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Duodenal web masquerading as pseudohypoaldosteronism of infancy
Journal of Clinical and Translational Endocrinology: Case Reports 15 (2020) 100056
Contents lists available at ScienceDirect
Journal of Clinical and Translational Endocrinology: Case Reports journal homepage: www.elsevier.com/locate/jctecasereports.com
Original Research
Duodenal web masquerading as pseudohypoaldosteronism of infancy Mireille El Bejjani∗, Nandu Thalange Department of Pediatrics, Al Jalila Children's Specialty Hospital, Dubai, United Arab Emirates
A R T I C LE I N FO
A B S T R A C T
Keywords: Pseudohypoaldosteronism Intestinal obstruction Duodenal web Hyponatremia Hyperkalemia
Introduction: We present the case of a 5-month-old girl with duodenal web masquerading as pseudohypoaldosteronism (PHA). Case presentation: A 5-month-old girl born to first-cousin parents was referred to our institution for evaluation following two hospitalizations with vomiting and dehydration, associated with severe hyponatremia and hyperkalemia. She had a history of chronic emesis and failure to thrive, with a reportedly normal abdominal and renal ultrasound at her local hospital. Our initial evaluation confirmed hyponatremia, with elevated renin and aldosterone. The suspected diagnosis was PHA type 1. We started treatment with sodium supplementation following which her electrolytes normalized and subsequently she maintained normal electrolyte balance with relative improvement in weight gain and reduced emesis. Three months’ later, she re-presented with severe bilious emesis. Abdominal X-ray showed gastric dilatation indicating upper small bowel obstruction. Urgent ultrasound showed a grossly distended, fluid-filled, hyper-peristaltic stomach and duodenum, with obstruction distal to the third part of the duodenum. This was confirmed by upper-GI fluoroscopic study with findings suggestive of a duodenal web or duodenal stenosis/partial atresia. At laparotomy, a duodenal web was found and the patient underwent duodenojejunostomy. Following surg ery, the patient had complete resolution of emesis with normalization of electrolytes, renin and aldosterone. She no longer required sodium supplementation. Conclusion: This rare case highlights the presentation of transient PHA secondary to intestinal obstruction in an infant. In this context, transient PHA is due to gastrointestinal losses of sodium and water resulting in decreased renal perfusion from dehydration and consequent rise in renin and aldosterone.
1. Introduction We present a rare case of transient PHA of infancy secondary to intestinal obstruction. Only one similar case has been previously reported in an infant [1]. Urinary tract infection or obstruction are the most commonly found causes of transient PHA of infancy [2]. 2. Case report The patient was a 5-month-old girl, born at term to first-cousin parents. She was small for gestational age (birth weight 2.0 Kg), and subsequently had suboptimal weight gain with recurrent emesis. She was referred to the endocrinology clinic for evaluation following two hospitalizations for vomiting and dehydration with severe hyponatremia and hyperkalemia. Records obtained from her second hospitalization indicate that she developed gastroenteritis with multiple episodes of vomiting and watery diarrhea, decreased oral intake and decreased urine output, which led to admission. Initial labs showed
severe hyponatremia, (Na+ 114 mEq/L), hypochloremia (Cl− 77 mEq/ L) and hyperkalemia, (K+ 7.3 mEq/L), with normal bicarbonate, (HCO− 3 23 mEq/L). She had a reported normal abdominal and renal ultrasound in her local hospital. She received hypertonic saline and salbutamol to correct her electrolyte imbalance and was maintained on intravenous fluids. She rapidly improved and was discharged home with a referral to our institution.She was reviewed in the endocrinology clinic the following week and appeared well. She had occasional nonbilious emesis after feeds, attributed to gastro-esophageal reflux. Physical examination was normal. She had a soft, non-bulging anterior fontanelle and normal external female genitalia with no virilization. However, investigations showed hyponatremia with a sodium of 129 mEq/ml and potassium of 3.9 mEq/L, with markedly elevated plasma renin activity (170 ng/ml/hr [normal 2–37 ng/ml/hr]) and aldosterone (275 ng/dl [normal 5–90 ng/dl]). She had normal 17α-hydroxyprogesterone (29ng/dl) and morning cortisol (11 μg/dl). Given her normal renal ultrasound, we suspected PHA type 1 and proceeded to genetic testing. Treatment with sodium supplementation was initiated
Abbreviations: eNaC, epithelial sodium Channel; MR, Mineralocorticoid Receptor; PHA, Pseudohypoaldosteronism ∗ Corresponding author. Department of Pediatrics, Al Jalila Children's Specialty Hospital Al Jaddaf, Dubai, PO Box: 7662, United Arab Emirates. E-mail address: [email protected] (M. El Bejjani). https://doi.org/10.1016/j.jecr.2020.100056 Received 8 August 2019; Received in revised form 19 January 2020; Accepted 24 January 2020 2214-6245/ © 2020 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
Journal of Clinical and Translational Endocrinology: Case Reports 15 (2020) 100056
M. El Bejjani and N. Thalange
Fig. 1. Mechanisms of transient pseudohypoaldosteronism. Transient PHA in infants may be secondary to urinary tract infection, hydronephrosis, or gastrointestinal obstruction. Gastrointestinal losses of sodium and water result in dehydration and reduced kidney perfusion, with increased sodium reabsorption in the proximal tubules and reduced sodium delivery to the distal nephrons. Reduced MR expression in infancy further enhances the clinical presentation of PHA. MR is also downregulated in a hypertonic environement which may occur in the setting of chronic dehydration.
