Potassium Pause: A Case of Cardiac Arrest Unmasking Distal Renal Tubular Acidosis

Potassium Pause: A Case of Cardiac Arrest Unmasking Distal Renal Tubular Acidosis | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Potassium Pause: A Case of Cardiac Arrest Unmasking Distal Renal Tubular Acidosis Pankaj Singhania, Abhranil Dhar, Ayush Agarwal This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7293894/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 11 You are reading this latest preprint version Abstract Background Distal renal tubular acidosis (dRTA) is an uncommon renal tubular disorder disorder marked by impaired distal nephron acid excretion, resulting in hyperchloremic metabolic acidosis, persistent alkaline urine, and significant potassium loss. Complications include growth failure and rickets in children, whereas in adults osteomalacia, polyuria, nephrocalcinosis and nephrolithiasis are common. Hypokalaemia an invariable feature presents depending on severity. Muscular weakness, proximal myopathy and quadriparesis in severe cases can be the presentations. Severe hypokalaemia may rarely precipitate life-threatening cardiac arrhythmias including cardiac arrest. Case : We describe a 37-year-old male who presented with acute quadriparesis due to severe hypokalaemia. While attempts at potassium correctio were underway he had a cardiac arrest due to profound hypokalaemia. There were five such episodes over a span of 45 minutes, each followed by successful resuscitation. Once stabilised and the potassium climbed to safe levels, a metabolic evaluation confirmed dRTA. Timely recognition and targeted electrolyte correction ensured full recovery. Conclusion Hypokalaemia is not common and is easily managed with oral or parenteral potassium therapy. Repeated cardiac arrest due to hypokalaemia is the highlight of this case and emphasises the need for prompt identification of dRTA to prevent fatal complications in recurrences. Distal renal tubular acidosis hypokalaemia cardiac arrest metabolic acidosis Figures Figure 1 Introduction Distal renal tubular acidosis is a rare cause of normal anion gap metabolic acidosis resulting from defective hydrogen ion secretion in the distal nephron. This defect promotes acid retention, potassium wasting, and persistently alkaline urine [ 1 , 2 ]. Though classically presenting as growth retardation, nephrolithiasis or osteomalacia, profound hypokalaemia may provoke neuromuscular paralysis or cardiac arrhythmias [ 3 ]. We report an unusual case of dRTA presenting dramatically as cardiac arrest. Case A 37-year-old male presented at the emergency with acute onset quadriparesis and carpopedal spasm. While initial blood investigations were pending, he suffered sudden cardiac arrest. Prompt cardiopulmonary resuscitation restored spontaneous circulation and he was shifted to intensive care unit (ICU). While in ICU, patient developed cardiac arrest again. There was a total of five cardiac arrests in a span of 45 minutes all of which were followed by successful resuscitation and he was finally intubated and put on mechanical ventilation. Electrocardiogram revealed T-wave inversion, U waves and tachycardia suggestive of severe hypokalaemia. (Figure A) Biochemistry confirmed serum potassium of 1.3 mmol/L. Arterial blood gas showed, pH 7.371, bicarbonate (HCO3) of 13.3 mEq/L and pCO2 34 mmHg. Intravenous potassium chloride was initiated. After initial stabilization, patient was extubated. Potassium improved to 3.1 mEq/L. Repeat ECG showed restoration of all wave forms and sinus rhythm (Figure B). During evaluation of underlying etiology for the hypokalaemia, urinary pH remained persistently alkaline at 6.6. Renal ultrasound showed increased cortical echogenicity. Serum creatinine was 1.9 mg/dl with an eGFR of 44 mL/min/1.73m². Thyroid function test was within normal range (TSH- 0.88 µIU/mL, fT4- 1.49 ng/dl). Autoimmune markers were negative. All these pointed towards a renal tubular pathology. A diagnosis of distal renal tubular acidosis was made based on clinical and biochemical parameters. The patient was subsequently managed with oral potassium citrate and alkali therapy. He recovered fully with resolution of neuromuscular weakness and was discharged on potassium citrate maintenance therapy. Discussion This case highlights a rare but critical presentation of dRTA with life-threatening hypokalaemia-induced cardiac arrest. The hallmark of dRTA is the triad of normal anion gap metabolic acidosis, hypokalaemia and inappropriately high urinary pH [ 1 , 4 ]. In dRTA, impaired distal acidification leads to acid retention while potassium is lost to maintain electrochemical neutrality [ 5 ]. Profound hypokalaemia prolongs ventricular repolarisation, predisposing to arrhythmias, cardiac arrest and sudden death [ 3 ]. The electrocardiogram typically shows U waves, T-wave flattening and ventricular tachyarrhythmias. Early identification of the biochemical pattern is essential, as prompt potassium repletion and alkali therapy are life-saving interventions [ 6 ]. Underlying causes of dRTA include autoimmune disorders like Sjögren’s syndrome, genetic defects, and drug-induced tubulointerstitial