UKMLA Renal & Electrolyte Emergencies: AKI, Hyperkalaemia

Renal medicine is the UKMLA specialty where the highest-weighted stems carry the tightest time-critical thresholds. Hyperkalaemia with ECG changes kills in minutes if the right drug isn't given. Acute kidney injury unrecognised during a fluid-resuscitation stem converts a passable mark into a dangerous management plan. Hyponatraemia corrected too aggressively causes central pontine myelinolysis — a distractor that recurs every few AKT papers. The exam weights renal content heavily because safe F1 practice depends on recognising kidney injury fast, classifying it correctly, and acting on electrolyte derangement before harm occurs.

A typical AKT paper contains 20–30 stems that touch renal or electrolyte content — roughly 10–15% of the total. They cluster into three groups: AKI recognition and management, CKD complications and staging, and acute electrolyte/acid-base emergencies. Each group has a rigid protocol (KDIGO for AKI, NICE NG203 for CKD, the hyperkalaemia triad, the Adrogue-Madias style hyponatraemia pathway) that is drillable for the AKT.

This masterclass walks through all three clusters, integrates ABG interpretation (which threads through every renal emergency), and closes with fluid-status assessment — the skill that determines whether a fluid bolus, a diuretic, or neither is the right next step. Aligned to KDIGO 2012, NICE NG148 (AKI), NICE NG203 (CKD), and the 2023 UK Kidney Association hyperkalaemia guideline.

Table of contents

1. Why renal carries exam weight
2. AKI — pre-renal, intrinsic, post-renal
3. KDIGO staging
4. Fluid management in AKI
5. Contrast-associated nephropathy
6. CKD — staging and progression
7. CKD complications — anaemia, bone disease, CV risk
8. Hyperkalaemia
9. Hyponatraemia
10. Hypernatraemia
11. Hypocalcaemia
12. Metabolic acidosis and the anion gap
13. Metabolic alkalosis
14. ABG interpretation algorithm
15. Fluid-status assessment
16. Common AKT question patterns
17. FAQ

1. Why renal carries exam weight

The GMC content map lists "acute kidney injury", "chronic kidney disease", "fluid depletion", "electrolyte abnormalities", and "dehydration" as core presentations — and renal pathology threads through cardiology (HF decompensation), endocrine (DKA, SIADH), infection (sepsis, urosepsis), and pharmacology (renal dosing, nephrotoxic drug recognition) stems.

Candidates lose renal marks most often through four recurring errors: failing to recognise pre-renal AKI in a septic patient who needs fluid resuscitation, picking the wrong drug for hyperkalaemia (insulin-dextrose without calcium gluconate cover), treating hyponatraemia too fast, and missing contrast nephropathy prophylaxis. All four are fixable with targeted drilling.

Your target: 75%+ subscore on renal/electrolyte Q-bank filters. Pair this post with the emergency presentations masterclass for shared acute-care framing (sepsis six, DKA, major haemorrhage) and the respiratory post for the ABG five-step interpretation.

2. AKI — pre-renal, intrinsic, post-renal

Definition (KDIGO). Any of:

• Rise in creatinine ≥26 μmol/L within 48 hours.
• Rise in creatinine ≥1.5× baseline within 7 days.
• Urine output <0.5 mL/kg/hour for 6+ hours.

Classification by cause (the pathophysiological triage):

Pre-renal (most common — 60%). Reduced renal perfusion.

• Hypovolaemia: haemorrhage, GI losses, burns, diuretic overuse, poor oral intake.
• Reduced cardiac output: HF decompensation, sepsis, cardiogenic shock.
• Renal artery stenosis.
• Drug-mediated: ACEi/ARBs (reduce GFR through efferent dilation), NSAIDs (reduce afferent flow).

Urinalysis: typically no blood/protein. Urea:creatinine ratio elevated (prerenal pattern). Responds to volume replacement.

Intrinsic (30%). Kidney parenchymal damage.