(MR), and results in excessive renal sodium losses. Autosomal recessive PHA is a more severe, multi-organ condition caused by mutation in genes encoding the subunits of the epithelial sodium channel (eNaC). The transient form of PHA1, also termed PHA type 3, is not genetic [3]. Urinary tract infection or obstruction are the primary causes most commonly associated with transient PHA in infancy [2]. The differential diagnosis included congenital adrenal hyperplasia, which was ruled out in our patient given the age at presentation, lack of virilization on examination, and normal 17α-hydroxyprogesterone level. Another consideration was neonatal Bartter syndrome due to mutation in the renal potassium channel ROMK, characterized by early postnatal severe hyperkalemia, along with hyponatremia and hyperreninemic hyperaldosteronism. However, in this context, potassium normalization is expected within the first week of life [4]. Other forms of Bartter's syndrome typically present with hypokalemia. Only one similar case of intestinal obstruction leading to transient PHA has been previously described in a 7-week-old infant with underlying congenital jejunal membrane [1]. Other reports of transient PHA have been described in association with extensive bowel resection in adults [5]. Aldosterone tightly regulates sodium and potassium homeostasis by acting on the MR which is expressed in the renal distal convoluted tubule. MR in turn promotes the expression of the genes encoding eNaC and the Na+/K+-ATPase [6]. Transient PHA is most commonly due to renal causes, but as in our case, maybe secondary to gastro-intestinal obstruction (see Fig. 1 for proposed mechanisms). In our case, the clinical picture of PHA at presentation was secondary to the gastrointestinal losses of sodium and water caused by the duodenal web, resulting in dehydration and poor kidney perfusion, with increased sodium reabsorption in the proximal tubules and reduced sodium delivery to the distal nephron causing hyperkalemia. Consequently, renin and aldosterone levels rose in response to decreased renal perfusion [7].
and she subsequently maintained normal electrolytes with improved weight gain and less frequent emesis. Three months’ later, she re-presented with severe bilious emesis. Abdominal X-ray showed a grossly dilated stomach indicating upper GI obstruction. Urgent ultrasound showed grossly distended, fluid-filled hyper-peristaltic stomach and duodenum, confirming obstruction distal to the third part of the duodenum. An upper-GI fluoroscopic study revealed distention of the duodenal bulb and descending loop. The third part of the duodenum showed funnel-shaped narrowing and obstruction to the flow of contrast. These findings suggested a duodenal web or duodenal stenosis/partial atresia. At laparotomy a duodenal web was found and she underwent duodenojejunostomy. Following surgical correction, the patient had complete resolution of emesis with normalization of electrolytes, renin and aldosterone. She no longer required sodium supplementation and her weight normalized. Subsequently, genetic testing for PHA was found to be negative. 3. Discussion We present a case of duodenal web masquerading as pseudohypoaldosteronism. Only one previous case has been described in an infant [1]. Her symptomatic improvement and normalization of electrolytes with salt supplementation added weight to the clinical diagnosis of Pseudohypoaldosteronism Type 1. The reportedly normal ultrasound examinations in her local hospital also supported this clinical diagnosis. Subsequently, her presentation with bilious emesis led to the diagnosis of duodenal web. PHA type 1 typically presents with failure to thrive, dehydration, hyponatremia, hyperkalemia, metabolic acidosis and high aldosterone and renin levels [3]. The autosomal dominant form of PHA1 is due to mutations in NR3C2 which encodes the mineralocorticoid receptor 2
