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<!--
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||
UID=208996
|
||
ConceptID=C0857899
|
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-->
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<!--imgCountBooks = 0--><h1 class="medgenTitle"><div class="MedGenTitleText">Decreased circulating aldosterone concentration</div></h1><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>208996</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0857899</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Finding</dd></dl></div></div><table class="medgenTable"><tbody><tr><td>Synonyms:</td>
|
||
<td>Decreased circulating aldosterone level; Hypoaldosteronism</td></tr>
|
||
<tr><td colspan="2" class="small"> </td></tr><tr><td>HPO:</td>
|
||
<td><a target="_blank" title="Human Phenotype Ontology" href="https://hpo.jax.org/app/browse/term/HP:0004319">HP:0004319</a></td></tr>
|
||
<tr><td>Monarch Initiative:</td>
|
||
<td><a href="https://monarchinitiative.org/disease/MONDO:0015900" target="_blank">MONDO:0015900</a></td></tr>
|
||
<tr><td>Orphanet:</td>
|
||
<td><a target="_blank" title="Orphanet: The portal for rare diseases and orphan drugs" href="http://www.orpha.net/consor/cgi-bin/OC_Exp.php?lng=EN&Expert=181419">ORPHA181419</a></td></tr></tbody></table></div><div class="rprt-body jig-ncbiinpagenav" data-jigconfig="smoothScroll: false, gotoTopLink: true, gotoTopLinkText: '', gotoTopLinkAttrs: {'title': 'Go to the top of the page'},allHeadingLevels: ['h1'], topOfPageTOC: true, tocId: 'my-toc'"><div id="rprt-tabs-1" class="rprt-tab"><div id="tb-termsProp-1"><div class="leftCol mgCol"><div>
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<div class="portlet mgSection" id="ID_100">
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Definition">Definition</h1><a sid="100" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln">Abnormally reduced levels of aldosterone. [from <a title="Human Phenotype Ontology" href="http://www.human-phenotype-ontology.org" class="defSource" target="_blank">HPO</a>]</div>
|
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</div>
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<div class="portlet mgSection" id="ID_118">
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Term_Hierarchy">Term Hierarchy</h1><a sid="118" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
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<div class="portlet_content ln HierarchyGTR"><div class="jig-ncbitabs"><ul><li><a href="#tabGTR">GTR</a></li><li><a href="#tabMGEN">MeSH</a></li></ul><div id="tabGTR"><div class="search_result"><div class="rprts"><div class="chiclet_legend"><span class="chiclet_list" style="position:static;"><span title="Clinical test" class="chiclet Ccolor round">C</span><span>Clinical test, </span><span title="Research test" class="chiclet Rcolor round">R</span><span>Research test, </span><span title="OMIM" class="chiclet Ocolor ">O</span><span>OMIM, </span><span title="GeneReview" class="chiclet Gcolor">G</span><span><em>GeneReviews</em>, </span><span title="ClinVar" class="chiclet Vcolor">V</span><span>ClinVar </span></span></div><div id="hierarchy" class="margin_t1"><div class="ds_tree"><ul><li class="matched_ds"><span class="chiclet_list"><span class="chiclet unavailable round" title="Clinical test">C</span><span class="chiclet unavailable round" title="Research Tests">R</span><span class="chiclet unavailable" title="OMIM">O</span><span class="chiclet unavailable" title="GeneReviews">G</span><span class="chiclet unavailable" title="ClinVar">V</span></span><span class="TLline">Decreased circulating aldosterone concentration</span></li></ul></div></div></div></div></div><div id="tabMGEN"><div class="ds_tree"><ul><li><span class="TLline"><a href="/medgen/867443" ref="tree=MeSH" title="MedGen record for Phenotypic abnormality">Phenotypic abnormality</a></span><ul><li><span class="TLline"><a href="/medgen/893021" ref="tree=MeSH" title="MedGen record for Abnormality of the endocrine system">Abnormality of the endocrine system</a></span><ul><li><span class="TLline"><a href="/medgen/867421" ref="tree=MeSH" title="MedGen record for Abnormality of renin-angiotensin system">Abnormality of renin-angiotensin system</a></span><ul><li><span class="TLline"><a href="/medgen/808216" ref="tree=MeSH" title="MedGen record for Abnormal circulating aldosterone concentration">Abnormal circulating aldosterone concentration</a></span><ul><li><span class="matched_ds">Decreased circulating aldosterone concentration</span><ul><li><span class="TLline"><a href="/medgen/899592" ref="tree=MeSH" title="MedGen record for Familial hypoaldosteronism">Familial hypoaldosteronism</a></span><ul><li><span class="TLline"><a href="/medgen/1842560" ref="tree=MeSH" title="MedGen record for Early-onset familial hypoaldosteronism">Early-onset familial hypoaldosteronism</a></span></li><li><span class="TLline"><a href="/medgen/1843290" ref="tree=MeSH" title="MedGen record for Late-onset familial hypoaldosteronism">Late-onset familial hypoaldosteronism</a></span></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></li></ul></div></div></div></div>
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</div>
