Kidney Disorders, Dialysis and Transplantation
When the kidneys fail, homeostasis fails. This lesson covers the nephron's filtration and reabsorption roles, the major causes of kidney failure, and the technologies that replace lost kidney function — haemodialysis, peritoneal dialysis, and transplantation.
Practise this lesson
Four printable worksheets that build from the foundations up to exam-style questions — start at whatever level suits you.
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 reading this lesson, consider: What factors should Aisha weigh up in deciding between dialysis and transplantation? Which would you choose, and why?
Know
- The structure of the nephron and its regions
- How each nephron region contributes to filtration/reabsorption
- Common causes of kidney failure
- How haemodialysis and peritoneal dialysis work
- How transplantation differs from dialysis
Understand
- Why diffusion across a semi-permeable membrane removes wastes without losing useful molecules
- Why dialysis cannot fully replace all kidney functions
- The immunological challenge of transplantation and why lifelong drugs are required
- Why transplantation generally offers better outcomes but carries higher initial risk
Can Do
- Label a nephron diagram with all five regions
- Explain haemodialysis using diffusion and concentration gradients
- Evaluate dialysis vs transplantation using criteria (effectiveness, risk, quality of life)
- Apply understanding to novel patient scenarios
Core Content
The five regions of the kidney's functional unit
Each kidney contains approximately 1 million nephrons. Each nephron has five key regions, each with a distinct filtration or reabsorption role.
Key Process (by region)
- Pressure filtration (glomerulus / Bowman's capsule)
- Bulk reabsorption (PCT)
- Counter-current multiplier (loop of Henle)
- Fine-tuning (DCT)
- Final concentration (collecting duct)
What moves
- Water, glucose, urea, ions → filtrate (proteins/cells stay)
- ~65% water, all glucose, most ions reabsorbed into blood
- Creates medullary salt gradient; descending loses water, ascending loses salt
- ADH controls water reabsorption; aldosterone controls Na⁺/K⁺
- ADH-regulated water reabsorption; concentrated urine formed
What to write in your book
- Glomerulus/Bowman's capsule → pressure filtration (small molecules into filtrate; proteins/cells stay).
- PCT → bulk reabsorption (~65% water, all glucose, most ions). Loop of Henle → counter-current multiplier (medullary salt gradient).
- DCT → fine-tuning (ADH/aldosterone). Collecting duct → final ADH-regulated water reabsorption → concentrated urine.
- ~1 million nephrons per kidney; kidney failure = homeostatic failure.
The functional unit of the kidney, of which each kidney has about 1 million, is the _____.
From diabetes to genetics — what destroys nephron function
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:
Diabetes (Type 2)
Chronic hyperglycaemia damages glomerular capillaries (diabetic nephropathy). Leading cause of ESRD in Australia (~37% of cases).
Hypertension
High blood pressure damages glomerular membranes over decades, reducing filtration area. Second most common cause (~25% of cases).
Polycystic Kidney Disease (PKD)
Autosomal dominant genetic condition. Fluid-filled cysts progressively replace functional nephron tissue. Familial — links to L17 (genetic disease).
Autoimmune (Glomerulonephritis)
Immune complexes deposit in the glomerular basement membrane, triggering inflammation that scars filtration membranes.
Infection / Pyelonephritis
Repeated bacterial kidney infections (usually ascending UTI) scar the renal cortex. More common in women and people with structural abnormalities.
Acute Injury (AKI)
Sudden damage from toxins (NSAIDs, contrast dye, certain antibiotics), crush injuries, or severe dehydration. Can recover if treated quickly.
What to write in your book
- ESRD = GFR < 15 mL/min; CKD affects ~10% of Australians.
- Leading causes: diabetes (~37%), hypertension (~25%), PKD (genetic, AD), glomerulonephritis (autoimmune), infection, acute injury.
- Chronic causes damage glomeruli/nephrons gradually; AKI is sudden and can recover.
- Dialysis replaces filtration only — not hormone production or full acid-base control.
What is the leading cause of end-stage renal disease (ESRD) in Australia?