• Acute tubular necrosis (ATN): ischaemic (prolonged pre-renal state), nephrotoxic (aminoglycosides, contrast, rhabdomyolysis, ethylene glycol).
• Acute interstitial nephritis (AIN): drug-induced (penicillins, PPIs, NSAIDs, rifampicin). Fever + rash + eosinophilia classic (but often absent).
• Glomerulonephritis: post-infectious, IgA nephropathy, lupus nephritis, anti-GBM (Goodpasture's), ANCA-vasculitis.
• Vascular: thrombotic microangiopathy (HUS, TTP), cholesterol emboli.

Urinalysis: red cell casts (glomerular), muddy brown casts (ATN), white cells + eosinophils (AIN).

Post-renal (10%). Urinary tract obstruction.

• Benign prostatic hyperplasia, prostate cancer.
• Bladder outlet obstruction.
• Ureteric obstruction: stones, malignancy, retroperitoneal fibrosis.
• Pelvic malignancy compression.

Imaging: renal tract US detects hydronephrosis; CT if cause unclear.

Investigation priority in new AKI:

1. Urinalysis (dipstick + microscopy).
2. Bladder scan for retention.
3. Renal tract USS.
4. Fluid assessment — JVP, capillary refill, blood pressure, lying-standing BP.
5. Medication review — stop nephrotoxics (ACEi/ARB, NSAIDs, metformin, contrast), adjust others.
6. Bloods — U&E, bicarbonate, magnesium, calcium, phosphate, CK (rhabdo), autoimmune screen if suspicion.
7. ABG/VBG — assess acid-base and potassium urgency.

AKT question pattern. Elderly patient with sepsis, creatinine jumped from 85 to 180 in 3 days. First step? Fluid resuscitation with crystalloid + identify and treat sepsis source + stop nephrotoxics.

3. KDIGO staging

Stage 1: creatinine 1.5–1.9× baseline OR rise ≥26 μmol/L within 48h; urine output <0.5 mL/kg/hour for ≥6h.

Stage 2: creatinine 2.0–2.9× baseline; urine output <0.5 mL/kg/hour for ≥12h.

Stage 3: creatinine ≥3.0× baseline OR creatinine ≥354 μmol/L OR initiation of RRT; urine output <0.3 mL/kg/hour for ≥24h OR anuria for ≥12h.

Indications for renal replacement therapy (AEIOU):

• Acidosis (pH <7.15 refractory to medical management)
• Electrolytes (refractory hyperkalaemia)
• Ingestion (dialysable toxin — methanol, ethylene glycol, lithium, salicylate)
• Overload (pulmonary oedema refractory to diuretics)
• Uraemia (pericarditis, encephalopathy, bleeding)

AKT question pattern. AKI patient with pH 7.12, K 7.2, pulmonary oedema unresponsive to furosemide. Action? Urgent dialysis referral.

4. Fluid management in AKI

Pre-renal AKI (volume-depleted):

• Crystalloid bolus 500 mL over 15 min (smaller/slower in elderly or cardiac history).
• Reassess fluid status after each bolus (JVP, BP, urine output).
• Continue boluses until euvolaemic or response plateaus.
• Target urine output >0.5 mL/kg/hour.
• Avoid dextrose solutions as resuscitation fluid (inadequate volume expansion).

Balanced crystalloid (Hartmann's, Plasma-Lyte) vs 0.9% saline:

• Hartmann's/Plasma-Lyte preferred in most AKI contexts per PLUS and SPLIT trials — reduces hyperchloraemic acidosis risk.
• 0.9% saline acceptable but use in moderation (causes hyperchloraemic metabolic acidosis at high volumes).
• Avoid Hartmann's in hyperkalaemia (contains 5 mmol/L potassium — small clinical effect but AKT sometimes tests this).

Post-renal AKI: relieve obstruction (catheterise for bladder outflow; percutaneous nephrostomy or ureteric stenting for ureteric obstruction).

Intrinsic AKI: treat specific cause (withdraw offending drug in AIN; steroids/immunosuppression in vasculitis/GN).

Fluid challenge failure. If euvolaemic and urine output not improving, do not push more fluid — risks pulmonary oedema. Consider RRT criteria and nephrology referral.