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<div class="portlet mgSection" id="ID_112">
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||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Conditions_with_this_feature">Conditions with this feature</h1><a sid="112" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln clinfeat">
|
||
<div class="divPopper rprt" id="rdis_39125"><div><strong>Polyglandular autoimmune syndrome, type 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>39125</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0085859</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Autoimmune polyglandular syndrome type I (APS1) is characterized by the presence of 2 of 3 major clinical symptoms: Addison disease, and/or hypoparathyroidism, and/or chronic mucocutaneous candidiasis (Neufeld et al., 1981). However, variable APS1 phenotypes have been observed, even among sibs. In addition, some patients may exhibit apparent isolated hypoparathyroidism, an early manifestation of APS1 with peak incidence at around age 5 years; over long-term follow-up, the development of additional features of APS1 may be observed (Cranston et al., 2022).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/39125">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_67439"><div><strong>Liddle syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>67439</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0221043</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">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.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/67439">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_82783"><div><strong>Deficiency of steroid 11-beta-monooxygenase</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>82783</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0268292</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">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).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/82783">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_82784"><div><strong>Corticosterone 18-monooxygenase deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>82784</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0268293</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">CMO type I deficiency is an autosomal recessive disorder caused by a defect in the penultimate biochemical step of aldosterone biosynthesis, the 18-hydroxylation of corticosterone (B) to 18-hydroxycorticosterone (18-OHB). This enzymatic defect results in decreased aldosterone and salt-wasting. In CMO I deficiency, aldosterone is undetectable, whereas its immediate precursor, 18-OHB, is low or normal. These patients have an increased ratio of corticosterone to 18-OHB (Portrat-Doyen et al., 1998). The CYP11B2 gene product also catalyzes the final step in aldosterone biosynthesis: the 18-oxidation of 18-OHB to aldosterone. A defect in that enzymatic step results in CMO type II deficiency (610600), an allelic disorder with an overlapping phenotype but distinct biochemical features. In CMO II deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18-OHB. These patients have a low ratio of corticosterone to 18-OHB (Portrat-Doyen et al., 1998).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/82784">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_82889"><div><strong>Glucocorticoid deficiency with achalasia</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>82889</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0271742</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Triple A syndrome is an inherited condition characterized by three specific features: achalasia, Addison disease, and alacrima. Achalasia is a disorder that affects the ability to move food through the esophagus, the tube that carries food from the throat to the stomach. It can lead to severe feeding difficulties and low blood glucose (hypoglycemia). Addison disease, also known as primary adrenal insufficiency, is caused by abnormal function of the small hormone-producing glands on top of each kidney (adrenal glands). The main features of Addison disease include fatigue, loss of appetite, weight loss, low blood pressure, and darkening of the skin. The third major feature of triple A syndrome is a reduced or absent ability to secrete tears (alacrima). Most people with triple A syndrome have all three of these features, although some have only two.\n\nMany of the features of triple A syndrome are caused by dysfunction of the autonomic nervous system. This part of the nervous system controls involuntary body processes such as digestion, blood pressure, and body temperature. People with triple A syndrome often experience abnormal sweating, difficulty regulating blood pressure, unequal pupil size (anisocoria), and other signs and symptoms of autonomic nervous system dysfunction (dysautonomia).\n\nPeople with this condition may have other neurological abnormalities, such as developmental delay, intellectual disability, speech problems (dysarthria), and a small head size (microcephaly). In addition, affected individuals commonly experience muscle weakness, movement problems, and nerve abnormalities in their extremities (peripheral neuropathy). Some develop optic atrophy, which is the degeneration (atrophy) of the nerves that carry information from the eyes to the brain. Many of the neurological symptoms of triple A syndrome worsen over time.