Why CKD Is a Core OSCE Topic
Chronic kidney disease affects approximately 3 million people in the UK. It is frequently encountered in ward rounds, outpatient clinics, and prescribing scenarios. OSCEs examine it in clinical reasoning stations (patient with eGFR 28 — what do you need to consider?), prescribing stations (drug dose adjustment in renal failure), and communication stations (explaining CKD to a patient). The focus is on staging, complication recognition, and safe prescribing.
💡 Tip
CKD is defined as abnormalities of kidney structure or function present for more than 3 months, with implications for health. A single eGFR result is not enough — always confirm with repeat testing at least 3 months apart (except AKI, which is separate).
KDIGO Staging — eGFR Categories
| Stage | eGFR (mL/min/1.73m²) | Description |
|---|---|---|
| G1 | 90 or above | Normal or high — with other markers of kidney damage |
| G2 | 60-89 | Mildly reduced — with other markers |
| G3a | 45-59 | Mildly to moderately reduced |
| G3b | 30-44 | Moderately to severely reduced |
| G4 | 15-29 | Severely reduced |
| G5 | Below 15 | Kidney failure (dialysis/transplant threshold) |
Albuminuria (ACR) Categories:
| Category | ACR (mg/mmol) | Description |
|---|---|---|
| A1 | Below 3 | Normal or mildly increased |
| A2 | 3-30 | Moderately increased |
| A3 | Above 30 | Severely increased |
CKD is described as G stage + A category: e.g., CKD G3b A2.
Common Causes
🧠 Mnemonic
DAVID — common causes of CKD:
- D iabetic nephropathy (most common in UK — 25-30%)
- A therosclerotic renovascular disease
- V ascular — hypertensive nephropathy
- I nflammatory — glomerulonephritis (IgA nephropathy, lupus nephritis)
- D rugs and obstructive (NSAIDs, analgesic nephropathy, polycystic kidney disease, recurrent UTI with obstruction)
Monitoring CKD — NICE Recommendations
Check eGFR and ACR:
- At least annually in all CKD patients
- Every 6 months in G3b-G4
- Every 3 months in G4-G5 (approaching dialysis threshold)
Rate of eGFR decline:
- Average: 1-2 mL/min/1.73m²/year naturally with ageing
- CKD progression: decline above 5 mL/min in 1 year or 10 mL/min in 5 years is significant — investigate for modifiable causes and refer
Slowing CKD Progression
| Intervention | Evidence | Target |
|---|---|---|
| BP control | Essential — reduces intraglomerular pressure | Below 140/90 (below 130/80 if diabetic nephropathy or ACR above 70) |
| ACE inhibitor or ARB | Reduces proteinuria and glomerular injury — first-line in CKD + proteinuria (A2/A3) regardless of BP | Both ACEi and ARB together — avoid (no additional benefit, increased harm) |
| SGLT-2 inhibitor | CREDENCE, DAPA-CKD trials — nephroprotection even in non-diabetic CKD | Empagliflozin/dapagliflozin if eGFR above 20 |
| Glycaemic control | HbA1c target 53 mmol/mol (7%) in diabetic CKD | |
| Smoking cessation | Accelerates CKD progression | |
| Dietary protein restriction | Modest benefit — refer to renal dietitian in G4-G5 | 0.8 g/kg/day |
| Avoid nephrotoxins | NSAIDs, IV contrast, aminoglycosides — avoid or use cautiously |
CKD Complications
Anaemia of CKD
- Normocytic, normochromic
- Due to: reduced erythropoietin (EPO) production, iron deficiency, shortened RBC lifespan
- Management: iron replacement first (oral or IV if poor absorption); erythropoiesis-stimulating agent (ESA — darbepoetin, epoetin) if iron-replete and Hb below 100 g/L; target Hb 100-120 g/L
- Refer to nephrology if Hb below 100 g/L and eGFR below 45
Renal Bone Disease (CKD-MBD)
- Low vitamin D (reduced 1-alpha hydroxylation) → low calcium → secondary hyperparathyroidism → high PTH → bone resorption + vascular calcification
- Management: active vitamin D (alfacalcidol or calcitriol — NOT plain vitamin D3 in severe CKD); phosphate binders (calcium carbonate, sevelamer) for hyperphosphataemia
Hyperkalaemia
- Reduced renal excretion of potassium
- Exacerbated by: ACE inhibitors/ARBs, potassium-sparing diuretics (spironolactone), dietary potassium
- Management: dietary restriction; stop/reduce offending drugs; patiromer or sodium zirconium cyclosilicate (ZS-9) for chronic management
Metabolic Acidosis
- Reduced H⁺ excretion and bicarbonate regeneration
- Oral sodium bicarbonate supplementation if persistent serum bicarbonate below 22 mmol/L