AKT question pattern. AKI patient now JVP raised, bilateral crackles, SpO₂ 88%. Next step? Stop fluids; IV furosemide; consider NIV; nephrology referral for possible dialysis.

5. Contrast-associated nephropathy

Definition. Creatinine rise ≥25% or ≥44 μmol/L within 48–72 hours of contrast administration, without other cause.

Risk factors:

• Pre-existing CKD (eGFR <60)
• Diabetes
• Age >75
• Heart failure
• Volume depletion
• Concurrent nephrotoxic drugs
• High-dose or repeated contrast

Prevention:

• IV 0.9% saline 1 mL/kg/hour for 12 hours before and 12 hours after contrast in high-risk patients.
• Stop nephrotoxics (ACEi, NSAIDs, metformin) on day of contrast; restart 48 hours later once creatinine stable.
• N-acetylcysteine — older recommendation, largely abandoned after AMACING trial showed no benefit.
• Use lowest dose of iso-osmolar or low-osmolar contrast.

Management once established. Supportive — fluid balance, treat hyperkalaemia, avoid further nephrotoxics. Usually self-resolving within 7–14 days.

AKT question pattern. Diabetic with eGFR 35 scheduled for CT with contrast. Action? Withhold metformin and ACEi on the day; IV saline prehydration 12 hours before and after; check creatinine 48 hours post.

6. CKD — staging and progression

CKD staging (NICE NG203):

Stages G1 and G2 require evidence of kidney damage (albuminuria, haematuria, imaging/biopsy findings) for diagnosis.

Albuminuria categories (ACR — urine albumin:creatinine ratio):

• A1: <3 mg/mmol (normal)
• A2: 3–30 mg/mmol (moderate)
• A3: >30 mg/mmol (severe)

Progression monitoring:

• Rapid progression = decline ≥5 mL/min/1.73 m²/year OR stage transition + ≥25% fall.
• Refer to nephrology: eGFR <30, ACR >70, rapid progression, resistant HTN, complications.

Key drug interventions:

• ACEi or ARB (ramipril, losartan) if ACR >3 mg/mmol — especially diabetic nephropathy. Slows progression.
• SGLT2 inhibitor (dapagliflozin, empagliflozin) in CKD — approved at eGFR ≥20 for diabetic and non-diabetic CKD with albuminuria. DAPA-CKD and EMPA-KIDNEY trials transformed practice. Major 2026-testable update.
• Statin (atorvastatin 20 mg) for CV risk.
• BP target <140/90 generally; <130/80 if ACR >70 (or diabetic with ACR >3).
• Smoking cessation, diet, exercise, weight management.

AKT question pattern. Diabetic patient with eGFR 42, ACR 45 mg/mmol. First-line nephroprotective drug additions? ACEi + SGLT2 inhibitor.

7. CKD complications — anaemia, bone disease, CV risk

CKD anaemia. Erythropoietin deficiency from damaged kidneys. Usually normocytic normochromic. Diagnose from stage G3 onwards.

• Investigate and replete iron first: target ferritin >100 (200 in dialysis patients) and transferrin saturation >20%. Often IV iron needed.
• ESA (erythropoiesis-stimulating agent) — darbepoetin alfa, epoetin alfa — if Hb <100 despite iron repletion. Target Hb 100–120 (higher targets cause cardiovascular harm).
• HIF-PHI agents (roxadustat) — emerging alternative.

CKD mineral and bone disorder (CKD-MBD).

• Hyperphosphataemia develops from G3b — reduce dietary phosphate; phosphate binders (sevelamer, calcium carbonate, lanthanum).
• Secondary hyperparathyroidism — phosphate rises + 1,25-vitamin D falls → PTH rises → bone resorption. Treat with activated vitamin D analogues (alfacalcidol, paricalcitol); cinacalcet for refractory.
• Vitamin D deficiency — supplement colecalciferol.
• Bone disease (renal osteodystrophy).

CV risk. CKD is the strongest non-traditional CV risk factor. Aggressive BP + lipid management. Antiplatelet if established atherosclerotic disease.

Metabolic acidosis in CKD. Oral sodium bicarbonate if bicarbonate <20 mmol/L — slows progression, improves nutrition.

