How to use these nephrology practice questions
These ten single-best-answer cases cover common nephrology decisions: urgent treatment, interpreting laboratory results and recognising patterns of kidney disease. They are practice questions, not a claim about the format of any particular examination. Read each case and select the best option; the explanation follows immediately so you can check your reasoning and identify why a tempting alternative is wrong.
For each question, name the finding that drives the decision before choosing an answer. In a clinical case, that may be an ECG change, a urine result, the timeline of symptoms or a specific biochemical pattern. A diagnosis alone is not always enough: many questions test the next safe action.
1. Hyperkalaemia with ECG changes
This question tests the first priority when potassium is high and the ECG suggests myocardial effects. A practice board on this topic can group the action, mechanism and follow-up decisions together.
A board on this topic ends up looking like this:
A 68-year-old with advanced chronic kidney disease has a potassium concentration of 7.1 mmol/L. The ECG shows tall, peaked T waves and a widening QRS complex. What is the most appropriate immediate treatment?
Intravenous calcium stabilises the cardiac membrane when hyperkalaemia is causing ECG changes. It does not lower serum potassium, so potassium-shifting and removal treatments are also required. Insulin with glucose can shift potassium intracellularly, but does not replace immediate membrane stabilisation in this presentation.
The key distinction is stabilisation versus potassium removal. Calcium acts quickly on cardiac membrane excitability but does not reduce the potassium concentration. Subsequent treatment should address shifting potassium into cells and removing it from the body, with repeat potassium and ECG assessment.
2. Acute kidney injury and urinary obstruction
This question tests recognition of a reversible post-renal cause and the action that relieves it. Look for evidence of retention rather than assuming that every acute creatinine rise is intrinsic kidney injury.
A practice question on this decision could look like this:
A 74-year-old man presents with oliguria and a rising creatinine. He has a palpable, painless bladder; bedside bladder scanning shows 900 mL of retained urine. What is the most appropriate next step?
The large residual volume and palpable bladder indicate urinary retention causing post-renal acute kidney injury. Prompt bladder decompression with a catheter is the immediate step, followed by monitoring for post-obstructive diuresis and investigation of the cause. Diuretics do not relieve the obstruction.
The strongest distractor is furosemide: oliguria can prompt thoughts of diuresis, but it does not correct a blocked outflow. After decompression, monitor urine output, fluid balance and electrolytes; the cause of retention also needs assessment.
3. Haematuria after a respiratory infection
This question tests how the interval between an infection and visible haematuria helps distinguish glomerular diagnoses.
A question focused on the timeline might be written like this:
A 22-year-old develops visible haematuria on the same day as a sore throat. Urine microscopy shows dysmorphic red cells, and kidney function is preserved. Which diagnosis best fits this timing?
IgA nephropathy can cause synpharyngitic haematuria, occurring during or shortly after an upper respiratory infection. Post-streptococcal glomerulonephritis more typically follows a latent interval after infection. The urine findings support a glomerular source but do not, on their own, identify its cause.
The timing is the discriminating clue; dysmorphic red cells indicate glomerular bleeding but are not specific to IgA nephropathy. In a real assessment, complement levels, infection history, kidney function and the wider clinical picture may guide further investigation.
4. Defining nephrotic-range proteinuria
This question checks a useful adult threshold. Be clear about the amount and the unit rather than relying on a vague description such as “heavy proteinuria”.
A threshold question could appear like this:
In an adult, which 24-hour urinary protein excretion is conventionally in the nephrotic range?
Nephrotic-range proteinuria in adults is conventionally defined as urinary protein excretion above 3.5 g per 24 hours. The threshold describes protein loss; nephrotic syndrome also involves clinical and biochemical features such as hypoalbuminaemia and oedema.
Do not treat the threshold as a complete diagnosis. A patient with proteinuria needs assessment of serum albumin, oedema, kidney function and urine findings, alongside investigation for an underlying glomerular or systemic cause.
5. Establishing chronic kidney disease
This question tests the duration required to distinguish chronic kidney disease from a single abnormal result or an episode of acute kidney injury.
A board section on diagnostic criteria might lead to this question:
Which finding meets the time-based definition of chronic kidney disease in an adult, assuming it is confirmed to persist?
An eGFR below 60 mL/min/1.73 m² persisting for at least three months meets the chronicity criterion for CKD. A single result cannot establish duration, and an abnormality may instead reflect acute illness or acute kidney injury. Persistent markers of kidney damage can also establish CKD even when eGFR is at least 60.
The strongest distractor is the single low eGFR: the value matters, but so does persistence. CKD can also be diagnosed through persistent markers of kidney damage, such as albuminuria, even when eGFR is not below 60.
6. Recognising an urgent dialysis indication
This question tests whether you can identify a complication that remains dangerous despite medical treatment, rather than using creatinine alone to decide about dialysis.
A decision-focused question could look like this:
A patient with acute kidney injury has severe hyperkalaemia with persistent ECG changes despite initial medical treatment. Which is the most appropriate next step?
