High-Yield Renal Medicine and Electrolytes for Exams

Renal medicine and electrolytes appear in nearly every exam block, often disguised inside cardiology, endocrine or emergency questions. Most marks come from a handful of skills: staging AKI and CKD, treating hyperkalaemia in the right order, working through hyponatraemia, and reading acid-base results. This guide is exam revision.

Acute kidney injury

Definition (KDIGO framework)

Causes

• Prerenal: hypovolaemia, sepsis, heart failure, drugs that reduce renal perfusion (ACE inhibitors, ARBs, NSAIDs).
• Intrinsic: acute tubular necrosis (ischaemia, contrast, aminoglycosides), glomerulonephritis, acute interstitial nephritis (drugs such as penicillins, PPIs, NSAIDs), rhabdomyolysis.
• Postrenal: obstruction (prostate, stones, tumour).

Management themes

• Assess volume status and treat hypovolaemia.
• Stop or hold nephrotoxic and renally risky drugs ("sick day" medicines: ACE inhibitors, ARBs, diuretics, metformin, NSAIDs, SGLT2 inhibitors).
• Ultrasound if obstruction is suspected or the cause is unclear.
• Urine dipstick for blood and protein (suggests glomerular disease).
• Indications for urgent dialysis: refractory hyperkalaemia, refractory acidosis, fluid overload resistant to diuretics, uraemic complications (pericarditis, encephalopathy), certain toxins.

Chronic kidney disease

CKD is abnormal kidney structure or function for more than three months. It is classified by GFR (G1–G5) and albuminuria (A1–A3).

Management themes

• Blood pressure control; ACE inhibitor or ARB for albuminuria.
• SGLT2 inhibitors to slow progression in many patients with CKD, with or without diabetes, per recent guidelines.
• Statins for cardiovascular risk.
• Manage complications: anaemia (check iron, then erythropoiesis-stimulating agents), CKD-mineral bone disorder (phosphate, PTH, vitamin D), acidosis.
• Adjust drug doses for eGFR.
• Plan renal replacement therapy or conservative care early.

Potassium

Hyperkalaemia

Causes: AKI or CKD, drugs (ACE inhibitors, ARBs, spironolactone, trimethoprim, potassium supplements), Addison disease, rhabdomyolysis, tumour lysis, acidosis. Always consider pseudohyperkalaemia from a haemolysed sample.

ECG changes progress from tall tented T waves to flattened P waves, broad QRS and sine wave, then arrest.

Treatment order (exam favourite):

1. Stabilise the myocardium: intravenous calcium gluconate or chloride if ECG changes or severe hyperkalaemia. It does not lower potassium.
2. Shift potassium into cells: insulin with glucose; nebulised salbutamol as an adjunct.
3. Remove potassium: potassium binders, loop diuretics if passing urine, dialysis if refractory.
4. Treat the cause and review drugs.
5. Monitor glucose after insulin.

Hypokalaemia

Causes: diuretics, vomiting, diarrhoea, hyperaldosteronism, insulin, beta-agonists, low magnesium. ECG: U waves, flat T waves. Replace potassium (oral if mild; intravenous at controlled rates if severe) and correct magnesium, or hypokalaemia will not correct.

Sodium

Hyponatraemia: a structured approach

1. Is it real? Exclude hyperglycaemia (translocational) and pseudohyponatraemia.
2. Serum osmolality: true hypotonic hyponatraemia has low osmolality.
3. Urine osmolality: low (below 100 mOsm/kg) suggests excess water intake (primary polydipsia, beer potomania).
4. Volume status and urine sodium:

SIADH causes: small cell lung cancer, pneumonia, CNS disease, drugs (SSRIs, carbamazepine, antipsychotics, cyclophosphamide), pain, postoperative state. Fluid restriction is first line.

Correction: severe symptoms (seizures, reduced consciousness) need hypertonic saline boluses with close monitoring. Chronic hyponatraemia must be corrected slowly within daily limits to avoid osmotic demyelination.

Hypernatraemia

Usually water loss with poor access to water (older adults, infants, impaired consciousness) or diabetes insipidus. Correct gradually.

Calcium, magnesium and phosphate in brief

• Hypercalcaemia: see high-yield endocrinology; fluids first.
• Hypomagnesaemia: PPIs, diuretics, alcohol; causes refractory hypokalaemia and hypocalcaemia.
• Hyperphosphataemia: CKD, tumour lysis.
• Refeeding syndrome: low phosphate, potassium and magnesium when feeding restarts after starvation.

Acid-base

Anion gap

Anion gap = sodium − (chloride + bicarbonate). A raised gap points to added acid.

Metabolic alkalosis: vomiting, diuretics, hyperaldosteronism.

Glomerular disease

Classic clues: IgA nephropathy causes haematuria one or two days after an upper respiratory infection; post-streptococcal glomerulonephritis appears one to three weeks after infection. Haemoptysis with AKI suggests anti-GBM disease or ANCA vasculitis.

Diuretics in one table

Common exam traps

• Treating hyperkalaemia with insulin before calcium when the ECG shows changes.
• Forgetting a haemolysed sample as a cause of high potassium.
• Correcting chronic hyponatraemia too fast.
• Missing thiazides as the cause of hyponatraemia in an older patient.
• Continuing ACE inhibitors, NSAIDs and metformin in AKI.
• Not correcting magnesium in refractory hypokalaemia.

How to revise

Practise electrolyte and acid-base questions in short, frequent sets; they rely on structured reasoning that improves with repetition. MediFlow Exam Prep includes data-interpretation vignettes with full explanations. See also high-yield endocrinology and diabetes.

Summary

• AKI: define, stage, find the cause, stop risky drugs.
• CKD: classify by GFR and albuminuria; protect kidneys and the heart.
• Hyperkalaemia: calcium, shift, remove, treat cause.
• Hyponatraemia: osmolality, urine tests, volume status, slow correction.
• Acid-base: use the anion gap.