Journal of Clinical and Translational Endocrinology: Case Reports 15 (2020) 100056
M. El Bejjani and N. Thalange
Acknowledgement
Additionally, advances in the understanding of the expression and regulation of the MR further elucidate the underlying mechanism of transient PHA in this context. It has been shown in vitro that hypertonicity induces post-transcriptional events that downregulate MR expression [8]. Moreover, the expression of MR varies throughout gestation and infancy, with transient expression seen between 15 and 24 weeks’ gestation, followed by a significant decrease in MR expression at birth coupled with reduced eNaC expression, despite very high levels of aldosterone [6].This will compound impaired regulation of sodium and potassium in the setting of severe dehydration in an infant. In our patient, reduced renal perfusion due to recurrent emesis led to a rise in aldosterone and renin levels. That, in addition to the downregulation of MR secondary to severe dehydration, resulted in the biochemical picture of PHA which resolved after surgical correction of the duodenal web. Although this clinical picture of transient PHA secondary to intestinal obtruction has seldom been reported, we speculate that it is under-recognized and is more common than it appears, given the higher incidence of gastrointestinal obstruction compared to transient PHA in neonates and infants. It should be considered in infants presenting with severe hyperkalemia and/or hyponatremia. In cases of apparent PHA, in addition to excluding a renal etiology, it is important to consider upper gastrointestinal obstruction as a possible cause.
We thank Dr. Ajay D'Souza, consultant pediatric radiologist at Al Jalila Children's Hospital for interpretation of radiographic studies. References [1] Nissen M, Dettmer P, Thränhardt R, Winter K, Niemeyer T, Tröbs RB. Congenital jejunal membrane causing transient pseudohypoaldosteronism and hypoprothrombinemia in a 7-week-old infant. Klin Pädiatr 2017;229(5):302–3. https://doi. org/10.1055/s-0043-113570. Epub 2017/08/14, PubMed PMID: 28806843. [2] Watanabe T. Renal mineralocorticoid receptor expression in early infancy and secondary pseudohypoaldosteronism type 1. Austin Pediatr 2017;4(1):1050. 2017. [3] Riepe FG. Pseudohypoaldosteronism. Endocr Dev. 2013;24:86–95. https://doi.org/ 10.1159/000342508. Epub 2013/02/01, PubMed PMID: 23392097. [4] Finer G, Shalev H, Birk OS, Galron D, Jeck N, Sinai-Treiman L, et al. Transient neonatal hyperkalemia in the antenatal (ROMK defective) Bartter syndrome. J Pediatr 2003;142(3):318–23. https://doi.org/10.1067/mpd.2003.100. PubMed PMID: 12640382. [5] Vantyghem MC, Hober C, Evrard A, Ghulam A, Lescut D, Racadot A, et al. Transient pseudo-hypoaldosteronism following resection of the ileum: normal level of lymphocytic aldosterone receptors outside the acute phase. J Endocrinol Invest 1999;22(2):122–7. https://doi.org/10.1007/BF03350891. PubMed PMID: 10195379. [6] Martinerie L, Munier M, Le Menuet D, Meduri G, Viengchareun S, Lombès M. The mineralocorticoid signaling pathway throughout development: expression, regulation and pathophysiological implications. Biochimie 2013;95(2):148–57. https://doi. org/10.1016/j.biochi.2012.09.030. Epub 2012/09/28, PubMed PMID: 23026756. [7] Watanabe T. Transient pseudohypoaldosteronism caused by intestinal abnormalities. Klin Pädiatr 2018;230(2):104. https://doi.org/10.1055/s-0043-120068. Epub 2017/ 12/13, PubMed PMID: 29237184. [8] Viengchareun S, Lema I, Lamribet K, Keo V, Blanchard A, Cherradi N, et al. Hypertonicity compromises renal mineralocorticoid receptor signaling through Tis11b-mediated post-transcriptional control. J Am Soc Nephrol 2014;25(10):2213–21. https://doi.org/10.1681/ASN.2013091023. Epub 2014/04/ 03, PubMed PMID: 24700863; PubMed Central PMCID: PMCPMC4178442.
