Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Persistent hypokalemia and hypomagnesemia usually have hereditary causes such as Gitelmans or Bartters syndrome. Making a diagnosis of hereditary tubulopathies requires genetic testing which is quite expensive, not readily available and which may prove challenging in resource limited settings. This outlines the importance of physiology-based management in resource-limited settings.
This was a single-patient case report of a patient admitted with COVID 19 and acute gastroenteritis and subsequently followed up as outpatient. Clinical follow up, spot and 24-hour urine electrolytes, renin/aldosterone panel, arterial blood gases, and genomic sequencing were done between August 2022 and March 2025.
This was a 38-year-old male who had presented to the hospital with mild COVID-19 pneumonia and acute gastroenteritis. At the time of first contact, his serum potassium was 2.32 mmol/L and serum magnesium 0.46 mmol/L, which were duly corrected. The patient was noted to have persistent hypokalemia and hypomagnesemia despite supplementation. Further history was notable for salt cravings for several years.
Two spot-urine profiles demonstrated a fractional excretion of sodium of 0.29–0.71 %, a fractional excretion of potassium of 8.0–9.4 % and striking hypocalciuria which was pointing towards a diagnosis of Gitelmans syndrome. Arterial blood gas showed a pH of 7.49 and the urine Cl⁻ was 174 mmol/L. Renin was markedly elevated with an elevated aldosterone. Anti-nuclear antibody and anti-dsDSNA antibody were negative.
The whole-exome/genome sequencing was negative, and a targeted Sanger sequencing confirmed an isolated heterozygous SLC12A1 c.2006A>C (p.Glu669Ala, variant of uncertain significance). The patient was started on low-dose spironolactone 25 mg once daily with potassium and magnesium supplementation which helped with the resolution of symptoms
We present a case of multiple electrolyte imbalance that fit the clinical diagnosis of Gitelman syndrome but did not have the classic biallelic SLC12A3 mutation on genetic testing. This highlights two importance points. Firstly, the value of genetic testing in in ruling out hereditary tubulopathies which can be expensive and not readily available in resource limited settings. Secondly, post-infectious causes like COVID-19 can unmask or precipitate Gitelman like phenotypes. The patient was effectively managed as acquired Gitelman syndrome with potassium and magnesium supplementation and with inexpensive mineralocorticoid blockade. This demonstrates that genetic testing might not always be accessible and therefore, clinical diagnosis becomes important, especially for acquired tubulopathies.