nephritis [ 2 , 5 ]. In our patient, secondary causes were ruled out, suggesting idiopathic dRTA. Chronic hypokalaemia in untreated cases may cause nephrocalcinosis, chronic kidney disease and osteomalacia. This case reiterates the importance of considering dRTA in any patient with unexplained hypokalaemia and metabolic acidosis with a normal anion gap. In emergency settings, recognition of characteristic ECG changes may aid diagnosis even before laboratory confirmation. Conclusion Distal RTA, though rare, can present with catastrophic hypokalaemia-induced arrhythmias which can be fatal. High clinical suspicion, urgent biochemical confirmation, aggressive potassium repletion and lifelong alkali therapy are crucial for preventing morbidity and mortality. Hypokalemia should always be investigated for the etiology to prevent recurrence and fatal complications. Learning points for clinicians Recognize distal RTA as a rare cause of life-threatening hypokalaemia. Look for dRTA in presence of normal anion gap metabolic acidosis with high urine pH. Early ECG changes can be clues. Rule out secondary causes of dRTA. Urgent potassium correction is critical. Lifelong alkali therapy prevents recurrence and complications. Abbreviations dRTA Distal Renal Tubular acidosis ICU Intensive Care Unit ECG Electrocardiogram HCO3 bicarbonate PCO2 Partial pressure of carbon dioxide TSH Thyroid stimulating hormone FT4 Free thyroxine Declarations Ethics approval and consent to participate: Consent from patient was obtained. As this is a case report, ethical approval was not required Consent for publication : Consent was obtained from the patient for publication Clinical trial number: not applicable Availability of data and material: all available data have been included in the manuscript. Competing interests: none declared Funding: none Acknowledgements: none References Soriano JR. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol. 2002;13(8):2160–2170. Batlle D, Haque SK. Genetic causes and mechanisms of distal renal tubular acidosis. Nephrol Dial Transplant. 2012;27(10):3691–3704. Gennari FJ. Hypokalemia. N Engl J Med. 1998;339(7):451–458. Karet FE. Mechanisms in hyperkalemic and hypokalemic renal tubular acidosis. J Am Soc Nephrol. 2009;20(2):251–254. Vasquez-Rios G, et al. Distal renal tubular acidosis and severe hypokalaemia: a case report. J Med Case Rep. 2019;13(1):103. Kalita J, et al. Renal tubular acidosis presenting as respiratory paralysis: a case report. Neurol India. 2010;58(1):106–108. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 10 Mar, 2026 Reviews received at journal 14 Oct, 2025 Reviews received at journal 11 Oct, 2025 Reviewers agreed at journal 06 Oct, 2025 Reviews received at journal 02 Oct, 2025 Reviewers agreed at journal 01 Oct, 2025 Reviewers agreed at journal 30 Sep, 2025 Reviewers invited by journal 29 Sep, 2025 Editor assigned by journal 08 Aug, 2025 Submission checks completed at journal 08 Aug, 2025 First submitted to journal 04 Aug, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7293894","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":527314834,"identity":"345ce9cb-8a50-406d-87c9-b3048cfcae69","order_by":0,"name":"Pankaj 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This defect promotes acid retention, potassium wasting, and persistently alkaline urine [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Though classically presenting as growth retardation, nephrolithiasis or osteomalacia, profound hypokalaemia may provoke neuromuscular paralysis or cardiac arrhythmias [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. We report an unusual case of dRTA presenting dramatically as cardiac arrest.\u003c/p\u003e"},{"header":"Case","content":"\u003cp\u003eA 37-year-old male presented at the emergency with acute onset quadriparesis and carpopedal spasm. While initial blood investigations were pending, he suffered sudden cardiac arrest. Prompt cardiopulmonary resuscitation restored spontaneous circulation and he was shifted to intensive care unit (ICU). While in ICU, patient developed cardiac arrest again. There was a total of five cardiac arrests in a span of 45 minutes all of which were followed by successful resuscitation and he was finally intubated and put on mechanical ventilation. Electrocardiogram revealed T-wave inversion, U waves and tachycardia suggestive of severe hypokalaemia. (Figure A) Biochemistry confirmed serum potassium of 1.3 mmol/L. Arterial blood gas showed, pH 7.371, bicarbonate (HCO3) of 13.3 mEq/L and pCO2 34 mmHg. Intravenous potassium chloride was initiated. After initial stabilization, patient was extubated. Potassium improved to 3.1 mEq/L. Repeat ECG showed restoration of all wave forms and sinus rhythm (Figure B). During evaluation of underlying etiology for the hypokalaemia, urinary pH remained persistently alkaline at 6.6. Renal ultrasound showed increased cortical echogenicity. Serum creatinine was 1.9 mg/dl with an eGFR of 44 mL/min/1.73m\u0026sup2;. Thyroid function test was within normal range (TSH- 0.88 \u0026micro;IU/mL, fT4- 1.49 ng/dl). Autoimmune markers were negative. All these pointed towards a renal tubular pathology. A diagnosis of distal renal tubular acidosis was made based on clinical and biochemical parameters.