Replacing filtration by diffusion across a semi-permeable membrane
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.
How it works
- Blood removed via fistula (surgically created AV connection), pumped through dialyser
- Dialysate flows counter-current to blood — maximises concentration gradient
- Urea, excess K⁺, excess Na⁺, creatinine diffuse out; glucose and proteins too large to cross membrane
- 3 sessions per week, ~4 hours each in a dialysis centre
How it works
- Dialysate fluid infused into the peritoneal cavity via a permanent catheter
- The peritoneum (abdominal lining) acts as the semi-permeable membrane
- Waste solutes diffuse from peritoneal blood vessels into dialysate
- Fluid drained and replaced 3–4 times daily (CAPD) or overnight with a cycler (APD)
- Can be done at home — greater independence than haemodialysis
What to write in your book
- Dialysis = diffusion of waste solutes across a semi-permeable membrane down a concentration gradient.
- Haemodialysis: blood via fistula → dialyser; dialysate counter-current; 3×/week, ~4 hr.
- Peritoneal dialysis: peritoneum = membrane; dialysate in abdomen; home-based, daily exchanges.
- Urea diffuses out (high in blood); glucose stays (equal both sides); proteins too large.
Dialysis removes urea from the blood by which principle?
Replacing the failed organ — and the immunological challenge
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.
The Procedure
- Donor and recipient are tissue-typed (HLA matching) to minimise rejection risk
- The new kidney is connected to the iliac artery and vein, and the ureter attached to the bladder
- Function can begin immediately (living donor) or after a few days (cadaveric)
- Lifelong immunosuppressant therapy required (e.g. tacrolimus, mycophenolate, prednisolone)
Types of Rejection
| 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 |
What to write in your book
- Transplant: HLA-matched donor kidney implanted in the pelvis (iliac artery/vein, ureter to bladder).
- Lifelong immunosuppressants (tacrolimus, mycophenolate, prednisolone) needed to prevent rejection.
- Rejection: hyperacute (pre-formed antibodies), acute (T-cell), chronic (fibrosis).
- Trade-off: immunosuppression ↑ infection and cancer (skin, lymphoma) risk.
A kidney transplant recipient must take lifelong immunosuppressant drugs to prevent rejection of the donor organ.
Dialysis uses a semi-permeable membrane to filter waste products from the blood when kidney function is impaired.
Kidney transplants never require immunosuppressive drugs because the kidney is not recognised as foreign tissue by the recipient's immune system.
Effectiveness, quality of life, longevity, risk, reversibility, availability and cost
| 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 |
What to write in your book
- Transplant: continuous, best quality of life and longevity (graft 12–15 yr) — but surgical risk, immunosuppression, organ shortage (3–5 yr wait), irreversible.
- Haemodialysis: 3×/week centre-based, fatigue; peritoneal: home-based, peritonitis risk.
- Cost: HD ~$70k/yr, PD ~$55k/yr, transplant ~$100k + $15k/yr drugs (cheaper long-term).
- Best choice depends on patient age, comorbidities, donor availability.
A transplanted kidney lasts forever, so a patient who receives one will never need dialysis again.
Haemodialysis filters blood through an artificial membrane, while peritoneal dialysis uses the patient's own peritoneal membrane.
Dialysis completely restores all kidney functions, including hormone production and blood pressure regulation.
Nephron Regions
- Glomerulus/Bowman's → pressure filtration
- PCT → bulk reabsorption (~65% water, glucose, ions)
- Loop of Henle → counter-current multiplier (salt gradient)
- DCT → fine-tuning (ADH/aldosterone); collecting duct → final water reabsorption
Causes of Failure
- Diabetes (leading ~37%), hypertension (~25%)
- PKD (genetic, AD), glomerulonephritis (autoimmune)
- Infection (pyelonephritis), acute injury (AKI)
Dialysis
- Diffusion across semi-permeable membrane down concentration gradient
- Haemodialysis: fistula → dialyser; 3×/week, ~4 hr; counter-current dialysate
- Peritoneal: peritoneum = membrane; home-based, daily exchanges
Transplant
- HLA-matched donor kidney in pelvis; lifelong immunosuppressants
- Rejection: hyperacute, acute (T-cell), chronic (fibrosis)
- Best outcomes but organ shortage + surgical risk; graft 12–15 yr
Nephron Region Functions
For each nephron region, describe its primary process and what substances move.