\n\nPeople with triple A syndrome frequently develop a thickening of the outer layer of skin (hyperkeratosis) on the palms of their hands and the soles of their feet. Other skin abnormalities may also be present in people with this condition.\n\nAlacrima is usually the first noticeable sign of triple A syndrome, as it becomes apparent early in life that affected children produce little or no tears while crying. They develop Addison disease and achalasia during childhood or adolescence, and most of the neurologic features of triple A syndrome begin during adulthood. The signs and symptoms of this condition vary among affected individuals, even among members of the same family.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/82889">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_87442"><div><strong>Congenital adrenal hypoplasia, X-linked</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>87442</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information."><span class="highlight" style="background-color:">C0342482</span></a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">NR0B1-related adrenal hypoplasia congenita includes both X-linked adrenal hypoplasia congenita (X-linked AHC) and Xp21 deletion (previously called complex glycerol kinase deficiency). X-linked AHC is characterized by primary adrenal insufficiency and/or hypogonadotropic hypogonadism (HH). Adrenal insufficiency is acute infantile onset (average age 3 weeks) in approximately 60% of affected males and childhood onset (ages 1-9 years) in approximately 40%. HH typically manifests in a male with adrenal insufficiency as delayed puberty (i.e., onset age >14 years) and less commonly as arrested puberty at about Tanner Stage 3. Rarely, X-linked AHC manifests initially in early adulthood as delayed-onset adrenal insufficiency, partial HH, and/or infertility. Heterozygous females very occasionally have manifestations of adrenal insufficiency or hypogonadotropic hypogonadism. Xp21 deletion includes deletion of NR0B1 (causing X-linked AHC) and GK (causing glycerol kinase deficiency), and in some cases deletion of DMD (causing Duchenne muscular dystrophy). Developmental delay has been reported in males with Xp21 deletion when the deletion extends proximally to include DMD or when larger deletions extend distally to include IL1RAPL1 and DMD.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/87442">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_90983"><div><strong>Apparent mineralocorticoid excess</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>90983</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C0342488</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">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).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/90983">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_332252"><div><strong>Glucocorticoid deficiency 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>332252</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1836621</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Familial isolated glucocorticoid deficiency (GCCD) is an adrenocortical failure characterized by very low levels of plasma cortisol despite high levels of plasma adrenocorticotropin (ACTH). Moreover, the adrenal response to ACTH is severely impaired. There is no mineralocorticoid deficiency and the renin-angiotensin system is not affected (summary by Genin et al., 2002). For a general phenotypic description and a discussion of genetic heterogeneity of familial glucocorticoid deficiency, see GCCD1 (202200).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/332252">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_343170"><div><strong>Pseudohyperaldosteronism type 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>343170</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C1854631</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">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.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/343170">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_483046"><div><strong>Corticosterone methyloxidase type 2 deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>483046</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C3463917</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">CMO type II deficiency is an autosomal recessive disorder caused by a defect in the final biochemical step of aldosterone biosynthesis, the 18-hydroxylation of 18-hydroxycorticosterone (18-OHB) to aldosterone. This enzymatic defect results in decreased aldosterone and salt-wasting associated with an increased serum ratio of 18-OHB to aldosterone. In CMO II deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18-OHB. These patients have a low ratio of corticosterone to 18-OHB (Portrat-Doyen et al., 1998). The CYP11B2 gene product also catalyzes an earlier step in aldosterone biosynthesis: the 18-hydroxylation of corticosterone to 18-OHB. A defect in that enzymatic step results in CMO type I deficiency (204300), an allelic disorder with an overlapping phenotype but distinct biochemical features. In CMO I deficiency, aldosterone is undetectable, whereas its immediate precursor, 18-OHB, is low or normal (Portrat-Doyen et al., 1998).