Persistent, life-threatening hyperkalaemia despite medical treatment is an urgent indication to assess for renal replacement therapy. Decisions are based on the clinical context and complications, not a single creatinine threshold. Continue appropriate stabilisation and monitoring while arranging urgent specialist management.
The strongest distractor is waiting for a creatinine number. Dialysis decisions are driven by the whole clinical picture and complications, including refractory electrolyte disturbance, severe acidosis, fluid overload or uraemic complications. Escalation should not wait for an arbitrary laboratory threshold.
7. Interpreting an anion gap
This question tests calculation and classification. Calculate the gap from the values provided, then decide what that result says about the metabolic acidosis.
A short calculation question might look like this:
A patient has sodium 140 mmol/L, chloride 104 mmol/L and bicarbonate 12 mmol/L. Using an anion gap calculated as sodium minus chloride minus bicarbonate, how should the result be classified?
The anion gap is 140 − 104 − 12 = 24 mmol/L, which is elevated using the conventional reference range. With a low bicarbonate, this is a high anion gap metabolic acidosis. Reference ranges vary by laboratory, and albumin affects interpretation of the gap.
The arithmetic is straightforward; the interpretation needs context. Check the laboratory’s reference range and consider albumin, which can lower the measured gap. The gap classifies the acid–base disturbance but does not identify its cause.
8. Severe symptomatic hyponatraemia
This question tests the initial response to severe neurological symptoms and the need to avoid overly rapid correction.
A management question might be framed like this:
A patient with marked hyponatraemia has a generalised seizure. What is the most appropriate immediate treatment approach?
Seizure with severe hyponatraemia is a medical emergency. Hypertonic saline is used to raise sodium initially under close monitoring, with the treatment target and subsequent correction rate managed carefully to reduce the risk of osmotic demyelination. Unrestricted rapid correction is unsafe.
The aim is initial improvement in severe symptoms, not immediate normalisation of sodium. The correction plan depends on the patient’s presentation and local protocols; monitor sodium closely and avoid excessive correction, especially when hyponatraemia is chronic or its duration is uncertain.
9. Pulmonary–renal syndrome
This question tests the association between rapidly progressive kidney injury, pulmonary haemorrhage and a specific antibody-mediated disease.
A pattern-recognition question could look like this:
A 31-year-old has rapidly rising creatinine, haemoptysis and bilateral pulmonary opacities. Kidney biopsy shows crescentic glomerulonephritis with linear IgG staining along the glomerular basement membrane. Which diagnosis best fits?
Pulmonary haemorrhage with rapidly progressive glomerulonephritis and linear IgG staining along the glomerular basement membrane is characteristic of anti-GBM disease. This is a time-critical pulmonary–renal syndrome requiring urgent specialist assessment and treatment.
The biopsy pattern is the decisive clue. IgA nephropathy is associated with mesangial IgA deposition, while membranous nephropathy typically causes a nephrotic presentation rather than this classic pulmonary–renal pattern. Suspected anti-GBM disease warrants urgent assessment; do not delay escalation while waiting for a routine appointment.
10. Albuminuric diabetic CKD
This question tests kidney-protective treatment in a patient with hypertension and significant albuminuria, while keeping contraindications and monitoring in view.
A treatment-choice question could look like this:
A patient with type 2 diabetes has hypertension, an eGFR of 48 mL/min/1.73 m² and persistent urine albumin-to-creatinine ratio of 500 mg/g. There is no contraindication. Which treatment is an appropriate kidney-protective choice?
For hypertension with albuminuric CKD, an ACE inhibitor or an angiotensin receptor blocker is an appropriate kidney-protective choice if tolerated and not contraindicated. Monitor blood pressure, creatinine and potassium after starting or increasing treatment. Combining an ACE inhibitor with an ARB is generally avoided because it increases adverse effects without routine benefit.
Check baseline blood pressure, creatinine and potassium, then monitor after starting or changing the dose. The result and clinical circumstances matter: assess for a significant creatinine rise, hyperkalaemia, hypotension and other reasons the medicine may not be suitable.
Review the pattern of lost marks
A correct answer is useful; knowing what you repeatedly miss is more useful for planning the next study session. Group errors by skill: recognising an emergency, interpreting a urine or blood result, or choosing treatment. A practice dashboard might make the weaker areas visible like this:
A weak-area summary on this set could look like this:
Start with the lowest-scoring section, but review the reason for each error before repeating the question. Was the relevant value overlooked, the diagnosis uncertain, or the first action confused with definitive treatment? Those require different fixes.
If the same detail costs marks twice, turn it into a short retrieval question and revisit it in a later session. For example, a potassium emergency needs a clear distinction between cardiac stabilisation, intracellular shifting and potassium removal.
A remediation card from a repeated error could be waiting here:
You lost this mark twice: in hyperkalaemia with ECG changes, what does intravenous calcium do—and what does it not do?
How MySummaries helps
Build a nephrology revision board from your own notes, then use it to generate question practice, flashcards and marked written answers. Review the errors that recur and turn them into focused revision. Open MySummaries.