Funding sources None. Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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Contents lists available at ScienceDirect
Journal of Clinical and Translational Endocrinology: Case Reports journal homepage: www.elsevier.com/locate/jctecasereports.com
Original Research
Duodenal web masquerading as pseudohypoaldosteronism of infancy Mireille El Bejjani∗, Nandu Thalange Department of Pediatrics, Al Jalila Children's Specialty Hospital, Dubai, United Arab Emirates
A R T I C LE I N FO
A B S T R A C T
Keywords: Pseudohypoaldosteronism Intestinal obstruction Duodenal web Hyponatremia Hyperkalemia
Introduction: We present the case of a 5-month-old girl with duodenal web masquerading as pseudohypoaldosteronism (PHA). Case presentation: A 5-month-old girl born to first-cousin parents was referred to our institution for evaluation following two hospitalizations with vomiting and dehydration, associated with severe hyponatremia and hyperkalemia. She had a history of chronic emesis and failure to thrive, with a reportedly normal abdominal and renal ultrasound at her local hospital. Our initial evaluation confirmed hyponatremia, with elevated renin and aldosterone. The suspected diagnosis was PHA type 1. We started treatment with sodium supplementation following which her electrolytes normalized and subsequently she maintained normal electrolyte balance with relative improvement in weight gain and reduced emesis. Three months’ later, she re-presented with severe bilious emesis. Abdominal X-ray showed gastric dilatation indicating upper small bowel obstruction. Urgent ultrasound showed a grossly distended, fluid-filled, hyper-peristaltic stomach and duodenum, with obstruction distal to the third part of the duodenum. This was confirmed by upper-GI fluoroscopic study with findings suggestive of a duodenal web or duodenal stenosis/partial atresia. At laparotomy, a duodenal web was found and the patient underwent duodenojejunostomy. Following surg ery, the patient had complete resolution of emesis with normalization of electrolytes, renin and aldosterone. She no longer required sodium supplementation. Conclusion: This rare case highlights the presentation of transient PHA secondary to intestinal obstruction in an infant. In this context, transient PHA is due to gastrointestinal losses of sodium and water resulting in decreased renal perfusion from dehydration and consequent rise in renin and aldosterone.
1. Introduction We present a rare case of transient PHA of infancy secondary to intestinal obstruction. Only one similar case has been previously reported in an infant [1]. Urinary tract infection or obstruction are the most commonly found causes of transient PHA of infancy [2]. 2. Case report The patient was a 5-month-old girl, born at term to first-cousin parents. She was small for gestational age (birth weight 2.0 Kg), and subsequently had suboptimal weight gain with recurrent emesis. She was referred to the endocrinology clinic for evaluation following two hospitalizations for vomiting and dehydration with severe hyponatremia and hyperkalemia. Records obtained from her second hospitalization indicate that she developed gastroenteritis with multiple episodes of vomiting and watery diarrhea, decreased oral intake and decreased urine output, which led to admission. Initial labs showed
severe hyponatremia, (Na+ 114 mEq/L), hypochloremia (Cl− 77 mEq/ L) and hyperkalemia, (K+ 7.3 mEq/L), with normal bicarbonate, (HCO− 3 23 mEq/L). She had a reported normal abdominal and renal ultrasound in her local hospital. She received hypertonic saline and salbutamol to correct her electrolyte imbalance and was maintained on intravenous fluids. She rapidly improved and was discharged home with a referral to our institution.She was reviewed in the endocrinology clinic the following week and appeared well. She had occasional nonbilious emesis after feeds, attributed to gastro-esophageal reflux. Physical examination was normal. She had a soft, non-bulging anterior fontanelle and normal external female genitalia with no virilization. However, investigations showed hyponatremia with a sodium of 129 mEq/ml and potassium of 3.9 mEq/L, with markedly elevated plasma renin activity (170 ng/ml/hr [normal 2–37 ng/ml/hr]) and aldosterone (275 ng/dl [normal 5–90 ng/dl]). She had normal 17α-hydroxyprogesterone (29ng/dl) and morning cortisol (11 μg/dl). Given her normal renal ultrasound, we suspected PHA type 1 and proceeded to genetic testing. Treatment with sodium supplementation was initiated
Abbreviations: eNaC, epithelial sodium Channel; MR, Mineralocorticoid Receptor; PHA, Pseudohypoaldosteronism ∗ Corresponding author. Department of Pediatrics, Al Jalila Children's Specialty Hospital Al Jaddaf, Dubai, PO Box: 7662, United Arab Emirates. E-mail address: [email protected] (M. El Bejjani). https://doi.org/10.1016/j.jecr.2020.100056 Received 8 August 2019; Received in revised form 19 January 2020; Accepted 24 January 2020 2214-6245/ © 2020 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
Journal of Clinical and Translational Endocrinology: Case Reports 15 (2020) 100056
M. El Bejjani and N. Thalange
Fig. 1. Mechanisms of transient pseudohypoaldosteronism. Transient PHA in infants may be secondary to urinary tract infection, hydronephrosis, or gastrointestinal obstruction. Gastrointestinal losses of sodium and water result in dehydration and reduced kidney perfusion, with increased sodium reabsorption in the proximal tubules and reduced sodium delivery to the distal nephrons. Reduced MR expression in infancy further enhances the clinical presentation of PHA. MR is also downregulated in a hypertonic environement which may occur in the setting of chronic dehydration.
