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<meta name="keywords" content="C0020428, aldosteronism, disease or syndrome, elevated plasma aldosterone, hyperaldosteronism, increased aldosterone, increased aldosterone production, increased circulating aldosterone concentration, mineralocorticoid excess, primary hyperaldosteronism, autosomal dominant, autosomal recessive, birth defects, chromosomal disease, chromosome, clinical features, clinical findings, clinical genetics, clinical recommendations, clinvar, congenital chromosomal disease, consumer genetic resources, cytogenetic location, disease characteristics, disease definitions, disease descriptions, disease ontology, disease synonyms, disease vocabulary, dysmorphology, entrez, familial disease, gene, gene-disease relationship, genereviews, genetic disease, genetic disorder, genetic terminology, genetic testing registry, genetics home reference, genomic disease, gtr, hereditary disease, heritable disease, hpo, human phenotype ontology, inherited disease, management guidelines, maternal inheritance, medgen, medical genetics, medical subject headings, mesh, mitochondrial inheritance, mode of inheritance, national center for biotechnology information, national institutes of health, national library of medicine, ncbi, nih, nlm, omim, ordo, orphanet, paternal inheritance, phenome, position statements, professional practice guidelines, rare disease, reference sequence, refseq, snomed ct, syndrome, undiagnosed diseases, x-linked recessive" /><meta name="description" content="Overproduction of the mineralocorticoid aldosterone by the adrenal cortex." /><meta name="robots" content="index,nofollow,noarchive" />
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<title>Increased circulating aldosterone concentration (Concept Id: C0020428)
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<!--
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UID=6960
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ConceptID=C0020428
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-->
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<!--imgCountBooks = 0--><h1 class="medgenTitle"><div class="MedGenTitleText">Increased circulating aldosterone concentration</div></h1><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>6960</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:">C0020428</span></a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div><table class="medgenTable"><tbody><tr><td>Synonym:</td>
|
||
<td>Hyperaldosteronism</td></tr>
|
||
<tr><td><span class="bold">SNOMED CT: </span></td>
|
||
<td>Aldosteronism (88213004); Hyperaldosteronism (88213004)</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:0000859">HP:0000859</a></td></tr>
|
||
<tr><td>Monarch Initiative:</td>
|
||
<td><a href="https://monarchinitiative.org/disease/MONDO:0003009" target="_blank">MONDO:0003009</a></td></tr>
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</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>
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||
<div class="portlet_content ln">Overproduction of the mineralocorticoid aldosterone by the adrenal cortex. [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="TLline">Increased 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">Increased circulating aldosterone concentration</span><ul><li><span class="TLline"><a href="/medgen/2172" ref="tree=MeSH" title="MedGen record for Bartter syndrome">Bartter syndrome</a></span><ul><li><span class="TLline"><a href="/medgen/893350" ref="tree=MeSH" title="MedGen record for Antenatal Bartter syndrome">Antenatal Bartter syndrome</a></span><ul><li><span class="TLline"><a href="/medgen/355727" ref="tree=MeSH" title="MedGen record for Bartter disease type 1">Bartter disease type 1</a></span></li><li><span class="TLline"><a href="/medgen/343428" ref="tree=MeSH" title="MedGen record for Bartter disease type 2">Bartter disease type 2</a></span></li><li><span class="TLline"><a href="/medgen/934787" ref="tree=MeSH" title="MedGen record for Bartter disease type 5">Bartter disease type 5</a></span></li></ul></li><li><span class="TLline"><a href="/medgen/335399" ref="tree=MeSH" title="MedGen record for Bartter disease type 3">Bartter disease type 3</a></span></li><li><span class="TLline"><a href="/medgen/355430" ref="tree=MeSH" title="MedGen record for Bartter disease type 4A">Bartter disease type 4A</a></span></li><li><span class="TLline"><a href="/medgen/934772" ref="tree=MeSH" title="MedGen record for Bartter disease type 4B">Bartter disease type 4B</a></span></li><li><span class="TLline"><a href="/medgen/824706" ref="tree=MeSH" title="MedGen record for Bartter syndrome type 4">Bartter syndrome type 4</a></span></li><li><span class="TLline"><a href="/medgen/811594" ref="tree=MeSH" title="MedGen record for Bartter syndrome with hypocalcemia">Bartter syndrome with hypocalcemia</a></span></li></ul></li><li><span class="TLline"><a href="/medgen/780028" ref="tree=MeSH" title="MedGen record for Familial hyperaldosteronism">Familial hyperaldosteronism</a></span><ul><li><span class="TLline"><a href="/medgen/340137" ref="tree=MeSH" title="MedGen record for Familial hyperaldosteronism type II">Familial hyperaldosteronism type II</a></span></li><li><span class="TLline"><a href="/medgen/824604" ref="tree=MeSH" title="MedGen record for Familial hyperaldosteronism type III">Familial hyperaldosteronism type III</a></span></li><li><span class="TLline"><a href="/medgen/824577" ref="tree=MeSH" title="MedGen record for Glucocorticoid-remediable aldosteronism">Glucocorticoid-remediable aldosteronism</a></span></li></ul></li><li><span class="TLline"><a href="/medgen/278002" ref="tree=MeSH" title="MedGen record for Primary hyperaldosteronism">Primary hyperaldosteronism</a></span><ul><li><span class="TLline"><a href="/medgen/892448" ref="tree=MeSH" title="MedGen record for Dexamethasone-suppressible primary hyperaldosteronism">Dexamethasone-suppressible primary hyperaldosteronism</a></span></li><li><span class="TLline"><a href="/medgen/892826" ref="tree=MeSH" title="MedGen record for Glucocortocoid-insensitive primary hyperaldosteronism">Glucocortocoid-insensitive primary hyperaldosteronism</a></span></li></ul></li><li><span class="TLline"><a href="/medgen/488835" ref="tree=MeSH" title="MedGen record for Secondary hyperaldosteronism">Secondary hyperaldosteronism</a></span></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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||
