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]