8. Hyperkalaemia

Classification and severity (2023 UK Kidney Association):

• Mild: K 5.5–5.9 mmol/L
• Moderate: K 6.0–6.4
• Severe: K ≥6.5 OR any ECG changes OR symptoms

ECG progression (memorise):

1. Tall tented T waves
2. Prolonged PR
3. Loss of P waves
4. Widened QRS
5. Sine wave pattern
6. Asystole/VF

Causes:

• AKI/CKD
• ACEi/ARB, spironolactone, amiloride, trimethoprim, NSAIDs
• Potassium supplements
• Rhabdomyolysis, tumour lysis
• Addison's disease
• Acidosis
• Pseudohyperkalaemia (haemolysed sample)

Management ladder (for severe or ECG changes):

1. Cardioprotection: IV calcium gluconate 10 mL of 10% over 5–10 min. Onset <5 min; duration 30–60 min. Stabilises cardiac membrane. Repeat if ECG changes persist after 5 min. (Calcium chloride in arrest.)
2. Shift K intracellularly:
   • IV insulin 10 units actrapid + 25 g dextrose (125 mL 20% glucose or equivalent) over 15–30 min. Monitor BMs for 6 hours (delayed hypoglycaemia risk).
   • Salbutamol 10–20 mg nebulised (synergistic with insulin-dextrose).
3. Remove K from body:
   • Sodium zirconium cyclosilicate (Lokelma) or patiromer — newer oral agents that bind K. NICE-approved.
   • Older calcium resonium less effective, used historically.
   • Haemodialysis if refractory or severe CKD.
4. Treat the cause: stop offending drugs, correct acidosis (sodium bicarbonate if pH <7.2), manage underlying AKI/CKD.

Sodium bicarbonate (8.4% 50 mL) is a legacy option for severe acidotic hyperkalaemia but no longer routinely first-line.

AKT question pattern. AKI patient, K 7.1, ECG shows tall tented T waves and widened QRS. First drug? IV calcium gluconate 10 mL 10% — cardiac membrane stabilisation is priority. Then insulin-dextrose + salbutamol.

9. Hyponatraemia

Classification by severity (symptoms) and chronicity:

• Mild: Na 130–134, often asymptomatic.
• Moderate: Na 125–129, headache, nausea, confusion.
• Severe: Na <125, seizures, coma, respiratory arrest.

Acute (<48 hours) vs chronic (>48 hours) matters enormously for correction rate.

Diagnostic workflow — the volume-status triage:

Step 1 — Assess volume status:

• Hypovolaemic: reduced JVP, dry mucous membranes, postural drop, tachycardia.
  • Renal loss (diuretics, Addison's, salt-losing nephropathy).
  • Extra-renal loss (GI losses, burns, third-spacing).
• Euvolaemic:
  • SIADH (commonest).
  • Hypothyroidism.
  • Adrenal insufficiency.
• Hypervolaemic: raised JVP, oedema, ascites.
  • Heart failure.
  • Cirrhosis.
  • Nephrotic syndrome.
  • Renal failure.

Step 2 — Urine osmolality and urine sodium:

• Urine osmolality <100 mOsm/kg → primary polydipsia or beer potomania.
• Urine osmolality >100 → inappropriate ADH activity or solute-related cause.
• Urine sodium <20 mmol/L → effective hypovolaemia (GI losses, HF, cirrhosis, nephrotic — kidney retaining sodium).
• Urine sodium >40 mmol/L → renal salt loss OR SIADH (kidneys wasting sodium inappropriately).

SIADH criteria:

• Euvolaemic hyponatraemia.
• Plasma osmolality <275 mOsm/kg.
• Urine osmolality >100 mOsm/kg (inappropriately concentrated).
• Urine sodium >40 mmol/L.
• Normal thyroid, adrenal, renal function.
• Not on diuretics.

SIADH causes:

• CNS: stroke, tumour, trauma, meningitis, SAH.
• Pulmonary: pneumonia, TB, small cell lung cancer (paraneoplastic).
• Drugs: SSRIs, carbamazepine, chlorpropamide, ecstasy, opiates.
• Other: nausea, pain, surgery.