(MR), and results in excessive renal sodium losses. Autosomal recessive PHA is a more severe, multi-organ condition caused by mutation in genes encoding the subunits of the epithelial sodium channel (eNaC). The transient form of PHA1, also termed PHA type 3, is not genetic [3]. Urinary tract infection or obstruction are the primary causes most commonly associated with transient PHA in infancy [2]. The differential diagnosis included congenital adrenal hyperplasia, which was ruled out in our patient given the age at presentation, lack of virilization on examination, and normal 17α-hydroxyprogesterone level. Another consideration was neonatal Bartter syndrome due to mutation in the renal potassium channel ROMK, characterized by early postnatal severe hyperkalemia, along with hyponatremia and hyperreninemic hyperaldosteronism. However, in this context, potassium normalization is expected within the first week of life [4]. Other forms of Bartter's syndrome typically present with hypokalemia. Only one similar case of intestinal obstruction leading to transient PHA has been previously described in a 7-week-old infant with underlying congenital jejunal membrane [1]. Other reports of transient PHA have been described in association with extensive bowel resection in adults [5]. Aldosterone tightly regulates sodium and potassium homeostasis by acting on the MR which is expressed in the renal distal convoluted tubule. MR in turn promotes the expression of the genes encoding eNaC and the Na+/K+-ATPase [6]. Transient PHA is most commonly due to renal causes, but as in our case, maybe secondary to gastro-intestinal obstruction (see Fig. 1 for proposed mechanisms). In our case, the clinical picture of PHA at presentation was secondary to the gastrointestinal losses of sodium and water caused by the duodenal web, resulting in dehydration and poor kidney perfusion, with increased sodium reabsorption in the proximal tubules and reduced sodium delivery to the distal nephron causing hyperkalemia. Consequently, renin and aldosterone levels rose in response to decreased renal perfusion [7].
and she subsequently maintained normal electrolytes with improved weight gain and less frequent emesis. Three months’ later, she re-presented with severe bilious emesis. Abdominal X-ray showed a grossly dilated stomach indicating upper GI obstruction. Urgent ultrasound showed grossly distended, fluid-filled hyper-peristaltic stomach and duodenum, confirming obstruction distal to the third part of the duodenum. An upper-GI fluoroscopic study revealed distention of the duodenal bulb and descending loop. The third part of the duodenum showed funnel-shaped narrowing and obstruction to the flow of contrast. These findings suggested a duodenal web or duodenal stenosis/partial atresia. At laparotomy a duodenal web was found and she underwent duodenojejunostomy. Following surgical correction, the patient had complete resolution of emesis with normalization of electrolytes, renin and aldosterone. She no longer required sodium supplementation and her weight normalized. Subsequently, genetic testing for PHA was found to be negative. 3. Discussion We present a case of duodenal web masquerading as pseudohypoaldosteronism. Only one previous case has been described in an infant [1]. Her symptomatic improvement and normalization of electrolytes with salt supplementation added weight to the clinical diagnosis of Pseudohypoaldosteronism Type 1. The reportedly normal ultrasound examinations in her local hospital also supported this clinical diagnosis. Subsequently, her presentation with bilious emesis led to the diagnosis of duodenal web. PHA type 1 typically presents with failure to thrive, dehydration, hyponatremia, hyperkalemia, metabolic acidosis and high aldosterone and renin levels [3]. The autosomal dominant form of PHA1 is due to mutations in NR3C2 which encodes the mineralocorticoid receptor 2
