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.
Autosomal dominant polycystic kidney disease is the most common inherited genetic kidney disorder and a common cause of end stage renal disease.PKD1 and PKD2 account for more than 90% of cases and patients frequently present between the third and fifth decades of life. Other recently identified gene variants, including GANAB, ALG8, ALG9, DNAJB11, and IFT140, are typically associated with milder or atypical cystic phenotypes. Hypertension frequently complicated ADPKD and the average age of diagnosing hypertension is 30 years to 34years. We, however, present an adolescent with bilateral kidney cysts, markedly enlarged kidneys and hypertension representing an unusually early and severe presentation of ADPKD in whom there is no family history.
Clinical data were obtained from the patient’s hospital records. Evaluation included history, physical examination, laboratory studies, and renal imaging (ultrasound and magnetic resonance imaging). Diagnosis was based on KDIGO 2025 criteria for ADPKD, which allow confirmation in the presence of multiple bilateral cysts and kidney enlargement in the absence of atypical extrarenal features
An 18-year-old male undergraduate student was referred to our facility on account of ultrasound findings of kidney cysts. He had presented to his primary care physician on account of heaviness around the left flank not associated with fever, hematuria, vomiting or swelling. His blood pressure on presenting to his primary care physician was 170/90mmHg and he was commenced on amlodipine 10mg daily and lisinopril 10mg daily. Abdominopelvic ultrasound revealed massively enlarged kidneys with multiple cysts which led to his referral. His medical history is notable for hypertension diagnosed at the age of 16 although no screening for secondary hypertension had been performed at the time. He was offered anti-hypertensives, but he had not been compliant with his medications.
On examination, he was afebrile, not pale or anicteric, and had no leg oedema. The abdomen was full, moved with respiration, and had no areas of tenderness. The left kidney was ballotable. His blood pressure was 140/90mmHg. The rest of the examination was unremarkable.
Urinalysis showed trace protein and blood.
Lab test
Value
Reference range
Sodium
139
130-146 mmol/L
Potassium
4.4
3.3-5.0mmol/L
Chloride
99
90-108mmol/L
Bicarbonate
22
10-24mmol/L
urea
5.7
1.6-8.0mmol/L
Creatinine
87
36-130umol/L
Calcium
2.28
2.20-2.70mmol/L
Total cholesterol
4.3
5.3mmol/L
LDL-C
2.8
2.6mmol/L
PCV
44
40-54%
Magnetic resonance imaging showed marked renomegaly with both kidneys containing multiple extensive varied sized oval shaped cystic lesions within, with complete thinning of the renal cortical mantle. The right kidney measured 16.0X10.1X9.4cm and the left kidney measured 17.2x10.1x11.4cm with a total kidney volume of 790ml and 1,030ml for the right and left kidney respectively.
Mayo classification: 1E
The patient was counselled, blood pressure control optimized, family screening was suggested and the patient offered tolvaptan. On learning about the possible complications of tolvaptan, the patient opted to defer the decision to commence tolvaptan and asked for the conversation to be revisited in 3 months.
Traditionally diagnosing ADPKD in the absence of a family history could be challenging particularly in resource poor setting where genetic testing is not readily available. The recent KDIGO 2025 diagnostic framework allowed us to make a diagnosis of ADPKD without family history or genetic testing. Presentation with large kidneys and hypertension at this age is not common. The presence of early onset hypertension and total kidney volume greater than expected for age puts him at risk of rapid ADPKD progression also demonstrated by his MAYO classification. This case with early severe disease onset raises a hypothesis of truncating or biallelic mutation or the presence of other modifiers. It is notable that a similar case report of an 18-year-old with severely enlarged kidneys had demonstrated GANAB gene mutation hitherto associated with mild disease. Thus, this case highlights the challenge of relying on imaging-based diagnosis and knowledge gaps that could have been addressed with genetic testing.
Although our patient deferred commencing tolvaptan, being able to make a diagnosis even in the absence of a family history or genetic testing allowed us to rapidly offer guideline-directed care aimed at driving optimal outcome.