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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>
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<div class="portlet_content ln clinfeat">
|
||
<div class="divPopper rprt" id="rdis_78631"><div><strong>Congenital secretory diarrhea, chloride type</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>78631</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.">C0267662</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Congenital secretory chloride diarrhea is an autosomal recessive form of severe chronic diarrhea characterized by excretion of large amounts of watery stool containing high levels of chloride, resulting in dehydration, hypokalemia, and metabolic alkalosis. The electrolyte disorder resembles the renal disorder Bartter syndrome (see 607364), except that chloride diarrhea is not associated with calcium level abnormalities (summary by Choi et al., 2009). Genetic Heterogeneity of Diarrhea Other forms of diarrhea include DIAR2 (251850), caused by mutation in the MYO5B gene (606540) on 18q21; DIAR3 (270420), caused by mutation in the SPINT2 gene (605124) on 19q13; DIAR4 (610370), caused by mutation in the NEUROG3 gene (604882) on 10q21; DIAR5 (613217), caused by mutation in the EPCAM gene (185535) on 2p21; DIAR6 (614616), caused by mutation in the GUCY2C gene (601330) on 12p12; DIAR7 (615863) caused by mutation in the DGAT1 gene (604900) on 8q24; DIAR8 (616868), caused by mutation in the SLC9A3 gene (182307) on 5p15; DIAR9 (618168), caused by mutation in the WNT2B gene (601968) on 1p13; DIAR10 (618183), caused by mutation in the PLVAP gene (607647) on 19p13; DIAR11 (618662), caused by deletion of the intestine critical region (ICR) on chromosome 16p13, resulting in loss of expression of the flanking gene PERCC1 (618656); DIAR12 (619445), caused by mutation in the STX3 gene (600876) on 11q12; and DIAR13 (620357), caused by mutation in the ACSL5 gene (605677) on chromosome 10q25.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/78631">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_260623"><div><strong>Autosomal dominant pseudohypoaldosteronism type 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>260623</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.">C1449842</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Autosomal dominant pseudohypoaldosteronism type I (PHA1A) is characterized by salt wasting resulting from renal unresponsiveness to mineralocorticoids. Patients may present with neonatal renal salt wasting with hyperkalaemic acidosis despite high aldosterone levels. These patients improve with age and usually become asymptomatic without treatment. Some adult patients with the disorder may have elevated aldosterone levels, but no history of clinical disease. This observation suggests that only those infants whose salt homeostasis is stressed by intercurrent illness and volume depletion develop clinically recognized PHA I (summary by Geller et al., 1998). Autosomal recessive pseudohypoaldosteronism type I (see PHA1B1, 264350), caused by mutation in any one of 3 genes encoding the epithelial sodium channel (ENaC), is a similar but more severe systemic disorder with persistence into adulthood.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/260623">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_335399"><div><strong>Bartter disease type 3</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>335399</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.">C1846343</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bartter syndrome refers to a group of disorders that are unified by autosomal recessive transmission of impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria. Clinical disease results from defective renal reabsorption of sodium chloride in the thick ascending limb (TAL) of the Henle loop, where 30% of filtered salt is normally reabsorbed (Simon et al., 1997). Patients with antenatal (or neonatal) forms of Bartter syndrome (e.g., BARTS1, 601678) typically present with premature birth associated with polyhydramnios and low birth weight and may develop life-threatening dehydration in the neonatal period. Patients with classic Bartter syndrome present later in life and may be sporadically asymptomatic or mildly symptomatic (summary by Simon et al., 1996 and Fremont and Chan, 2012). Genetic Heterogeneity of Bartter Syndrome Antenatal Bartter syndrome type 1 (601678) is caused by loss-of-function mutations in the butmetanide-sensitive Na-K-2Cl cotransporter NKCC2 (SLC12A1; 600839). Antenatal Bartter syndrome type 2 (241200) is caused by loss-of-function mutations in the ATP-sensitive potassium channel ROMK (KCNJ1; 600359). One form of neonatal Bartter syndrome with sensorineural deafness, Bartter syndrome type 4A (602522), is caused by mutation in the BSND gene (606412). Another form of neonatal Bartter syndrome with sensorineural deafness, Bartter syndrome type 4B (613090), is caused by simultaneous mutation in both the CLCNKA (602024) and CLCNKB (602023) genes. Also see autosomal dominant hypocalcemia-1 with Bartter syndrome (601198), which is sometimes referred to as Bartter syndrome type 5 (Fremont and Chan, 2012), caused by mutation in the CASR gene (601199). See Gitelman syndrome (GTLMN; 263800), which is often referred to as a mild variant of Bartter syndrome, caused by mutation in the thiazide-sensitive sodium-chloride cotransporter SLC12A3 (600968).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/335399">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_340137"><div><strong>Familial hyperaldosteronism type II</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>340137</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.">C1854107</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Familial hyperaldosteronism type II (HALD2) is an autosomal dominant disorder characterized by hypertension due to increased aldosterone, often with hypokalemia. Patients usually present before age 20 years, although some may present in infancy. The disorder shows incomplete penetrance and variable expressivity; some patients may have normal blood pressure but have an increased aldosterone:renin ratio (ARR) on laboratory testing. Spironolactone is an effective treatment (summary by Scholl et al., 2018). For a general phenotypic description and a discussion of genetic heterogeneity of familial hyperaldosteronism, see HALD1 (103900).