Phys Clinical Cases · renal
Polycystic Kidney Disease (ADPKD) — DCE Clinical Case
DCE short-case station: the abdominal examination in ADPKD — bilateral ballotable renal masses, cystic hepatomegaly, hernias, blood pressure and hypertensive fundi — with presentation template and probing questions.
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Target exams
Approach — what the examiner is testing
This station is not "palpate an abdomen". It tests whether you can find bilateral renal masses correctly, stage their consequences, and survey the extrarenal disease — then synthesise rather than list. The ballotable kidney is a vanishingly rare sign in modern medicine and ADPKD is its classic source, so examiners watch your ballottement technique closely [7].
Before touching the patient: blood pressure measured properly, both arms, after rest — hypertension is the earliest manifestation of ADPKD and the most modifiable driver of progression, so measuring it yourself is part of the examination, not an afterthought [2].
Examination sequence
General inspection. Comfort at rest (chronic pain is common and undertreated), abdominal distension or visible asymmetry from massive kidneys or liver, sclera for the pallor of CKD, and a quick mental note of body habitus and any flank scars from prior cyst surgery or nephrectomy [7].
Hands and arms. Nails for the leuconychia of hypoalbuminaemia or Lindsay nails of CKD; asterixis if advanced disease is in the differential; then the blood pressure you have already measured [2].
Fundi. Two minutes that stage his hypertension: arteriolar narrowing, silver wiring, AV nipping — and the absence of haemorrhages or papilloedema, which you state explicitly because their presence would change the urgency of everything [2].
Abdomen — the core. Distension, scars, visible masses. Palpate each flank bimanually: one hand in the loin lifting forward, the other palpating from the front — a renal mass is ballotable (bounces between your hands), moves with respiration, is dull to percussion, and you can often get above it (unlike a spleen). In ADPKD both kidneys are enlarged, firm to hard, and may be nodular; the right is usually easier. Then the liver — palpable, smooth or irregularly nodular, sometimes massively so; measure the span and say whether it feels cystic [7].
Hernial orifices and genitourinary surface. Inguinal and incisional hernias are commoner in ADPKD and matter practically — they complicate future peritoneal dialysis — so examine the orifices and say why [6].
Cardiovascular survey. A displaced apex or fourth sound for left ventricular hypertrophy from years of hypertension; at the precordium listen for the mid-systolic click of mitral valve prolapse, found in about a quarter of ADPKD patients, and for aortic regurgitation [4] [2].
Finish. Offer a urine dipstick (haematuria, proteinuria), state that you would check for ankle oedema and fluid status, and offer to complete the family history — the examiner is listening for the extrarenal survey: aneurysm history in the family, liver, valves, hernias, diverticular disease [3] [5].
Presentation template (deliver this to the examiner)
"Mr Okafor has a blood pressure of 152/94 mmHg measured with an appropriate cuff after rest, grade 2 hypertensive retinopathy without haemorrhages or papilloedema, and a sustained apex beat consistent with hypertensive heart disease. On abdominal examination he has bilaterally enlarged, ballotable renal masses that move with respiration — the right approximately 16 cm by palpation — and a palpable, nodular liver edge 4 cm below the costal margin. There are no hernias. My synthesis: ADPKD with polycystic liver involvement and suboptimally controlled hypertension, with mass-effect symptoms. I would document his renal function and eGFR trajectory, quantify his kidney and liver volumes on imaging to stage progression by Mayo class, intensify his blood-pressure management with an ACE inhibitor first line, review his pain, and complete the extrarenal survey — including whether any family member has had a cerebral aneurysm, which would trigger MR angiography for him." [2] [6] [3]
If you find peritonism or localised tenderness
Say immediately that acute abdominal pain in an ADPKD patient has its own differential: cyst haemorrhage (pain with haematuria, settling), an infected cyst (fever, high inflammatory markers, often negative cultures), a stone — and in the dialysis or transplant population, diverticulitis with possible perforation, which runs a more complicated course in ADPKD and lowers your threshold for surgical review and cross-sectional imaging [5] [7].
Probing questions
"How do you distinguish his renal masses from splenomegaly or a gastric mass?" — "By the renal signs: each mass is ballotable between my two hands, moves with respiration, is dull to percussion, and I can get above it — a spleen has a notch, cannot be balloted, and I cannot get above it. Bilaterality and the nodular liver beside it complete the syndrome: two enlarged kidneys plus hepatomegaly plus hypertension is ADPKD until proven otherwise." [7] [1]
"His wife asks whether his blood pressure matters now that the diagnosis is made." — "It matters more than anything else I can modify today. Hypertension in ADPKD is renal in origin — cyst compression drives intrarenal renin release — it arrives before renal function falls, and controlling it slows organ damage: in the young patient with preserved GFR the HALT-PKD trial supports a target below 110/75 as tolerated, with an ACE inhibitor or ARB first line. At 152/94 he is under-treated, and that is the most actionable finding of my examination." [2]
"What would make you image his brain?" — "A trigger, not a reflex. I do not screen every ADPKD patient for intracranial aneurysms — I screen the enriched-risk ones: a family history of aneurysm or subarachnoid haemorrhage, a prior rupture, a high-risk occupation, or pre-transplant assessment. The test is MR angiography, and most small screen-detected aneurysms in ADPKD are managed with interval imaging rather than intervention. And every patient, screened or not, gets the thunderclap-headache safety-net advice." [3] [6]
"He asks whether his children should be scanned." — "That is a counselling conversation before it is a scan. Each child has a 50% risk; the choice to be tested is theirs when they are old enough to make it, because the result has insurance and family-planning consequences. If they proceed as adults, age-calibrated ultrasound is the first-line test — and the message I leave him with is that finding it early is when blood-pressure control and progression staging do the most good." [1] [6]
References
- [1]Pei Y, Obaji J, Dupuis A, et al. Unified criteria for ultrasonographic diagnosis of ADPKD J Am Soc Nephrol, 2009.PMID 18945943
- [2]Schrier RW, Abebe KZ, Perrone RD, et al. Blood pressure in early autosomal dominant polycystic kidney disease N Engl J Med, 2014.PMID 25399733
- [3]Irazabal MV, Huston J 3rd, Kubly V, et al. Extended follow-up of unruptured intracranial aneurysms detected by presymptomatic screening in patients with autosomal dominant polycystic kidney disease Clin J Am Soc Nephrol, 2011.PMID 21551026
- [4]Hossack KF, Leddy CL, Johnson AM, et al. Echocardiographic findings in autosomal dominant polycystic kidney disease N Engl J Med, 1988.PMID 3419455
- [5]Lederman ED, McCoy G, Conti DJ, et al. Diverticulitis and polycystic kidney disease Am Surg, 2000.PMID 10695753
- [6]Kidney Disease: Improving Global Outcomes (KDIGO) ADPKD Work Group KDIGO 2025 Clinical Practice Guideline for the Evaluation, Management, and Treatment of Autosomal Dominant Polycystic Kidney Disease (ADPKD) Kidney Int, 2025.PMID 39848759
- [7]Ong AC, Devuyst O, Knebelmann B, et al. Autosomal dominant polycystic kidney disease: the changing face of clinical management Lancet, 2015.PMID 26090645