Management:

• Hypovolaemic: IV 0.9% saline + treat cause.
• Euvolaemic (SIADH): fluid restrict 750–1000 mL/day first-line. Second-line: tolvaptan (vasopressin receptor antagonist) or demeclocycline.
• Hypervolaemic: fluid restrict + treat underlying cause (diuretics in HF, albumin in cirrhosis).
• Severe symptomatic (seizures, coma): hypertonic 3% saline 150 mL bolus over 10 min, repeat once if needed; aim Na rise 5 mmol/L in first hour.

Correction rate: Never more than 10 mmol/L in 24 hours (ideally 8 mmol/L) to avoid central pontine myelinolysis (osmotic demyelination syndrome). Present with locked-in syndrome days after overcorrection.

AKT question pattern. Small-cell lung cancer patient, Na 118, euvolaemic, urine osmolality 450, urine sodium 55. Diagnosis? SIADH. Management? Fluid restrict + treat underlying malignancy.

10. Hypernatraemia

Definition. Na >145 mmol/L. Almost always dehydration.

Causes:

• Water loss: diabetes insipidus (cranial — DDAVP; nephrogenic — thiazides, lithium, chronic hypercalcaemia), sweat losses, GI losses without replacement.
• Reduced intake: elderly, dementia, immobility, ICU.
• Sodium gain: hypertonic saline, Cushing's (rare).

Management:

• Slow correction — aim <10 mmol/L fall in 24 hours to avoid cerebral oedema.
• Oral rehydration if possible.
• IV 5% dextrose (or 0.45% saline) — choose based on co-existing volume status.
• If severely volume-depleted, start with 0.9% saline to restore circulation before switching to hypotonic.

11. Hypocalcaemia

Classification (corrected calcium):

• Mild: 2.00–2.19 mmol/L.
• Moderate: 1.90–1.99.
• Severe: <1.90.

Signs. Trousseau's (carpal spasm on BP cuff inflation) and Chvostek's (facial twitch on tapping facial nerve). Neuromuscular irritability, perioral tingling, carpopedal spasm, tetany, seizures, prolonged QT, Torsades.

Causes:

• Hypoparathyroidism (post-thyroidectomy, autoimmune).
• Vitamin D deficiency.
• CKD (failure to convert 25-OH to 1,25-OH vitamin D).
• Hyperphosphataemia (rhabdomyolysis, tumour lysis).
• Acute pancreatitis.
• Hypomagnesaemia (common in alcoholics, chronic PPI).
• Sepsis.

Management:

• Severe or symptomatic: IV calcium gluconate 10 mL of 10% over 10 min, then infusion 100 mL 10% calcium gluconate in 1L saline/dextrose over 12–24 hours.
• Replete magnesium (correction unlikely without this).
• Oral calcium + vitamin D for chronic.
• Treat underlying cause.

AKT question pattern. Post-thyroidectomy patient, corrected Ca 1.72, perioral tingling, positive Chvostek's. Action? IV calcium gluconate 10 mL 10% + oral calcium/vitamin D supplementation.

12. Metabolic acidosis and the anion gap

Anion gap. Na − (Cl + HCO₃). Normal 8–16 mmol/L.

High anion gap (MUDPILES):

• Methanol
• Uraemia
• Diabetic ketoacidosis
• Paraldehyde (old), propylene glycol (modern addition — from lorazepam/pentobarbital infusions)
• Iron, Isoniazid
• Lactic acidosis (sepsis, tissue hypoxia, metformin, ischaemia)
• Ethylene glycol (antifreeze)
• Salicylate (aspirin overdose)

Normal anion gap (hyperchloraemic):

• GI bicarb loss (diarrhoea, high-output stoma).
• Renal tubular acidosis (types 1, 2, 4).
• Addison's.
• Acetazolamide.
• Hyperchloraemic acidosis (saline over-resuscitation).

Management. Treat underlying cause. Sodium bicarbonate only for severe (pH <7.1) and specific causes (salicylate overdose, ESRD). DKA is treated with insulin + fluids, not bicarbonate.