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/340137">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_343428"><div><strong>Bartter disease type 2</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>343428</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.">C1855849</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bartter syndrome refers to a group of disorders that are unified by autosomal recessive transmission of impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria. Clinical disease results from defective renal reabsorption of sodium chloride in the thick ascending limb (TAL) of the Henle loop, where 30% of filtered salt is normally reabsorbed (Simon et al., 1997). Patients with antenatal forms of Bartter syndrome typically present with premature birth associated with polyhydramnios and low birth weight and may develop life-threatening dehydration in the neonatal period. Patients with classic Bartter syndrome (see BARTS3, 607364) present later in life and may be sporadically asymptomatic or mildly symptomatic (summary by Simon et al., 1996 and Fremont and Chan, 2012). For a discussion of genetic heterogeneity of Bartter syndrome, see 607364.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/343428">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_355430"><div><strong>Bartter disease type 4A</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>355430</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.">C1865270</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bartter syndrome refers to a group of disorders that are unified by autosomal recessive transmission of impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria. Clinical disease results from defective renal reabsorption of sodium chloride in the thick ascending limb (TAL) of the Henle loop, where 30% of filtered salt is normally reabsorbed (Simon et al., 1997). Patients with antenatal (or neonatal) forms of Bartter syndrome typically present with premature birth associated with polyhydramnios and low birth weight and may develop life-threatening dehydration in the neonatal period. Patients with classic Bartter syndrome (see BARTS3, 607364) present later in life and may be sporadically asymptomatic or mildly symptomatic (summary by Simon et al., 1996 and Fremont and Chan, 2012). For a discussion of genetic heterogeneity of Bartter syndrome, see 607364.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/355430">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_355727"><div><strong>Bartter disease type 1</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>355727</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.">C1866495</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bartter syndrome refers to a group of disorders that are unified by autosomal recessive transmission of impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria. Clinical disease results from defective renal reabsorption of sodium chloride in the thick ascending limb (TAL) of the Henle loop, where 30% of filtered salt is normally reabsorbed (Simon et al., 1997). Patients with antenatal forms of Bartter syndrome typically present with premature birth associated with polyhydramnios and low birth weight and may develop life-threatening dehydration in the neonatal period. Patients with classic Bartter syndrome (see BARTS3, 607364) present later in life and may be sporadically asymptomatic or mildly symptomatic (summary by Simon et al., 1996 and Fremont and Chan, 2012). For a discussion of genetic heterogeneity of Bartter syndrome, see 607364.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/355727">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_411243"><div><strong>EAST syndrome</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>411243</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.">C2748572</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Syndrome with characteristics of seizures, sensorineural deafness, ataxia, intellectual deficit, and electrolyte imbalance. It has been described in five patients from four families. The disease is caused by homozygous or compound heterozygous mutations in the KCNJ10 gene, encoding a potassium channel expressed in the brain, spinal cord, inner ear and kidneys. Transmission is autosomal recessive.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/411243">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_462405"><div><strong>Congenital adrenal insufficiency with 46, XY sex reversal OR 46,XY disorder of sex development-adrenal insufficiency due to CYP11A1 deficiency</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>462405</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.">C3151055</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">P450scc deficiency is a rare disorder that can present as acute adrenal insufficiency in infancy or childhood. ACTH and plasma renin activity are grossly elevated and adrenal steroids are inappropriately low or absent; the 46,XY patients have female external genitalia, sometimes with clitoromegaly. The phenotypic spectrum ranges from prematurity, complete underandrogenization, and severe early-onset adrenal failure to term birth with clitoromegaly and later-onset adrenal failure (summary by Kim et al., 2008). Although hormonal and phenotypic features can resemble those of congenital lipoid adrenal hyperplasia (lipoid CAH; 201710), no patient with P450scc deficiency has been described with the massive adrenal enlargement typical of lipoid CAH (summary by Sahakitrungruang et al., 2011).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/462405">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_824577"><div><strong>Glucocorticoid-remediable aldosteronism</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>824577</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.">C3838731</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">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.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/824577">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_824604"><div><strong>Familial hyperaldosteronism type III</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>824604</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.">C3838758</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">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).</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/824604">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_934723"><div><strong>Hyperaldosteronism, familial, type IV</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>934723</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.">C4310756</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove nowrap">See: <a href="/medgen/934723">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_934772"><div><strong>Bartter disease type 4B</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>934772</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.">C4310805</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