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/483046">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1648476"><div><strong>Liddle syndrome 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1648476</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4748251</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">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.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1648476">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1648443"><div><strong>Liddle syndrome 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1648443</dd><dt><span class="dotprefix"> •</span>Concept ID: </dt><dd><a href="/medgen/docs/help/#sources" target="_blank" title="Concept Unique Identifier from NLM's Unified Medical Language system (UMLS) Click for more information.">C4748292</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">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.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/1648443">Condition Record</a></div></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_90983" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Apparent mineralocorticoid excess</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_87442" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital adrenal hypoplasia, X-linked</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_82784" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Corticosterone 18-monooxygenase deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_483046" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Corticosterone methyloxidase type 2 deficiency</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_82783" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Deficiency of steroid 11-beta-monooxygenase</a></div><div class="jig-moreless" data-jigconfig="class: 'moveDown', moreText: 'See full list (12)', lessText: 'Show less', nodeBefore: 0"><span id="clinMore">
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_332252" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Glucocorticoid deficiency 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_82889" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Glucocorticoid deficiency with achalasia</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_67439" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Liddle syndrome</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1648476" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Liddle syndrome 2</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1648443" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Liddle syndrome 3</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_39125" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Polyglandular autoimmune syndrome, type 1</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_343170" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Pseudohyperaldosteronism type 2</a></div></span></div></div>
|
||
</div>
|
||
|
||
<div class="portlet mgSection" id="ID_105">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Professional_guidelines">Professional guidelines</h1><a sid="105" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln"><h3 class="subhead">PubMed<a class="help jig-ncbi-popper" data-jig="ncbipopper" href="#guidelinesHelpPM"><img class="pulldown" src="//static.pubmed.gov/portal/portal3rc.fcgi/4223267/img/4204968" /></a></h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/34993603">Potassium and fiber: a controversial couple in the nutritional management of children with chronic kidney disease.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">El Amouri A,
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Delva K,
|
||
Foulon A,
|
||
Vande Moortel C,
|
||
Van Hoeck K,
|
||
Glorieux G,
|
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Van Biesen W,
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Vande Walle J,
|
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Raes A,
|
||
Snauwaert E,
|
||
Eloot S</span><br />
|
||
<span class="medgenPMjournal">Pediatr Nephrol</span>
|
||
2022 Jul;37(7):1657-1665.
|
||
Epub 2022 Jan 7
|
||
doi: 10.1007/s00467-021-05365-5.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34993603" target="_blank">34993603</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/33179734">Variability of Aldosterone Measurements During Adrenal Venous Sampling for Primary Aldosteronism.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yozamp N,
|
||
Hundemer GL,
|
||
Moussa M,
|
||
Underhill J,
|
||
Fudim T,
|
||
Sacks B,
|
||
Vaidya A</span><br />
|
||
<span class="medgenPMjournal">Am J Hypertens</span>
|
||
2021 Feb 18;34(1):34-45.
|
||
doi: 10.1093/ajh/hpaa151.
|
||
<span class="bold">PMID: </span><a href="/pubmed/33179734" target="_blank">33179734</a><a href="/pmc/articles/PMC7891268" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/8491965">Paracentesis in the management of cirrhotic ascites.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Ginès P,
|
||
Arroyo V</span><br />
|
||
<span class="medgenPMjournal">J Hepatol</span>
|
||
1993;17 Suppl 2:S14-8.
|
||
doi: 10.1016/s0168-8278(05)80449-0.