13. Metabolic alkalosis

Types:

• Chloride-responsive (urine Cl <20 mmol/L): vomiting, NG suction, diuretics, post-hypercapnia.
• Chloride-resistant (urine Cl >20): hyperaldosteronism, Cushing's, Bartter/Gitelman, severe hypokalaemia.

Management. IV 0.9% saline + potassium replacement for chloride-responsive. Treat endocrine cause for chloride-resistant.

14. ABG interpretation algorithm

Use the five-step framework from the respiratory post. Recap:

Step 1 — Hypoxia? PaO₂ <10 on air.

Step 2 — pH. Acidosis <7.35; alkalosis >7.45.

Step 3 — Primary disorder (respiratory vs metabolic).

• pH ↓ + CO₂ ↑ → respiratory acidosis.
• pH ↓ + HCO₃ ↓ → metabolic acidosis.
• pH ↑ + CO₂ ↓ → respiratory alkalosis.
• pH ↑ + HCO₃ ↑ → metabolic alkalosis.

Step 4 — Compensation. Partial compensation = pH still abnormal. Full compensation = pH normalised (rare; usually only in chronic respiratory acidosis).

Step 5 — Anion gap if metabolic acidosis.

Complex disorders. Some ABGs show two primary disorders (mixed). Expected compensation ranges:

• Metabolic acidosis: PaCO₂ should fall by 1.2 × fall in HCO₃. If PaCO₂ is higher, co-existing respiratory acidosis.
• Metabolic alkalosis: PaCO₂ should rise by 0.7 × rise in HCO₃. If lower, co-existing respiratory alkalosis.

AKT question pattern. Severe sepsis, pH 7.18, pCO₂ 3.2, HCO₃ 10, lactate 5.5. Classification? Metabolic acidosis (high anion gap from lactate) with respiratory compensation. Underlying: septic lactic acidosis.

15. Fluid-status assessment

Deciding whether to give fluids, withhold them, or diurese is one of the most tested F1 decisions.

Hypovolaemic signs:

• Tachycardia, hypotension, low JVP, dry mucous membranes, reduced capillary refill >2s.
• Postural BP drop (>20 mmHg systolic) or postural tachycardia (>30 bpm).
• Oliguria (<0.5 mL/kg/hour).
• Concentrated urine; high urea:creatinine ratio.
• Cool peripheries, reduced skin turgor.

Hypervolaemic signs:

• Raised JVP, peripheral oedema, bibasal crackles, hypoxia.
• Pulmonary oedema on CXR.
• S3 gallop.
• Hepatomegaly, ascites.

Euvolaemic. Normal JVP, no oedema, normal capillary refill, adequate urine output. BP within patient's usual range.

Practical approach:

1. Passive leg raise — if BP/UO improves, volume-responsive.
2. IV fluid challenge 250–500 mL — reassess.
3. Central venous pressure and bedside echo (IVC collapsibility) in ICU settings.

Pitfalls:

• JVP can be falsely low if patient agitated/tachypnoeic.
• Pitting oedema can coexist with intravascular depletion (nephrotic, cirrhotic).
• Tachycardia may be absent in beta-blocked patients.

MLA Prep tags every fluid-management question by underlying pathology and fluid-status category — so your practice distinguishes volume-responsive from volume-overloaded AKI in the exam. Start the free diagnostic for your renal/fluid subscore in 20 minutes.

16. Common AKT question patterns

Seven renal stem templates recur on AKT papers.

Template 1 — Pre-renal vs intrinsic AKI. Stem gives context (sepsis, hypovolaemia, nephrotoxic drugs) + urinalysis. Task: categorise and pick first action.

Template 2 — KDIGO staging + RRT decision. Stem gives creatinine trend + urine output + electrolyte/acid-base parameters. Task: identify stage and whether dialysis criteria met.

Template 3 — Hyperkalaemia emergency. K + ECG findings. First drug is almost always IV calcium gluconate if ECG changes or K ≥6.5.

Template 4 — Hyponatraemia workup. Volume + urine osmolality + urine sodium → triage to hypovolaemic/euvolaemic/hypervolaemic. Identify SIADH vs cardiac vs renal cause.