|
||
<div class="spaceAbove">Bartter syndrome refers to a group of disorders that are unified by autosomal recessive transmission of impaired salt reabsorption in the thick ascending loop of Henle with pronounced salt wasting, hypokalemic metabolic alkalosis, and hypercalciuria. Clinical disease results from defective renal reabsorption of sodium chloride in the thick ascending limb (TAL) of the Henle loop, where 30% of filtered salt is normally reabsorbed (Simon et al., 1997). Patients with antenatal (or neonatal) forms of Bartter syndrome (e.g., BARTS1, 601678) typically present with premature birth associated with polyhydramnios and low birth weight and may develop life-threatening dehydration in the neonatal period. Patients with classic Bartter syndrome present later in life and may be sporadically asymptomatic or mildly symptomatic (summary by Simon et al., 1996 and Fremont and Chan, 2012). For a discussion of genetic heterogeneity of Bartter syndrome, see 607364.</div>
|
||
<div class="spaceAbove nowrap">See: <a href="/medgen/934772">Condition Record</a></div></div>
|
||
<div class="divPopper rprt" id="rdis_1785163"><div><strong>Hypokalemic tubulopathy and deafness</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1785163</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.">C5543621</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Hypokalemic tubulopathy and deafness (HKTD) is an autosomal recessive disorder characterized by hypokalemic tubulopathy with renal salt wasting, disturbed acid-base homeostasis, and sensorineural deafness (Schlingmann et al., 2021).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1785163">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1823950"><div><strong>Pseudohypoaldosteronism, type IB1, autosomal recessive</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1823950</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.">C5774176</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Autosomal recessive pseudohypoaldosteronism type I, including PHA1B1, is characterized by renal salt wasting and high concentrations of sodium in sweat, stool, and saliva. The disorder involves multiple organ systems and is especially threatening in the neonatal period. Laboratory evaluation shows hyponatremia, hyperkalemia, and increased plasma renin activity with high serum aldosterone concentrations. Respiratory tract infections are common in affected children and may be mistaken for cystic fibrosis (CF; 219700). Aggressive salt replacement and control of hyperkalemia results in survival, and the disorder appears to become less severe with age (review by Scheinman et al., 1999). A milder, autosomal dominant form of type I pseudohypoaldosteronism (PHA1A; 177735) is caused by mutations in the mineralocorticoid receptor gene (MCR, NR3C2; 600983). Gitelman syndrome (263800), another example of primary renal tubular salt wasting, is due to mutation in the thiazide-sensitive sodium-chloride cotransporter (SLC12A3; 600968). Hanukoglu and Hanukoglu (2016) provided a detailed review of the ENaC gene family, including structure, function, tissue distribution, and associated inherited diseases.</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1823950">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1824028"><div><strong>Pseudohypoaldosteronism, type IB2, autosomal recessive</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1824028</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.">C5774255</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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<div class="spaceAbove">Autosomal recessive pseudohypoaldosteronism type IB2 (PHA1B2) is characterized by renal salt wasting and high concentrations of sodium in sweat, stool, and saliva. The disorder involves multiple organ systems and is especially threatening in the neonatal period. Laboratory evaluation shows hyponatremia, hyperkalemia, and increased plasma renin activity with high serum aldosterone concentrations. Respiratory tract infections are common in affected children and may be mistaken for cystic fibrosis (CF; 219700). Aggressive salt replacement and control of hyperkalemia results in survival, and the disorder appears to become less severe with age (review by Scheinman et al., 1999).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1824028">Condition Record</a></div></div>
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<div class="divPopper rprt" id="rdis_1824029"><div><strong>Pseudohypoaldosteronism, type IB3, autosomal recessive</strong><div class="aux"><div class="resc"><dl class="rprtid"><dt>MedGen UID: </dt><dd>1824029</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.">C5774256</a></dd><dt><span class="dotprefix"> •</span></dt><dd>Disease or Syndrome</dd></dl></div></div></div>
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||
<div class="spaceAbove">Autosomal recessive pseudohypoaldosteronism type IB3 (PHA1B3) is characterized by renal salt wasting and high concentrations of sodium in sweat, stool, and saliva. The disorder involves multiple organ systems and is especially threatening in the neonatal period. Laboratory evaluation shows hyponatremia, hyperkalemia, and increased plasma renin activity with high serum aldosterone concentrations. Respiratory tract infections are common in affected children and may be mistaken for cystic fibrosis (CF; 219700). Aggressive salt replacement and control of hyperkalemia results in survival, and the disorder appears to become less severe with age (review by Scheinman et al., 1999).</div>