|
||
<span class="bold">PMID: </span><a href="/pubmed/8491965" target="_blank">8491965</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(decreased%20circulating%20aldosterone%20concentration)%20AND%20(%22english%20and%20humans%22%5BFilter%5D)%20AND%20(%20(%22practice%20guideline%22%5BFilter%5D)%20OR%20(practice*%5Btitl%5D%20AND%20(guideline%5Btitl%5D%20OR%20parameter%5Btitl%5D%20OR%20resource%5Btitl%5D%20OR%20bulletin%5Btitl%5D%20OR%20best%5Btitl%5D))%20OR%20(genetic*%5Btitl%5D%20AND%20(evaluation%5Btitl%5D%20OR%20counseling%5Btitl%5D%20OR%20screening%5Btitl%5D%20OR%20test*%5Btitl%5D))%20OR%20(clinical%5Btitl%5D%20AND%20((expert%5Btitl%5D%20AND%20consensus%5Btitl%5D)%20OR%20utility%5Btitl%5D%20OR%20guideline*%5Btitl%5D))%20OR%20(management%5Btitl%5D%20AND%20(clinical%5Btitl%5D%20OR%20diagnos*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20pain%5Btitl%5D%20OR%20surveillance%5Btitl%5D%20OR%20emergency%5Btitl%5D%20OR%20guideline*%5Btitl%5D%20OR%20therap*))%20OR%20(treatment%5Btitl%5D%20AND%20((evaluation%5Btitl%5D%20AND%20diagnosis%5Btitl%5D)%20OR%20(assessment%5Btitl%5D%20AND%20prevention%5Btitl%5D)%20OR%20therap*))%20OR%20(Diagnos*%5Btitl%5D%20AND%20(prenatal%5Btitl%5D%20OR%20treatment%5Btitl%5D%20OR%20follow-up%5Btitl%5D%20OR%20statement%5Btitl%5D%20OR%20criteria%5Btitl%5D%20OR%20newborn%5Btitl%5D%20OR%20differential%5Btitl%5D%20OR%20neonatal%5Btitl%5D%20OR%20neonate%5Btitl%5D))%20OR%20(guideline*%5Btitl%5D%20AND%20(pharmacogenetic*%5Btitl%5D%20OR%20recommendation%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20evidence-based%5Btitl%5D%20OR%20consensus%5Btitl%5D%20OR%20(technical%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20(molecular%5Btitl%5D%20AND%20testing%5Btitl%5D)))%20OR%20(risk%5Btitl%5D%20AND%20assessment%5Btitl%5D)%20OR%20(recommendation*%5Btitl%5D%20AND%20(statement%5Btitl%5D%20OR%20Evidence-based%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(care%20AND%20((Patient%5Btitl%5D%20AND%20standard*%5Btitl%5D)%20OR%20primary%5Btitl%5D%20OR%20psychosocial%5Btitl%5D))%20OR%20(Health%5Btitl%5D%20AND%20supervision%5Btitl%5D)%20OR%20(statement%5Btitl%5D%20AND%20(policy%5Btitl%5D%20OR%20position%5Btitl%5D%20OR%20Consensus%5Btitl%5D))%20OR%20(pharmacogenetics%5Btitl%5D%20AND%20(Dosing%5Btitl%5D%20OR%20therap*%5Btitl%5D%20OR%20genotype*%5Btitl%5D%20OR%20drug*%5Btitl%5D))%20OR%20(Chemotherapy%5Btitl%5D%20AND%20decision*%5Btitl%5D)%20OR%20(screening%5Btitl%5D%20AND%20(newborn%5Btitl%5D%20OR%20neonat*%5Btitl%5D%20OR%20detection%5Btitl%5D%20OR%20diagnos*%5Btitl%5D))%20OR%20(criteria%5Btitl%5D%20OR%20genotype*%5Btitl%5D)%20)%20NOT%20(%22Case%20reports%22%5BPublication%20type%5D%20OR%20%22clinical%20study%22%5BPublication%20Type%5D%20OR%20%22randomized%20controlled%20trial%22%5BPublication%20Type%5D)" title="PubMed search">See all (15)</a></div></div>
|
||
</div>
|
||
<div class="display-none help-popup" id="guidelinesHelpPM">These guidelines are articles in PubMed that match specific search criteria developed by MedGen to capture the most relevant practice guidelines. This list may not be comprehensive and may include broader topics as well. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div><div class="display-none help-popup" id="guidelinesHelpCurated">These guidelines are manually curated by the MedGen team
|
||
to supplement articles available in PubMed. See the <a href="/medgen/docs/faq/" title="Frequently asked questions" target="_blank">FAQ</a> for details.</div>
|
||
<div class="portlet mgSection" id="ID_103">
|
||
<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Recent_clinical_studies">Recent clinical studies</h1><a sid="103" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
|
||
<div class="portlet_content ln"><h3 class="subhead">Etiology</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/34603502">The Level and Significance of Circulating Angiotensin-III in Patients with Coronary Atherosclerosis.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yao G,
|
||
Li W,
|
||
Liu W,
|
||
Xing J,
|
||
Zhang C</span><br />
|
||
<span class="medgenPMjournal">J Renin Angiotensin Aldosterone Syst</span>
|
||
2021;2021:1704762.