\u003c/p\u003e\u003cp\u003eThe patient was subsequently managed with oral potassium citrate and alkali therapy. He recovered fully with resolution of neuromuscular weakness and was discharged on potassium citrate maintenance therapy.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis case highlights a rare but critical presentation of dRTA with life-threatening hypokalaemia-induced cardiac arrest. The hallmark of dRTA is the triad of normal anion gap metabolic acidosis, hypokalaemia and inappropriately high urinary pH [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. In dRTA, impaired distal acidification leads to acid retention while potassium is lost to maintain electrochemical neutrality [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eProfound hypokalaemia prolongs ventricular repolarisation, predisposing to arrhythmias, cardiac arrest and sudden death [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The electrocardiogram typically shows U waves, T-wave flattening and ventricular tachyarrhythmias. Early identification of the biochemical pattern is essential, as prompt potassium repletion and alkali therapy are life-saving interventions [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eUnderlying causes of dRTA include autoimmune disorders like Sj\u0026ouml;gren\u0026rsquo;s syndrome, genetic defects, and drug-induced tubulointerstitial nephritis [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. In our patient, secondary causes were ruled out, suggesting idiopathic dRTA. Chronic hypokalaemia in untreated cases may cause nephrocalcinosis, chronic kidney disease and osteomalacia.\u003c/p\u003e\u003cp\u003eThis case reiterates the importance of considering dRTA in any patient with unexplained hypokalaemia and metabolic acidosis with a normal anion gap. In emergency settings, recognition of characteristic ECG changes may aid diagnosis even before laboratory confirmation.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eDistal RTA, though rare, can present with catastrophic hypokalaemia-induced arrhythmias which can be fatal. High clinical suspicion, urgent biochemical confirmation, aggressive potassium repletion and lifelong alkali therapy are crucial for preventing morbidity and mortality. Hypokalemia should always be investigated for the etiology to prevent recurrence and fatal complications.\u003c/p\u003e\n\u003ch3\u003eLearning points for clinicians\u003c/h3\u003e\n\u003cp\u003e\u003cul\u003e\u003cli\u003e\u003cp\u003eRecognize distal RTA as a rare cause of life-threatening hypokalaemia.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eLook for dRTA in presence of normal anion gap metabolic acidosis with high urine pH.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eEarly ECG changes can be clues.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eRule out secondary causes of dRTA.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eUrgent potassium correction is critical.\u003c/p\u003e\u003c/li\u003e\u003cli\u003e\u003cp\u003eLifelong alkali therapy prevents recurrence and complications.\u003c/p\u003e\u003c/li\u003e\u003c/ul\u003e\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003edRTA\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eDistal Renal Tubular acidosis\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eICU\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eIntensive Care Unit\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eECG\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eElectrocardiogram\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eHCO3\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ebicarbonate\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003ePCO2\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003ePartial pressure of carbon dioxide\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eTSH\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eThyroid stimulating hormone\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003cdiv class=\"DefinitionListEntry\"\u003e\u003cdiv class=\"Term\"\u003eFT4\u003c/div\u003e\u003cdiv class=\"Description\"\u003e\u003cp\u003eFree thyroxine\u003c/p\u003e\u003c/div\u003e\u003c/div\u003e\u003c/div\u003e"},{"header":"Declarations","content":"\u003cul type=\"disc\"\u003e\n \u003cli\u003eEthics approval and consent to participate: Consent from patient was obtained. As this is a case report, ethical approval was not required\u003c/li\u003e\n \u003cli\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e: Consent was obtained from the patient for publication\u003c/li\u003e\n \u003cli\u003e\u003cstrong\u003eClinical trial number: not applicable\u003c/strong\u003e\u003c/li\u003e\n \u003cli\u003eAvailability of data and material: all available data have been included in the manuscript.\u003c/li\u003e\n \u003cli\u003eCompeting interests: none declared\u003c/li\u003e\n \u003cli\u003eFunding: none\u003c/li\u003e\n \u003cli\u003eAcknowledgements: none\u003c/li\u003e\n\u003c/ul\u003e"},{"header":"References","content":"\u003col start=\"1\" type=\"1\"\u003e\n \u003cli\u003eSoriano JR. Renal tubular acidosis: the clinical entity.