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<div class="spaceAbove nowrap">See: <a href="/medgen/1824029">Condition Record</a></div></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_260623" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Autosomal dominant pseudohypoaldosteronism type 1</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_355727" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bartter disease type 1</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_343428" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bartter disease type 2</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_335399" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bartter disease type 3</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_355430" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bartter disease type 4A</a></div><div class="jig-moreless" data-jigconfig="class: 'moveDown', moreText: 'See full list (17)', lessText: 'Show less', nodeBefore: 0"><span id="clinMore">
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_934772" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Bartter disease type 4B</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_462405" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital adrenal insufficiency with 46, XY sex reversal OR 46,XY disorder of sex development-adrenal insufficiency due to CYP11A1 deficiency</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_78631" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Congenital secretory diarrhea, chloride type</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_411243" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">EAST syndrome</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_340137" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Familial hyperaldosteronism type II</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_824604" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Familial hyperaldosteronism type III</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_824577" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Glucocorticoid-remediable aldosteronism</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_934723" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hyperaldosteronism, familial, type IV</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1785163" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Hypokalemic tubulopathy and deafness</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1823950" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Pseudohypoaldosteronism, type IB1, autosomal recessive</a></div>
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<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1824028" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Pseudohypoaldosteronism, type IB2, autosomal recessive</a></div>
|
||
<div class="hangingIndent"><a title="click for more information" class="jig-ncbipopper" href="#rdis_1824029" data-jigconfig="hasArrow: true, openEvent: 'click', closeEvent: 'mouseout', openAnimation: 'fadeIn', closeAnimation: 'fadeOut', triggerPosition: 'center right', destPosition: 'center left', arrowDirection: 'left'">Pseudohypoaldosteronism, type IB3, autosomal recessive</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/39851221">Mechanisms Underlying Iron Deficiency-Induced Cardiac Disorders: Implications for Treatment.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Cirovic A,
|
||
Starcevic A,
|
||
Ivanovski A,
|
||
Bogicevic D,
|
||
Orisakwe OE,
|
||
Cirovic A</span><br />
|
||
<span class="medgenPMjournal">Discov Med</span>
|
||
2025 Jan;37(192):31-41.
|
||
doi: 10.24976/Discov.Med.202537192.3.
|
||
<span class="bold">PMID: </span><a href="/pubmed/39851221" target="_blank">39851221</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35816262">Adrenal insufficiency in pregnancy: Physiology, diagnosis, management and areas for future research.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lee JH,
|
||
Torpy DJ</span><br />
|
||
<span class="medgenPMjournal">Rev Endocr Metab Disord</span>
|
||
2023 Feb;24(1):57-69.
|
||
Epub 2022 Jul 11
|
||
doi: 10.1007/s11154-022-09745-6.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35816262" target="_blank">35816262</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/29154418">Measuring non-polyaminated lipocalin-2 for cardiometabolic risk assessment.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Yang K,
|
||
Deng HB,
|
||
Man AWC,
|
||
Song E,
|
||
Zhang J,
|
||
Luo C,
|
||
Cheung BMY,
|
||
Yuen KY,
|
||
Jensen PS,
|
||
Irmukhamedov A,
|
||
Elie AGIM,
|
||
Vanhoutte PM,
|
||
Xu A,
|
||
De Mey JGR,
|
||
Wang Y</span><br />
|
||
<span class="medgenPMjournal">ESC Heart Fail</span>
|
||
2017 Nov;4(4):563-575.
|
||
Epub 2017 Jun 27
|
||
doi: 10.1002/ehf2.12183.
|
||
<span class="bold">PMID: </span><a href="/pubmed/29154418" target="_blank">29154418</a><a href="/pmc/articles/PMC5695172" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=(increased%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 (17)</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/38270079">Optimizing the aldosterone-to-renin ratio cut-off for screening primary aldosteronism based on cardiovascular risk: a collaborative study.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">He C,
|
||
Li R,
|
||
Yang J,
|
||
Shen H,
|
||
Wang Y,
|
||
Chen X,
|
||
Luo W,
|
||
Zeng Q,
|
||
Ma L,
|
||
Song Y,
|
||
Cheng Q,
|
||
Wang Z,
|
||
Wu FF,
|
||
Li Q,
|
||
Yang S,
|
||
Hu J</span><br />
|
||
<span class="medgenPMjournal">Clin Exp Hypertens</span>
|
||
2024 Dec 31;46(1):2301571.
|
||
Epub 2024 Jan 25
|
||
doi: 10.1080/10641963.2023.2301571.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38270079" target="_blank">38270079</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/36795035">Circulating maternal prorenin and oocyte and preimplantation embryo development: the Rotterdam Periconception Cohort.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Wiegel RE,
|
||
Danser AHJ,
|
||
van Duijn L,
|
||
Willemsen SP,
|
||
Laven JSE,
|
||
Steegers EAP,
|
||
Baart EB,
|
||
Steegers-Theunissen RPM</span><br />
|
||
<span class="medgenPMjournal">Hum Reprod</span>
|
||
2023 Apr 3;38(4):582-595.
|
||
doi: 10.1093/humrep/dead030.