|
||
Epub 2021 Sep 21
|
||
doi: 10.1155/2021/1704762.
|
||
<span class="bold">PMID: </span><a href="/pubmed/34603502" target="_blank">34603502</a><a href="/pmc/articles/PMC8478585" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/33179734">Variability of Aldosterone Measurements During Adrenal Venous Sampling for Primary Aldosteronism.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yozamp N,
|
||
Hundemer GL,
|
||
Moussa M,
|
||
Underhill J,
|
||
Fudim T,
|
||
Sacks B,
|
||
Vaidya A</span><br />
|
||
<span class="medgenPMjournal">Am J Hypertens</span>
|
||
2021 Feb 18;34(1):34-45.
|
||
doi: 10.1093/ajh/hpaa151.
|
||
<span class="bold">PMID: </span><a href="/pubmed/33179734" target="_blank">33179734</a><a href="/pmc/articles/PMC7891268" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/31104255">Levels of angiotensin peptides in healthy and cardiovascular/renal-diseased paediatric population-an investigative review.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Suessenbach FK,
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Burckhardt BB</span><br />
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<span class="medgenPMjournal">Heart Fail Rev</span>
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2019 Sep;24(5):709-723.
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doi: 10.1007/s10741-019-09797-y.
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<span class="bold">PMID: </span><a href="/pubmed/31104255" target="_blank">31104255</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/15160833">Pathophysiologic role of the renin-angiotensin-aldosterone and sympathetic nervous systems in heart failure.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Adams KF Jr</span><br />
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<span class="bold">PMID: </span><a href="/pubmed/15160833" target="_blank">15160833</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/8510388">Potassium supplementation ameliorates mineralocorticoid-induced sodium retention.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Krishna GG,
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<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Decreased%20circulating%20aldosterone%20concentration%22%20AND%20Etiology%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (115)</a></div><h3 class="subhead">Diagnosis</h3>
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<div class="nl"><a target="_blank" href="/pubmed/32208780">Soluble angiotensin IV receptor levels in preeclampsia: is there a variation?</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Khaliq OP,
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<div class="portlet_content ln"><span class="medgenPMauthor">Yozamp N,
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Hundemer GL,
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Moussa M,
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Underhill J,
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Fudim T,
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Sacks B,
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Vaidya A</span><br />
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<div class="nl"><a target="_blank" href="/pubmed/27018313">B-Type Natriuretic Peptide, Aldosterone, and Fluid Management in ARDS.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Semler MW,
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Marney AM,
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Rice TW,
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Nian H,
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Yu C,
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Wheeler AP,
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<div class="nl"><a target="_blank" href="/pubmed/15974890">Role of cardiovascular aldosterone in hypertension.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Takeda Y</span><br />
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<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Decreased%20circulating%20aldosterone%20concentration%22%20AND%20Diagnosis%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (39)</a></div><h3 class="subhead">Therapy</h3>
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<div class="nl"><a target="_blank" href="/pubmed/31104255">Levels of angiotensin peptides in healthy and cardiovascular/renal-diseased paediatric population-an investigative review.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Suessenbach FK,
|
||
Burckhardt BB</span><br />
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<span class="medgenPMjournal">Heart Fail Rev</span>
|
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2019 Sep;24(5):709-723.
