Secondary hyperaldosteronism and medullary nephrocalcinosis caused by self-administered and uncontrolled laxative use in an adolescent patient

Secondary hyperaldosteronism is respondent aldosterone secretion increase, occurring due to some diseases or drug use. It may be accompanied by normal arterial pressure with/without water retention or arterial hypertension without water retention. Secondary hyperaldosteronism without arterial hypertension and without water retention is usually caused by the use of laxative and diuretic drugs. This condition is characterized by the lack of salt wasting symptoms, presence of myalgia and muscle weakness resulting from hypokalemia, calcium oxalate crystalluria and sonographic signs of medullary nephrocalcinosis. Such characteristics of water-salt exchange and presence of nephrocalcinosis in combination with hypercalciuria are defined as Bartter-like syndrome. Peculiarity of the given clinical case is determined not by a diagnostic difficulty of secondary hyperaldosteronism but concealment of long term self-administered use of laxatives > 2 years without medical indications in a female patient, resulting in medullary nephrocalcinosis. A well-informed patient may endanger medical practice, because it is impossible to foresee everything including the uncontrolled self-administered drug use leading to the undesirable consequences.

1. Jones C, Mughal Z. Disorders of mineral metabolismus and nephrolithiasis. In: Webb N, Postlethwait RJ, ed. Clinical pediatric nephrology. 3rd ed. New York: Oxford University Press; 2003. рp. 73–101.

2. Van’t Hoff W. Renal tubular disorders. In: Webb NJ, Postlethwaite RJ, eds. Clinical pediatric nephrology. 3rd ed. New York: Oxford Press; 2003. pp. 103–112.

3. Diamond FB, Jr., Root AW. Disorders of mineral homeostasis in the newborn, infant, child, and adolescent. In: Sperling MA, editor. Pediatric Endocrinology. 3rd ed. Chapter 17. Elsevier Science; 2008.

4. Postlethwait RJ, ed. Clinical paediatric nephrology. 2nd ed. Oxford: Batterworth-Heinemann Ltd; 1994. 411 р.

5. Matsunoshita N, Nozu K, Shono A, et al. Differential diagnosis of Bartter syndrome, Gitelman syndrome, and pseudo-Bartter/Gitelman syndrome based on clinical characteristics. Genet Med. 2016;18(2):180−188. doi: https://doi.org/1010.1038/gim.2015.56.

6. Hizal MG, Ciki K, Esref S, et al. Clinical features of pseudo-Bartter syndrome in cystic fibrosis. Eur Resp J. 2017;50:PA1343. doi: https://doi.org/1010.1183/1393003.congress-2017.pa1343.

7. Faraji-Goodarzi M. Pseudo-Bartter syndrome in children with cystic fibrosis. Clin Case Rep. 2019;7(6):1123−1126. doi: https://doi.org/1010.1002/ccr3.2180.

8. Sakalli H, Bucak HI. Type IV neonatal Bartter syndrome complicated with congenital chloride diarrhea. Am J Case Rep. 2012; 13:230−233. doi: https://doi.org/1010.12659/AJCR.883446.

9. Krieg M, Bohnheit HG, Breustedt HJ, et al. Endokrinologie I: in frage und antwort. Springer-Verlag Berlin Heidelberg; 1989. 287 р.

10. Stolecke H. (Hrsg.) Endokrinologie des Kindes- und Jugendalters. Springer-Verlag Berlin Heidelberg; 1982. 666 р.