Understanding how kidneys fail, how technology compensates, and how we weigh transplantation against life-long dialysis — a genuine clinical trade-off with no perfect answer.
Use the PDF for classwork, homework or revision. It includes key ideas, activities, questions, an extend task and success-criteria proof.
Discovery: Aisha is 42. Her doctor tells her both kidneys are failing — her GFR is 11 mL/min (normal: 90+). She has two choices: start haemodialysis three times a week for the rest of her life, or go on the transplant waiting list (average wait: 4–5 years in Australia) and receive a donor kidney.
Before you read on, write your initial thoughts below:
Remember to connect the concepts in this lesson to the broader evolutionary framework. Each mechanism builds on what you have learned previously.
Each kidney contains approximately 1 million nephrons. Each nephron has five key regions, each with a distinct filtration or reabsorption role:
Chronic kidney disease (CKD) affects ~10% of Australians. Kidney failure (End-Stage Renal Disease, ESRD) occurs when GFR falls below 15 mL/min. Key causes include:
Chronic hyperglycaemia damages glomerular capillaries (diabetic nephropathy). Leading cause of ESRD in Australia (~37% of cases).
High blood pressure damages glomerular membranes over decades, reducing filtration area. Second most common cause (~25% of cases).
Autosomal dominant genetic condition. Fluid-filled cysts progressively replace functional nephron tissue. Familial — links to L16 (genetic disease).
Immune complexes deposit in the glomerular basement membrane, triggering inflammation that scars filtration membranes.
Repeated bacterial kidney infections (usually ascending UTI) scar the renal cortex. More common in women and people with structural abnormalities.
Sudden damage from toxins (NSAIDs, contrast dye, certain antibiotics), crush injuries, or severe dehydration. Can recover if treated quickly.
Dialysis uses the principle of diffusion across a semi-permeable membrane to remove waste solutes from blood while retaining useful large molecules (proteins) and cells.
A kidney transplant replaces the failed organ with a donor kidney (from a living or cadaveric donor). The recipient's failed kidneys are usually left in place — the donor kidney is implanted in the pelvis where surgical connection is easier.
| Type | Timing | Mechanism | Management |
|---|---|---|---|
| Hyperacute | Minutes–hours | Pre-formed antibodies against donor ABO/HLA | Prevented by cross-match testing before surgery |
| Acute | Days–weeks | T-cell mediated immune attack on donor antigens | High-dose corticosteroids; adjust immunosuppressants |
| Chronic | Months–years | Slow immune-mediated fibrosis of the transplant | Optimise immunosuppression; eventual re-listing |
| Criterion | Haemodialysis | Peritoneal Dialysis | Kidney Transplant |
|---|---|---|---|
| Effectiveness | Removes wastes 3x/week — not continuous | Daily — more continuous than HD | Continuous; restores most kidney functions |
| Quality of life | Centre-based; 12 h/week; fatigue common | Home-based; more flexible | Near-normal lifestyle after recovery |
| Longevity | 5–10 yr average survival (ESRD) | Similar to HD; peritonitis risk | Median graft survival 12–15 yr; patient survival superior to dialysis |
| Risk | Infection at access site; hypotension; clotting | Peritonitis; catheter infection | Surgical risk; chronic rejection; immunosuppression complications |
| Reversibility | Can switch modalities | Can switch to HD | Permanent; must continue drugs even if graft fails |
| Availability | Widely available | Widely available | Wait list 3–5 yr (Australia); organ shortage |
| Cost (AUS) | ~$70,000/yr (public) | ~$55,000/yr (public) | ~$100k surgery + ~$15k/yr drugs; cheaper long-term |
Diabetes (leading), hypertension, PKD (genetic), glomerulonephritis (autoimmune), infections, acute injury.
Blood circulated through dialyser; diffusion across semi-permeable membrane removes urea, K⁺, creatinine down concentration gradient; dialysate flows counter-current to maximise gradient. 3x/week, ~4 hr each session.