|
||
doi: 10.1007/s10741-019-09797-y.
|
||
<span class="bold">PMID: </span><a href="/pubmed/31104255" target="_blank">31104255</a></div>
|
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<div class="nl"><a target="_blank" href="/pubmed/26657712">Does Aldosterone Play a Significant Role for Regulation of Vascular Tone?</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lyngsø KS,
|
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Assersen K,
|
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Dalgaard EG,
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Skott O,
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Jensen BL,
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Hansen PB</span><br />
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<div class="nl"><a target="_blank" href="/pubmed/8510388">Potassium supplementation ameliorates mineralocorticoid-induced sodium retention.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Krishna GG,
|
||
Kapoor SC</span><br />
|
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<span class="medgenPMjournal">Kidney Int</span>
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1993 May;43(5):1097-103.
|
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doi: 10.1038/ki.1993.154.
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<span class="bold">PMID: </span><a href="/pubmed/8510388" target="_blank">8510388</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/3295362">Influence of a low sodium diet on the renal response to amino acid infusions in humans.</a></div>
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Miranda B,
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1987 Apr;31(4):992-9.
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<div class="nl"><a target="_blank" href="/pubmed/6328987">Effects of captopril on hepatic venous pressure and blood flow in patients with liver cirrhosis.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Eriksson LS,
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<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Decreased%20circulating%20aldosterone%20concentration%22%20AND%20Therapy%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (148)</a></div><h3 class="subhead">Prognosis</h3>
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<div class="nl"><a target="_blank" href="/pubmed/32580658">Elevated Angiotensin 1-7/Angiotensin II Ratio Predicts Favorable Outcomes in Patients With Heart Failure.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Wang K,
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Basu R,
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Poglitsch M,
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Bakal JA,
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Oudit GY</span><br />
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<span class="bold">PMID: </span><a href="/pubmed/32580658" target="_blank">32580658</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/28008098">B-type natriuretic peptide increases cortisol and catecholamine concentrations in healthy subjects.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Grimm G,
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Resl M,
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Heinisch BB,
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Hülsmann M,
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<span class="bold">PMID: </span><a href="/pubmed/28008098" target="_blank">28008098</a></div>
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||
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<div class="nl"><a target="_blank" href="/pubmed/27018313">B-Type Natriuretic Peptide, Aldosterone, and Fluid Management in ARDS.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Semler MW,
|
||
Marney AM,
|
||
Rice TW,
|
||
Nian H,
|
||
Yu C,
|
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Wheeler AP,
|
||
Brown NJ;
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NIH NHLBI ARDS Network</span><br />
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<span class="medgenPMjournal">Chest</span>
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2016 Jul;150(1):102-11.
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Epub 2016 Mar 23
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doi: 10.1016/j.chest.2016.03.017.
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<span class="bold">PMID: </span><a href="/pubmed/27018313" target="_blank">27018313</a><a href="/pmc/articles/PMC4980545" target="_blank" class="PubMedFree">Free PMC Article</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/23525530">Short-term responses of the kidney to high altitude in mountain climbers.</a></div>
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Alper SL</span><br />
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<span class="medgenPMjournal">Nephrol Dial Transplant</span>
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2014 Mar;29(3):497-506.
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Epub 2013 Mar 22
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doi: 10.1093/ndt/gft051.