Journal of Clinical and Translational Endocrinology: Case Reports 15 (2020) 100056
M. El Bejjani and N. Thalange
Acknowledgement
Additionally, advances in the understanding of the expression and regulation of the MR further elucidate the underlying mechanism of transient PHA in this context. It has been shown in vitro that hypertonicity induces post-transcriptional events that downregulate MR expression [8]. Moreover, the expression of MR varies throughout gestation and infancy, with transient expression seen between 15 and 24 weeks’ gestation, followed by a significant decrease in MR expression at birth coupled with reduced eNaC expression, despite very high levels of aldosterone [6].This will compound impaired regulation of sodium and potassium in the setting of severe dehydration in an infant. In our patient, reduced renal perfusion due to recurrent emesis led to a rise in aldosterone and renin levels. That, in addition to the downregulation of MR secondary to severe dehydration, resulted in the biochemical picture of PHA which resolved after surgical correction of the duodenal web. Although this clinical picture of transient PHA secondary to intestinal obtruction has seldom been reported, we speculate that it is under-recognized and is more common than it appears, given the higher incidence of gastrointestinal obstruction compared to transient PHA in neonates and infants. It should be considered in infants presenting with severe hyperkalemia and/or hyponatremia. In cases of apparent PHA, in addition to excluding a renal etiology, it is important to consider upper gastrointestinal obstruction as a possible cause.
We thank Dr. Ajay D'Souza, consultant pediatric radiologist at Al Jalila Children's Hospital for interpretation of radiographic studies. References [1] Nissen M, Dettmer P, Thränhardt R, Winter K, Niemeyer T, Tröbs RB. Congenital jejunal membrane causing transient pseudohypoaldosteronism and hypoprothrombinemia in a 7-week-old infant. Klin Pädiatr 2017;229(5):302–3. https://doi. org/10.1055/s-0043-113570. Epub 2017/08/14, PubMed PMID: 28806843. [2] Watanabe T. Renal mineralocorticoid receptor expression in early infancy and secondary pseudohypoaldosteronism type 1. Austin Pediatr 2017;4(1):1050. 2017. [3] Riepe FG. Pseudohypoaldosteronism. Endocr Dev. 2013;24:86–95. https://doi.org/ 10.1159/000342508. Epub 2013/02/01, PubMed PMID: 23392097. [4] Finer G, Shalev H, Birk OS, Galron D, Jeck N, Sinai-Treiman L, et al. Transient neonatal hyperkalemia in the antenatal (ROMK defective) Bartter syndrome. J Pediatr 2003;142(3):318–23. https://doi.org/10.1067/mpd.2003.100. PubMed PMID: 12640382. [5] Vantyghem MC, Hober C, Evrard A, Ghulam A, Lescut D, Racadot A, et al. Transient pseudo-hypoaldosteronism following resection of the ileum: normal level of lymphocytic aldosterone receptors outside the acute phase. J Endocrinol Invest 1999;22(2):122–7. https://doi.org/10.1007/BF03350891. PubMed PMID: 10195379. [6] Martinerie L, Munier M, Le Menuet D, Meduri G, Viengchareun S, Lombès M. The mineralocorticoid signaling pathway throughout development: expression, regulation and pathophysiological implications. Biochimie 2013;95(2):148–57. https://doi. org/10.1016/j.biochi.2012.09.030. Epub 2012/09/28, PubMed PMID: 23026756. [7] Watanabe T. Transient pseudohypoaldosteronism caused by intestinal abnormalities. Klin Pädiatr 2018;230(2):104. https://doi.org/10.1055/s-0043-120068. Epub 2017/ 12/13, PubMed PMID: 29237184. [8] Viengchareun S, Lema I, Lamribet K, Keo V, Blanchard A, Cherradi N, et al. Hypertonicity compromises renal mineralocorticoid receptor signaling through Tis11b-mediated post-transcriptional control. J Am Soc Nephrol 2014;25(10):2213–21. https://doi.org/10.1681/ASN.2013091023. Epub 2014/04/ 03, PubMed PMID: 24700863; PubMed Central PMCID: PMCPMC4178442.
Funding sources None. Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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