\u0026nbsp;\u003cem\u003eJ Am Soc Nephrol.\u003c/em\u003e 2002;13(8):2160–2170.\u003c/li\u003e\n \u003cli\u003eBatlle D, Haque SK. Genetic causes and mechanisms of distal renal tubular acidosis. \u003cem\u003eNephrol Dial Transplant.\u003c/em\u003e 2012;27(10):3691–3704.\u003c/li\u003e\n \u003cli\u003eGennari FJ. Hypokalemia. \u003cem\u003eN Engl J Med.\u003c/em\u003e 1998;339(7):451–458.\u003c/li\u003e\n \u003cli\u003eKaret FE. Mechanisms in hyperkalemic and hypokalemic renal tubular acidosis. \u003cem\u003eJ Am Soc Nephrol.\u003c/em\u003e 2009;20(2):251–254.\u003c/li\u003e\n \u003cli\u003eVasquez-Rios G, et al. Distal renal tubular acidosis and severe hypokalaemia: a case report. \u003cem\u003eJ Med Case Rep.\u003c/em\u003e 2019;13(1):103.\u003c/li\u003e\n \u003cli\u003eKalita J, et al. Renal tubular acidosis presenting as respiratory paralysis: a case report. \u003cem\u003eNeurol India.\u003c/em\u003e 2010;58(1):106–108.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"journal-of-rare-diseases","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [Journal of Rare Diseases](https://link.springer.com/journal/44162)","snPcode":"44162","submissionUrl":"https://submission.nature.com/new-submission/44162/3","title":"Journal of Rare Diseases","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Distal renal tubular acidosis, hypokalaemia, cardiac arrest, metabolic acidosis","lastPublishedDoi":"10.21203/rs.3.rs-7293894/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7293894/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e\u003cp\u003eDistal renal tubular acidosis (dRTA) is an uncommon renal tubular disorder disorder marked by impaired distal nephron acid excretion, resulting in hyperchloremic metabolic acidosis, persistent alkaline urine, and significant potassium loss. Complications include growth failure and rickets in children, whereas in adults osteomalacia, polyuria, nephrocalcinosis and nephrolithiasis are common. Hypokalaemia an invariable feature presents depending on severity. Muscular weakness, proximal myopathy and quadriparesis in severe cases can be the presentations. Severe hypokalaemia may rarely precipitate life-threatening cardiac arrhythmias including cardiac arrest.\u003c/p\u003e\u003ch2\u003eCase\u003c/h2\u003e\u003cp\u003e: We describe a 37-year-old male who presented with acute quadriparesis due to severe hypokalaemia. While attempts at potassium correctio were underway he had a cardiac arrest due to profound hypokalaemia. There were five such episodes over a span of 45 minutes, each followed by successful resuscitation. Once stabilised and the potassium climbed to safe levels, a metabolic evaluation confirmed dRTA. Timely recognition and targeted electrolyte correction ensured full recovery.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e\u003cp\u003eHypokalaemia is not common and is easily managed with oral or parenteral potassium therapy. Repeated cardiac arrest due to hypokalaemia is the highlight of this case and emphasises the need for prompt identification of dRTA to prevent fatal complications in recurrences.\u003c/p\u003e","manuscriptTitle":"Potassium Pause: A Case of Cardiac Arrest Unmasking Distal Renal Tubular Acidosis","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-10-12 14:31:12","doi":"10.21203/rs.3.rs-7293894/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-10T21:25:16+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-10-14T12:39:12+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-10-11T16:17:24+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"247972207395614380274615514614359183951","date":"2025-10-06T07:23:41+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-10-02T21:01:02+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"211430093684714744664849395926373071414","date":"2025-10-01T23:05:32+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"328318243867427469679701454500330823087","date":"2025-09-30T13:51:16+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-09-29T21:32:27+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-08-08T14:31:52+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-08-08T14:30:04+00:00","index":"","fulltext":""},{"type":"submitted","content":"Journal of Rare Diseases","date":"2025-08-04T18:31:31+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"journal-of-rare-diseases","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [Journal of Rare Diseases](https://link.springer.com/journal/44162)","snPcode":"44162","submissionUrl":"https://submission.nature.com/new-submission/44162/3","title":"Journal of Rare Diseases","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Open","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"54cf2a68-4c83-4e3f-9be8-485266f11d98","owner":[],"postedDate":"October 12th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-04-27T09:42:06+00:00","versionOfRecord":[],"versionCreatedAt":"2025-10-12 14:31:12","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7293894","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7293894","identity":"rs-7293894","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}