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<span class="bold">PMID: </span><a href="/pubmed/23525530" target="_blank">23525530</a><a href="/pmc/articles/PMC3938295" target="_blank" class="PubMedFree">Free PMC Article</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/6413258">Plasma dopamine: regulation and significance.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Van Loon GR</span><br />
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<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Decreased%20circulating%20aldosterone%20concentration%22%20AND%20Prognosis%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (31)</a></div><h3 class="subhead">Clinical prediction guides</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/33179734">Variability of Aldosterone Measurements During Adrenal Venous Sampling for Primary Aldosteronism.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yozamp N,
|
||
Hundemer GL,
|
||
Moussa M,
|
||
Underhill J,
|
||
Fudim T,
|
||
Sacks B,
|
||
Vaidya A</span><br />
|
||
<span class="medgenPMjournal">Am J Hypertens</span>
|
||
2021 Feb 18;34(1):34-45.
|
||
doi: 10.1093/ajh/hpaa151.
|
||
<span class="bold">PMID: </span><a href="/pubmed/33179734" target="_blank">33179734</a><a href="/pmc/articles/PMC7891268" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/31104255">Levels of angiotensin peptides in healthy and cardiovascular/renal-diseased paediatric population-an investigative review.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Suessenbach FK,
|
||
Burckhardt BB</span><br />
|
||
<span class="medgenPMjournal">Heart Fail Rev</span>
|
||
2019 Sep;24(5):709-723.
|
||
doi: 10.1007/s10741-019-09797-y.
|
||
<span class="bold">PMID: </span><a href="/pubmed/31104255" target="_blank">31104255</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/26657712">Does Aldosterone Play a Significant Role for Regulation of Vascular Tone?</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lyngsø KS,
|
||
Assersen K,
|
||
Dalgaard EG,
|
||
Skott O,
|
||
Jensen BL,
|
||
Hansen PB</span><br />
|
||
<span class="medgenPMjournal">J Cardiovasc Pharmacol</span>
|
||
2016 Jul;68(1):1-10.
|
||
doi: 10.1097/FJC.0000000000000345.
|
||
<span class="bold">PMID: </span><a href="/pubmed/26657712" target="_blank">26657712</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/23525530">Short-term responses of the kidney to high altitude in mountain climbers.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Goldfarb-Rumyantzev AS,
|
||
Alper SL</span><br />
|
||
<span class="medgenPMjournal">Nephrol Dial Transplant</span>
|
||
2014 Mar;29(3):497-506.
|
||
Epub 2013 Mar 22
|
||
doi: 10.1093/ndt/gft051.
|
||
<span class="bold">PMID: </span><a href="/pubmed/23525530" target="_blank">23525530</a><a href="/pmc/articles/PMC3938295" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/3755560">Haemodynamic role of vasopressin released during Finnish sauna.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Bussien JP,
|
||
Gaillard RC,
|
||
Nussberger J,
|
||
Waeber B,
|
||
Hofbauer KG,
|
||
Turnill D,
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Brögger R,
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Brunner HR</span><br />
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<span class="medgenPMjournal">Acta Endocrinol (Copenh)</span>
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1986 Jun;112(2):166-71.
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doi: 10.1530/acta.0.1120166.
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<span class="bold">PMID: </span><a href="/pubmed/3755560" target="_blank">3755560</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Decreased%20circulating%20aldosterone%20concentration%22%20AND%20Clinical%20prediction%20guides%2Fbroad%5Bfilter%5D%20%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (86)</a></div></div>
|
||
</div>
|
||
</div></div></div></div></div></div></div>
|
||
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|
||
|
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|
||
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|
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|
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|
||
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|
||
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|
||
<h2 class="offscreen_noflow">Supplemental Content</h2>
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<div class="portlet_content ln"><ul><li><a href="http://www.orpha.net/consor/cgi-bin/OC_Exp.php?Expert=181419" target="_blank">Orphanet</a></li><li><a href="https://clinicaltrials.gov/search?cond=Decreased%20circulating%20aldosterone%20concentration" target="_blank">ClinicalTrials.gov</a></li></ul></div>
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<div class="portlet_head mgSectionHead ui-widget-header"><h1 class="nl" id="Practice_guidelines">Practice guidelines</h1><a sid="121" href="#" class="portlet_shutter" title="Show/hide content"></a></div>
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