Peritoneum acts as membrane; dialysate infused into abdominal cavity; daily exchanges; home-based.
HLA-matched donor kidney implanted in pelvis; lifelong immunosuppressants required; types of rejection: hyperacute, acute (T-cell), chronic (fibrosis). Best long-term outcomes but organ shortage and surgical risk.
Try this: Compare dialysis and kidney transplant across cost, quality of life, survival rate, and eligibility criteria.
This comparator helps you evaluate why transplant is generally preferred but not available to all patients.
Dialysis filters blood artificially but requires lifelong sessions and dietary restrictions. Kidney transplant restores normal kidney function and quality of life but requires immunosuppressants and a suitable donor. Transplant survival rates are higher, but organ shortage limits availability.
Try this: Match each kidney treatment to the stage of kidney disease and the patient profile for which it is most appropriate.
This matcher reinforces the progression from lifestyle management through to end-stage renal disease treatments.
Early kidney disease is managed with blood pressure control, diet, and medication. As function declines, dialysis becomes necessary. Transplant is the definitive treatment for end-stage disease. The best treatment depends on disease stage, patient health, and resource availability.
For each nephron region, describe its primary process and what substances move.
Explain why urea moves from blood into dialysate during haemodialysis, but glucose does not. Use the terms concentration gradient and semi-permeable membrane in your answer.
Aisha (from Think First) is 42 years old. She has no major comorbidities. She has a 38-year-old sibling willing to be tested as a living donor. Use what you now know to:
1. Which nephron region is primarily responsible for reabsorbing all filtered glucose from the filtrate?
2. In haemodialysis, why does urea move from blood into the dialysate, but plasma proteins do not?
3. Polycystic kidney disease (PKD) is best described as:
4. A transplant recipient is prescribed tacrolimus and prednisolone long-term. The most likely reason these drugs increase the patient's cancer risk is:
5. Which statement about peritoneal dialysis compared to haemodialysis is correct?
Question 1 (4 marks): Describe how haemodialysis removes urea from the blood. In your answer, refer to the role of the semi-permeable membrane, the concentration gradient, and the significance of counter-current dialysate flow.
Question 2 (5 marks): Compare haemodialysis and kidney transplantation as treatments for end-stage renal disease. In your comparison, consider effectiveness, quality of life, longevity, and risk. Conclude with a justified recommendation for a 35-year-old otherwise healthy patient.
Question 3 (6 marks): Explain how the structure of the nephron enables the kidney to produce concentrated urine while retaining essential substances. In your answer, refer to at least THREE nephron regions and identify the hormones involved in regulating water reabsorption.
1. B — The PCT is the site of bulk reabsorption. All glucose filtered at the glomerulus is actively reabsorbed in the PCT via Na⁺/glucose co-transporters; none reaches the loop of Henle or collecting duct under normal conditions.
2. C — Urea is a small molecule (MW ~60 Da) that passes freely through the dialysis membrane. Plasma proteins (albumin MW ~69,000 Da) are too large to cross. No active transport is involved — movement is entirely by diffusion down the concentration gradient.
3. A — PKD is caused by mutations in PKD1 or PKD2 genes (autosomal dominant). Cysts grow progressively over decades, compressing and destroying nephrons. It is not infectious or autoimmune.
4. D — Immunosuppressants reduce the immune system's ability to perform immune surveillance — the process by which T-cells and NK cells destroy abnormal/precancerous cells. With reduced surveillance, transformed cells can proliferate unchecked. The drugs do not directly mutate DNA.
5. B — PD uses the peritoneum as the membrane and can be done at home (continuous ambulatory PD) or overnight (automated PD). It provides more continuous clearance (daily vs 3x/week for HD). It does NOT use a machine with hollow fibres — that is haemodialysis.
Return to your initial recommendation for Aisha. Has your advice changed? Explain what you now understand about HLA matching, rejection risk, and why a living-related donor (her sibling) offers a better match than a cadaveric donor.