Biology • Year 12 • Module 8 • Lesson 20
Kidney Disorders, Dialysis and Transplantation
Apply dialysis mechanisms and transplant criteria to patient data, real GFR trends and Australian clinical context.
1. Interpret GFR data — two patients over time
The graph below shows estimated GFR (eGFR) over 12 years for two patients. Patient A has type 2 diabetes; Patient B has polycystic kidney disease (PKD). The dashed line at 15 mL/min marks the ESRD threshold (dialysis or transplant required). 8 marks
Hypothetical data illustrating typical eGFR trajectories. After ANZData Registry report patterns, Australian Institute of Health and Welfare (2023).
1.1 Describe the trend in eGFR for each patient from year 0 to year 12. Include approximate values. 2 marks
1.2 At approximately what year does Patient A reach the ESRD threshold? Using lesson content, explain the mechanism by which chronic hyperglycaemia led to this outcome. 3 marks
1.3 Patient B's eGFR decline is initially slower but accelerates. Suggest why PKD causes an accelerating rate of decline, using the mechanism described in the lesson. 2 marks
1.4 At year 12, Patient B's eGFR is approximately 16. The nephrologist recommends listing for transplant. State one reason why transplantation is preferred over haemodialysis for a patient who has not yet reached ESRD but is approaching it. 1 mark
2. Cause-and-effect chain — haemodialysis removing urea
Fill in the empty effect boxes to trace how haemodialysis removes urea from blood, step by step. The first cause is given. 5 marks
| Cause | Effect (fill in) |
|---|---|
| Blood is pumped from the patient via an arteriovenous fistula into the dialyser. | |
| The dialysate contains near-zero urea concentration; blood contains high urea concentration. | |
| Urea molecules are small relative to the pores of the semi-permeable membrane. | |
| The dialysate flows counter-current (opposite direction) to blood flow through the dialyser. | |
| Overall outcome (so…): | |
3. Compare haemodialysis and peritoneal dialysis
Complete the comparison table using information from the lesson. 6 marks — 1 per row
| Feature | Haemodialysis | Peritoneal dialysis |
|---|---|---|
| Membrane used | ||
| Frequency | ||
| Setting | ||
| Key risk | ||
| Continuity of clearance | ||
| Access method |
4. Apply to a real scenario — Aisha's treatment decision
Aisha is 42 years old. Her nephrologist reports a GFR of 11 mL/min. She works full-time as a nurse, has two teenage children, and lives 180 km from the nearest haemodialysis centre in regional NSW. Her sister has offered to donate a kidney and their HLA match is rated "good." 5 marks
4.1 Identify two specific reasons why haemodialysis at a dialysis centre would present major practical challenges for Aisha. 2 marks
4.2 Explain why a living-related donor kidney (from Aisha's sister) is likely to offer better long-term outcomes than a cadaveric donor kidney. Use one specific criterion from the lesson. 2 marks
4.3 After transplant, Aisha is prescribed tacrolimus for life. State one benefit and one risk of this long-term immunosuppression. 1 mark
Q1.1 — Trend description (2 marks)
Patient A (diabetes) shows a steep, roughly linear decline from ~88 mL/min at year 0 to ~12 mL/min by year 9, then stabilises very low (~8 mL/min) in years 10–12 [1]. Patient B (PKD) shows a slow initial decline from ~85 mL/min at year 0, accelerating from year 6 onward, reaching ~16 mL/min by year 12 — just above the ESRD threshold [1].
Q1.2 — Patient A reaches ESRD threshold and mechanism (3 marks)
Patient A crosses the 15 mL/min ESRD threshold at approximately year 9 [1]. Chronic hyperglycaemia causes persistent elevated blood glucose, which damages the capillary endothelium within the glomerulus (diabetic nephropathy) [1]. This thickens the glomerular basement membrane, reduces the filtration surface area, and causes glomerulosclerosis, progressively reducing GFR over years to decades [1].
Q1.3 — PKD: accelerating decline (2 marks)
In PKD, fluid-filled cysts grow progressively over time. Early in the disease, many nephrons remain functional despite cyst formation [1]. As cysts enlarge and multiply, they compress and replace an increasing proportion of nephron tissue — so the rate of nephron loss (and eGFR decline) accelerates as more nephrons are destroyed simultaneously, consistent with the steepening curve after year 6 [1].
Q1.4 — Reason transplant is preferred (1 mark)
Any one of: transplant provides continuous kidney function (not just 3×/week); patient survival is superior to dialysis for eligible patients; quality of life is substantially better; dialysis would need to begin at ESRD and continue for years on the transplant waiting list.
Q2 — Cause-and-effect chain
Row 1 effect: Blood flows through the hollow fibre channels inside the dialyser, positioned adjacent to the flowing dialysate (separated only by the semi-permeable membrane).
Row 2 effect: A steep concentration gradient for urea is established — urea moves from high concentration (blood) toward low concentration (dialysate) down the gradient.
Row 3 effect: Urea diffuses freely across the membrane from blood into dialysate; plasma proteins (too large) and red blood cells remain in the blood.
Row 4 effect: The concentration gradient is maintained along the entire length of the dialyser (fresh low-urea dialysate always meets blood that still has relatively higher urea), maximising the total amount of urea removed per session.
Overall outcome: Blood is returned to the patient with substantially reduced urea and waste solute concentration, temporarily restoring acceptable plasma biochemistry until the next session.
Q3 — Comparison table
Membrane: HD — synthetic hollow fibres in the dialyser; PD — peritoneum (abdominal lining).
Frequency: HD — 3 sessions per week, ~4 hours each; PD — daily exchanges (CAPD: 3–4 per day; APD: overnight cycler).
Setting: HD — typically at a dialysis centre; PD — home-based.
Key risk: HD — infection at the fistula/access site, hypotension; PD — peritonitis (bacterial infection of the peritoneal cavity).
Continuity of clearance: HD — intermittent (3×/week); PD — more continuous (daily).
Access method: HD — arteriovenous fistula (surgically created); PD — permanent abdominal catheter.
Q4.1 — Practical challenges for Aisha (2 marks)
Any two of: (1) Aisha lives 180 km from the nearest dialysis centre — three return trips per week (~1080 km/week) is incompatible with full-time work and parenting [1]; (2) Each session is ~4 hours plus travel — approximately 12 hours/week in dialysis alone, creating severe fatigue and childcare difficulties [1]; (3) Distance means emergency access to dialysis in the event of a session being missed or an emergency is difficult.
Q4.2 — Living-related donor advantage (2 marks)
A living-related donor (sibling) typically offers better HLA matching than a cadaveric donor because siblings share 50% of their alleles on average and can be tested and matched in advance [1]. Better HLA matching reduces the risk of acute T-cell mediated rejection and chronic rejection, extending graft survival — median graft survival is longer for well-matched living-donor kidneys than for cadaveric donors [1]. Accept also: function begins immediately with a living donor (no delayed graft function); or that the wait for a cadaveric donor is 4–5 years in Australia.
Q4.3 — Tacrolimus benefit and risk (1 mark)
Benefit: Prevents acute rejection — tacrolimus suppresses T-cell activation, preventing the immune system from attacking the donor kidney's foreign HLA antigens. Risk: Increased susceptibility to opportunistic infection and certain cancers (especially skin cancer and lymphoma), because reduced immune surveillance allows pathogens and abnormal cells to proliferate unchecked. [1 mark for correctly identifying one benefit and one risk]