Template 5 — Acid-base classification. ABG interpretation with anion gap if metabolic acidosis.

Template 6 — Contrast nephropathy prophylaxis. Pre-contrast management in high-risk patient.

Template 7 — CKD drug management. ACEi + SGLT2 + statin + BP target for progressive CKD.

17. FAQ

How many AKT marks come from renal/electrolyte content? Approximately 20–30 of 200 stems touch renal or electrolyte content directly; more if you include prescribing (renal dosing) and fluid management.

Is sodium bicarbonate still used in hyperkalaemia? Rarely routinely. Modern guidance favours calcium gluconate + insulin-dextrose + salbutamol + K binders. Sodium bicarbonate is considered in severe acidotic hyperkalaemia (pH <7.2).

Do I need to know exact insulin-dextrose doses? Yes. 10 units actrapid + 25 g dextrose (equivalent to 125 mL 20% or 250 mL 10%) is the standard AKT-testable dose.

When are SGLT2 inhibitors safe in CKD? Initiation at eGFR ≥20 (dapagliflozin, empagliflozin). Continue at lower eGFRs. No longer restricted to T2DM — approved for non-diabetic CKD with albuminuria.

How fast can you correct hyponatraemia? Maximum 10 mmol/L in 24 hours (ideally 8). Overcorrection risks central pontine myelinolysis (locked-in syndrome, typically 2–6 days later).

What's the role of tolvaptan? Vasopressin V2 antagonist. SIADH refractory to fluid restriction. Also used in ADPKD to slow progression.

Is Hartmann's safe in AKI? Yes — current evidence favours balanced crystalloid over 0.9% saline in most AKI settings. The low potassium in Hartmann's (5 mmol/L) is clinically insignificant except at very high volumes.

What's the target Hb in CKD anaemia? 100–120 g/L. Higher targets cause cardiovascular harm (TREAT, CHOIR, CREATE trials).

When should I start dialysis in CKD progression? No single threshold. Consider when eGFR <10–15 + symptoms (uraemia, fluid overload, acidosis, electrolyte derangement) OR progressive malnutrition. Usually planned 6 months ahead with vascular access creation.

How is rhabdomyolysis managed? IV fluids aggressively (3–6 L/day initial target) to maintain urine output >1 mL/kg/hour. Monitor CK, K, Ca, urate, myoglobin. Treat hyperkalaemia per protocol. Urinary alkalinisation (sodium bicarbonate) remains debated; not routinely recommended.

What about nephrotic and nephritic syndromes? Nephrotic (proteinuria >3.5 g/day, hypoalbuminaemia, oedema, hyperlipidaemia) — minimal change disease, FSGS, membranous nephropathy, diabetic. Treat oedema (diuretics), proteinuria (ACEi/ARB), consider steroids for primary glomerular disease. Nephritic (haematuria, proteinuria, hypertension, oliguria, AKI) — IgA nephropathy, post-streptococcal GN, anti-GBM (Goodpasture's), ANCA vasculitis. Urgent nephrology referral.

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Renal and electrolyte content rewards protocol discipline more than almost any other block. Three clusters (AKI, CKD, electrolytes), one ABG algorithm, and seven question templates cover the whole surface area. Drill the hyperkalaemia ladder (calcium gluconate → insulin-dextrose → salbutamol → binders → dialysis), the hyponatraemia volume triage, and the KDIGO staging criteria — those three alone convert a feared specialty into a high-confidence subscore.

Pair this masterclass with the emergency presentations post for shared acute-care framing, the respiratory masterclass for ABG interpretation, the NICE guidelines post for renal dosing and nephrotoxic drug recognition, and the content map post for weighting within your study plan. The 12-week plan slots renal alongside endocrine in weeks 4–5.

MLA Prep's renal module covers all three clusters above with KDIGO-aligned AKI stems, NICE NG203 CKD questions, hyperkalaemia emergency drills, and a dedicated ABG interpretation drill set — every question tagged to the 2026 UKA guideline line it's testing. Start the free diagnostic to benchmark your renal subscore, or compare plans for full access.