Fluid Retention and Hypertension
- Loop diuretics (furosemide) — useful up to eGFR 15
- Dietary sodium restriction
Safe Prescribing in CKD
⚠️ Red Flag
Drugs requiring dose adjustment or avoidance in CKD (common OSCE pitfalls):
- Metformin: Stop if eGFR below 30; reduce dose if eGFR 30-44
- NSAIDs: Avoid in all CKD — worsen progression, precipitate AKI
- Nitrofurantoin: Avoid if eGFR below 30 (inadequate urine concentration + peripheral neuropathy risk)
- Opioids: Morphine metabolites accumulate — use fentanyl or alfentanil instead
- DOACs: Rivaroxaban and edoxaban require dose reduction or avoidance; dabigatran avoid if eGFR below 30
- Gentamicin: High nephrotoxicity — avoid or use with strict monitoring (pre-dose and 1-hour post-dose levels)
- Digoxin: Narrow therapeutic index; accumulates in CKD — reduce dose and monitor levels
Nephrology Referral Criteria (NICE)
Refer if any of the following:
- eGFR below 30 (G4-G5)
- eGFR falling rapidly (above 5 mL/min/year)
- ACR above 70 (A3) — likely glomerulonephritis
- Haematuria + proteinuria (possible glomerulonephritis)
- Suspected rare or genetic causes
- Uncontrolled hypertension despite 4 agents
- CKD complications not manageable in primary care
Frequently Asked Questions
"What is the difference between AKI and CKD?"
AKI is a rapid (hours to days) decline in renal function — potentially reversible, occurring on a normal or CKD background. CKD is a sustained (more than 3 months) structural or functional abnormality — largely irreversible and progressive. The key clinical tool is timeline and baseline: if eGFR has been stable for months then acutely falls, it is AKI; if it has been progressively declining over years, it is CKD. Ultrasound findings also help: small kidneys in CKD; normal or large in AKI.
"Why does CKD cause anaemia even before dialysis?"
The kidney produces approximately 90% of circulating erythropoietin (EPO), which stimulates red cell production in the bone marrow. As functional kidney mass is lost, EPO production falls proportionally. Additionally, uraemic toxins shorten red cell survival, and many CKD patients are iron deficient (poor intake, blood loss from dialysis). Iron deficiency must be corrected before prescribing an ESA — otherwise the ESA will be ineffective.
"What is the role of ACE inhibitors in CKD and when should they be stopped?"
ACE inhibitors (and ARBs) reduce intraglomerular pressure by dilating the efferent arteriole, thereby decreasing proteinuria and slowing CKD progression. They are recommended in all CKD patients with A2 or A3 albuminuria regardless of blood pressure. An expected rise in creatinine of up to 30% (or eGFR fall up to 25%) is acceptable and should not prompt discontinuation. Stop if: creatinine rises more than 30% (suggests bilateral renal artery stenosis), K+ above 6.0 mmol/L, or if the patient develops AKI.
"At what stage is dialysis usually started in CKD?"
Renal replacement therapy (dialysis or transplantation) is usually considered when eGFR falls below 10-15 mL/min/1.73m² (Stage G5). However, the decision is based on symptoms, rate of decline, and patient preference — not eGFR alone. Key symptoms indicating need for dialysis: uraemic encephalopathy, pericarditis, refractory pulmonary oedema, severe metabolic acidosis, and refractory hyperkalaemia. Patients should be referred to nephrology well before this stage (ideally eGFR below 30) for RRT planning, access formation (AV fistula), and transplant assessment.
"What dietary advice should be given to CKD patients?"
Protein: 0.8 g/kg/day in CKD G3b-G5 (avoid high-protein diets — excess urea from catabolism); Potassium: restrict if above 6.0 mmol/L (avoid bananas, potatoes, tomatoes); Phosphate: restrict in CKD G3b-G5 (avoid dairy, nuts, cola drinks); Sodium: below 6 g/day (reduces BP and fluid retention); Fluid: restrict only if fluid overloaded or anuric on dialysis. All CKD patients with G3b or above should be referred to a renal dietitian.
Related Posts
- Acute Kidney Injury OSCE — AKI superimposed on CKD and shared management principles
- Hypertension Management OSCE — BP control as the cornerstone of CKD progression prevention
- Blood Results Interpretation OSCE — interpreting eGFR, creatinine, electrolytes, and bicarbonate