|
||
<span class="bold">PMID: </span><a href="/pubmed/36795035" target="_blank">36795035</a><a href="/pmc/articles/PMC10068267" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/27105159">The Coxib case: Are EP receptors really guilty?</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Santilli F,
|
||
Boccatonda A,
|
||
Davì G,
|
||
Cipollone F</span><br />
|
||
<span class="medgenPMjournal">Atherosclerosis</span>
|
||
2016 Jun;249:164-73.
|
||
Epub 2016 Apr 6
|
||
doi: 10.1016/j.atherosclerosis.2016.04.004.
|
||
<span class="bold">PMID: </span><a href="/pubmed/27105159" target="_blank">27105159</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25194457">Effects of aldosterone on insulin sensitivity and secretion.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Luther JM</span><br />
|
||
<span class="medgenPMjournal">Steroids</span>
|
||
2014 Dec;91:54-60.
|
||
Epub 2014 Sep 4
|
||
doi: 10.1016/j.steroids.2014.08.016.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25194457" target="_blank">25194457</a><a href="/pmc/articles/PMC4252580" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<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 />
|
||
<span class="medgenPMjournal">Kidney Int</span>
|
||
1993 May;43(5):1097-103.
|
||
doi: 10.1038/ki.1993.154.
|
||
<span class="bold">PMID: </span><a href="/pubmed/8510388" target="_blank">8510388</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Increased%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 (189)</a></div><h3 class="subhead">Diagnosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38299345">Proteomic Associations of NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) in Heart Failure With Preserved Ejection Fraction.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Azzo JD,
|
||
Dib MJ,
|
||
Zagkos L,
|
||
Zhao L,
|
||
Wang Z,
|
||
Chang CP,
|
||
Ebert C,
|
||
Salman O,
|
||
Gan S,
|
||
Zamani P,
|
||
Cohen JB,
|
||
van Empel V,
|
||
Richards AM,
|
||
Javaheri A,
|
||
Mann DL,
|
||
Rietzschel ER,
|
||
Schafer PH,
|
||
Seiffert DA,
|
||
Gill D,
|
||
Burgess S,
|
||
Ramirez-Valle F,
|
||
Gordon DA,
|
||
Cappola TP,
|
||
Chirinos JA</span><br />
|
||
<span class="medgenPMjournal">Circ Heart Fail</span>
|
||
2024 Feb;17(2):e011146.
|
||
Epub 2024 Feb 1
|
||
doi: 10.1161/CIRCHEARTFAILURE.123.011146.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38299345" target="_blank">38299345</a><a href="/pmc/articles/PMC7615693" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/38270079">Optimizing the aldosterone-to-renin ratio cut-off for screening primary aldosteronism based on cardiovascular risk: a collaborative study.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">He C,
|
||
Li R,
|
||
Yang J,
|
||
Shen H,
|
||
Wang Y,
|
||
Chen X,
|
||
Luo W,
|
||
Zeng Q,
|
||
Ma L,
|
||
Song Y,
|
||
Cheng Q,
|
||
Wang Z,
|
||
Wu FF,
|
||
Li Q,
|
||
Yang S,
|
||
Hu J</span><br />
|
||
<span class="medgenPMjournal">Clin Exp Hypertens</span>
|
||
2024 Dec 31;46(1):2301571.
|
||
Epub 2024 Jan 25
|
||
doi: 10.1080/10641963.2023.2301571.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38270079" target="_blank">38270079</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/35816262">Adrenal insufficiency in pregnancy: Physiology, diagnosis, management and areas for future research.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Lee JH,
|
||
Torpy DJ</span><br />
|
||
<span class="medgenPMjournal">Rev Endocr Metab Disord</span>
|
||
2023 Feb;24(1):57-69.
|
||
Epub 2022 Jul 11
|
||
doi: 10.1007/s11154-022-09745-6.
|
||
<span class="bold">PMID: </span><a href="/pubmed/35816262" target="_blank">35816262</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25194457">Effects of aldosterone on insulin sensitivity and secretion.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Luther JM</span><br />
|
||
<span class="medgenPMjournal">Steroids</span>
|
||
2014 Dec;91:54-60.
|
||
Epub 2014 Sep 4
|
||
doi: 10.1016/j.steroids.2014.08.016.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25194457" target="_blank">25194457</a><a href="/pmc/articles/PMC4252580" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/21585422">Role of mineralocorticoid action in the brain in salt-sensitive hypertension.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Oki K,
|
||
Gomez-Sanchez EP,
|
||
Gomez-Sanchez CE</span><br />
|
||
<span class="medgenPMjournal">Clin Exp Pharmacol Physiol</span>
|
||
2012 Jan;39(1):90-5.
|
||
doi: 10.1111/j.1440-1681.2011.05538.x.
