC, Hinson JS, Sevransky JE, Rothman RE, Wright DW, Martin GS, Khanna AK; Vitamin C, Thiamine, and Steroids in Sepsis (VICTAS) Investigators
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Circulation 2016 Mar 15;133(11):1115-24. doi: 10.1161/CIRCULATIONAHA.115.018622. PMID: 26976916Free PMC Article
Briasoulis A, Androulakis E, Christophides T, Tousoulis D
Heart Fail Rev 2016 Mar;21(2):169-76. doi: 10.1007/s10741-016-9533-z. PMID: 26872673
Kovesdy CP, Quarles LD
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MacFadyen RJ
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Clinical prediction guides

Busse LW, Schaich CL, Chappell MC, McCurdy MT, Staples EM, Ten Lohuis CC, Hinson JS, Sevransky JE, Rothman RE, Wright DW, Martin GS, Khanna AK; Vitamin C, Thiamine, and Steroids in Sepsis (VICTAS) Investigators
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Kovesdy CP, Quarles LD
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Ellenbogen KA, Morillo CA, Wood MA, Gilligan DM, Eckberg DL, Smith ML
Pacing Clin Electrophysiol 1997 Mar;20(3 Pt 2):788-94. doi: 10.1111/j.1540-8159.1997.tb03905.x. PMID: 9080511

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