|
||
<span class="bold">PMID: </span><a href="/pubmed/21585422" target="_blank">21585422</a><a href="/pmc/articles/PMC3164934" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Increased%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 (92)</a></div><h3 class="subhead">Therapy</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38299345">Proteomic Associations of NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) in Heart Failure With Preserved Ejection Fraction.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Azzo JD,
|
||
Dib MJ,
|
||
Zagkos L,
|
||
Zhao L,
|
||
Wang Z,
|
||
Chang CP,
|
||
Ebert C,
|
||
Salman O,
|
||
Gan S,
|
||
Zamani P,
|
||
Cohen JB,
|
||
van Empel V,
|
||
Richards AM,
|
||
Javaheri A,
|
||
Mann DL,
|
||
Rietzschel ER,
|
||
Schafer PH,
|
||
Seiffert DA,
|
||
Gill D,
|
||
Burgess S,
|
||
Ramirez-Valle F,
|
||
Gordon DA,
|
||
Cappola TP,
|
||
Chirinos JA</span><br />
|
||
<span class="medgenPMjournal">Circ Heart Fail</span>
|
||
2024 Feb;17(2):e011146.
|
||
Epub 2024 Feb 1
|
||
doi: 10.1161/CIRCHEARTFAILURE.123.011146.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38299345" target="_blank">38299345</a><a href="/pmc/articles/PMC7615693" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/38270079">Optimizing the aldosterone-to-renin ratio cut-off for screening primary aldosteronism based on cardiovascular risk: a collaborative study.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">He C,
|
||
Li R,
|
||
Yang J,
|
||
Shen H,
|
||
Wang Y,
|
||
Chen X,
|
||
Luo W,
|
||
Zeng Q,
|
||
Ma L,
|
||
Song Y,
|
||
Cheng Q,
|
||
Wang Z,
|
||
Wu FF,
|
||
Li Q,
|
||
Yang S,
|
||
Hu J</span><br />
|
||
<span class="medgenPMjournal">Clin Exp Hypertens</span>
|
||
2024 Dec 31;46(1):2301571.
|
||
Epub 2024 Jan 25
|
||
doi: 10.1080/10641963.2023.2301571.
|
||
<span class="bold">PMID: </span><a href="/pubmed/38270079" target="_blank">38270079</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/30592365">Adrenomedullin in heart failure: pathophysiology and therapeutic application.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Voors AA,
|
||
Kremer D,
|
||
Geven C,
|
||
Ter Maaten JM,
|
||
Struck J,
|
||
Bergmann A,
|
||
Pickkers P,
|
||
Metra M,
|
||
Mebazaa A,
|
||
Düngen HD,
|
||
Butler J</span><br />
|
||
<span class="medgenPMjournal">Eur J Heart Fail</span>
|
||
2019 Feb;21(2):163-171.
|
||
Epub 2018 Dec 28
|
||
doi: 10.1002/ejhf.1366.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30592365" target="_blank">30592365</a><a href="/pmc/articles/PMC6607488" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<div class="nl"><a target="_blank" href="/pubmed/25194457">Effects of aldosterone on insulin sensitivity and secretion.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Luther JM</span><br />
|
||
<span class="medgenPMjournal">Steroids</span>
|
||
2014 Dec;91:54-60.
|
||
Epub 2014 Sep 4
|
||
doi: 10.1016/j.steroids.2014.08.016.
|
||
<span class="bold">PMID: </span><a href="/pubmed/25194457" target="_blank">25194457</a><a href="/pmc/articles/PMC4252580" target="_blank" class="PubMedFree">Free PMC Article</a></div>
|
||
|
||
<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>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Increased%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 (236)</a></div><h3 class="subhead">Prognosis</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/38299345">Proteomic Associations of NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) in Heart Failure With Preserved Ejection Fraction.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Azzo JD,
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Dib MJ,
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Zagkos L,
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Zhao L,
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Ebert C,
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Gan S,
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Zamani P,
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Cohen JB,
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van Empel V,
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Richards AM,
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Javaheri A,
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Mann DL,
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Rietzschel ER,
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Schafer PH,
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Seiffert DA,
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Gill D,
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Burgess S,
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Gordon DA,
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2024 Feb;17(2):e011146.
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Epub 2024 Feb 1
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<span class="bold">PMID: </span><a href="/pubmed/38299345" target="_blank">38299345</a><a href="/pmc/articles/PMC7615693" target="_blank" class="PubMedFree">Free PMC Article</a></div>
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||
<div class="nl"><a target="_blank" href="/pubmed/36795035">Circulating maternal prorenin and oocyte and preimplantation embryo development: the Rotterdam Periconception Cohort.</a></div>
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||
<div class="portlet_content ln"><span class="medgenPMauthor">Wiegel RE,
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Danser AHJ,
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van Duijn L,
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Willemsen SP,
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Laven JSE,
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Steegers EAP,
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Baart EB,
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Steegers-Theunissen RPM</span><br />
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2023 Apr 3;38(4):582-595.
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doi: 10.1093/humrep/dead030.
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<span class="bold">PMID: </span><a href="/pubmed/36795035" target="_blank">36795035</a><a href="/pmc/articles/PMC10068267" target="_blank" class="PubMedFree">Free PMC Article</a></div>
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||
<div class="nl"><a target="_blank" href="/pubmed/23333370">Circulating aldosterone and mortality in female nursing home residents.</a></div>
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||
<div class="portlet_content ln"><span class="medgenPMauthor">Tomaschitz A,
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Pilz S,
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Pieske B,
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Ritz E,
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März W,
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Meinitzer A,
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Dobnig H,
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Amrein K,
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Kienreich K,
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Verheyen N,
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Kraigher-Krainer E,
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Drechsler C,
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Colantonio C,
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Wagner D,
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2013 Mar;48(3):313-8.
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<span class="bold">PMID: </span><a href="/pubmed/23333370" target="_blank">23333370</a></div>
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<div class="nl"><a target="_blank" href="/pubmed/12667625">Adrenomedullin and heart failure.</a></div>
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||
<div class="portlet_content ln"><span class="medgenPMauthor">Rademaker MT,
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Cameron VA,
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Charles CJ,
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Lainchbury JG,
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Nicholls MG,
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Richards AM</span><br />
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<span class="medgenPMjournal">Regul Pept</span>
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2003 Apr 15;112(1-3):51-60.
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doi: 10.1016/s0167-0115(03)00022-3.
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<span class="bold">PMID: </span><a href="/pubmed/12667625" target="_blank">12667625</a></div>
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||
<div class="nl"><a target="_blank" href="/pubmed/11567664">Plasminogen activator inhibitor type-1 in cardiovascular disease. Status report 2001.</a></div>
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<div class="portlet_content ln"><span class="medgenPMauthor">Huber K,
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Christ G,
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<span class="medgenPMjournal">Thromb Res</span>
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2001 Sep 30;103 Suppl 1:S7-19.
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doi: 10.1016/s0049-3848(01)00293-6.
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<span class="bold">PMID: </span><a href="/pubmed/11567664" target="_blank">11567664</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Increased%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 (60)</a></div><h3 class="subhead">Clinical prediction guides</h3>
|
||
<div class="nl"><a target="_blank" href="/pubmed/36795035">Circulating maternal prorenin and oocyte and preimplantation embryo development: the Rotterdam Periconception Cohort.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Wiegel RE,
|
||
Danser AHJ,
|
||
van Duijn L,
|
||
Willemsen SP,
|
||
Laven JSE,
|
||
Steegers EAP,
|
||
Baart EB,
|
||
Steegers-Theunissen RPM</span><br />
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||
<span class="medgenPMjournal">Hum Reprod</span>
|
||
2023 Apr 3;38(4):582-595.
|
||
doi: 10.1093/humrep/dead030.
|
||
<span class="bold">PMID: </span><a href="/pubmed/36795035" target="_blank">36795035</a><a href="/pmc/articles/PMC10068267" 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.
|
||
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/30592365">Adrenomedullin in heart failure: pathophysiology and therapeutic application.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Voors AA,
|
||
Kremer D,
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||
Geven C,
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||
Ter Maaten JM,
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||
Struck J,
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||
Bergmann A,
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||
Pickkers P,
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||
Metra M,
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||
Mebazaa A,
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||
Düngen HD,
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||
Butler J</span><br />
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||
<span class="medgenPMjournal">Eur J Heart Fail</span>
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||
2019 Feb;21(2):163-171.
|
||
Epub 2018 Dec 28
|
||
doi: 10.1002/ejhf.1366.
|
||
<span class="bold">PMID: </span><a href="/pubmed/30592365" target="_blank">30592365</a><a href="/pmc/articles/PMC6607488" target="_blank" class="PubMedFree">Free PMC Article</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,
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||
Jensen BL,
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||
Hansen PB</span><br />
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||
<span class="medgenPMjournal">J Cardiovasc Pharmacol</span>
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||
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/11906484">Val-Tyr as a natural antihypertensive dipeptide can be absorbed into the human circulatory blood system.</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMauthor">Matsui T,
|
||
Tamaya K,
|
||
Seki E,
|
||
Osajima K,
|
||
Matsumoto K,
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||
Kawasaki T</span><br />
|
||
<span class="medgenPMjournal">Clin Exp Pharmacol Physiol</span>
|
||
2002 Mar;29(3):204-8.
|
||
doi: 10.1046/j.1440-1681.2002.03628.x.
|
||
<span class="bold">PMID: </span><a href="/pubmed/11906484" target="_blank">11906484</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Increased%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 (147)</a></div></div>
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<div class="nl"><a target="_blank" href="/pubmed/14768652">NIH state-of-the-science statement on management of the clinically inapparent adrenal mass ("incidentaloma").</a></div>
|
||
<div class="portlet_content ln"><span class="medgenPMjournal">NIH Consens State Sci Statements</span>
|
||
2002 Feb 4-6;19(2):1-25.
|
||
<span class="bold">PMID: </span><a href="/pubmed/14768652" target="_blank">14768652</a></div>
|
||
<div><a target="_blank" href="https://pubmed.ncbi.nlm.nih.gov/?term=%22Increased%20circulating%20aldosterone%20concentration%22%20AND%20systematic%5Bsb%5D%20AND%20%22english%20and%20humans%22%5Bfilter%5D%20NOT%20comment%5BPTYP%5D%20NOT%20letter%5BPTYP%5D" title="PubMed search">See all (1)</a></div></div>
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