Classify the Cause and Mechanism of Kidney Damage
For each scenario: (a) identify the cause of kidney damage; (b) classify it as chronic or acute; (c) explain the mechanism by which kidney function is impaired.
- A 58-year-old patient has had Type 2 diabetes for 20 years. Their eGFR has declined gradually from 90 to 22 mL/min/1.73m² over the past decade. Urinalysis shows proteinuria.
- A 24-year-old patient presents with flank pain, fever and cloudy urine. Blood tests show elevated creatinine. They have a history of recurrent UTIs.
- A patient with a family history of PKD develops enlarged kidneys visible on ultrasound. Multiple cysts are present in both kidneys. eGFR is declining slowly but steadily.
- After a marathon in extreme heat, an athlete collapses with severe dehydration. Creatinine rises sharply over 48 hours but returns to normal after IV fluid resuscitation.
- A 35-year-old patient has blood pressure consistently above 160/100 mmHg despite medication. Over 15 years, eGFR declines from 110 to 35. Renal biopsy shows glomerular sclerosis.
A fresh set drawn from this lesson's question bank — feedback shown immediately. +5 XP per correct · +25 XP all correct
Pick your answer, then rate your confidence — that tells the system what to drill next.
ApplyBand 4(4 marks) 1. 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.
AnalyseBand 4–5(5 marks) 2. Compare haemodialysis and kidney transplantation as treatments for end-stage renal disease. Consider effectiveness, quality of life, longevity, and risk. Conclude with a justified recommendation for a 35-year-old otherwise healthy patient.
EvaluateBand 5–6(6 marks) 3. Explain how the structure of the nephron enables the kidney to produce concentrated urine while retaining essential substances. Refer to at least THREE nephron regions and identify the hormones involved in regulating water reabsorption.
Show all answers
Multiple choice
MC answers and full explanations are shown inline as you complete each question. Use the retry button to attempt a fresh set from the lesson bank.
Activity 1 — Nephron Region Functions
Glomerulus/Bowman's capsule: pressure filtration — water, glucose, urea and ions are forced into the filtrate; proteins and blood cells are too large and stay in the blood. PCT: bulk reabsorption — ~65% of water, all glucose, and most ions are reabsorbed back into the blood. Loop of Henle: counter-current multiplier — the descending limb loses water and the ascending limb pumps out salt, creating a medullary salt (osmotic) gradient. DCT: fine-tuning of ions and water under ADH and aldosterone control. Collecting duct: final ADH-regulated water reabsorption (through aquaporins) using the medullary gradient → concentrated urine.
Activity 2 — Classify the Cause
1. (a) Diabetic nephropathy; (b) chronic; (c) chronic hyperglycaemia damages glomerular capillaries and the basement membrane (non-enzymatic glycation), reducing filtration and causing proteinuria. 2. (a) Pyelonephritis (kidney infection); (b) acute on a background of recurrent UTIs; (c) ascending bacterial infection inflames and scars the renal cortex, impairing filtration; elevated creatinine reflects reduced clearance. 3. (a) Polycystic kidney disease; (b) chronic (genetic, autosomal dominant); (c) fluid-filled cysts progressively replace functional nephron tissue, reducing the number of working nephrons and lowering eGFR over time. 4. (a) Acute kidney injury (pre-renal); (b) acute; (c) severe dehydration reduces blood volume and renal perfusion, lowering GFR; creatinine rises sharply but recovers with IV fluids because the nephrons are not permanently damaged. 5. (a) Hypertensive nephropathy; (b) chronic; (c) sustained high blood pressure damages and scleroses the glomeruli over years, reducing filtration area and GFR (biopsy shows glomerular sclerosis).
Short Answer Model Answers
SA1 (4 marks): The patient's blood is pumped from a fistula through the dialyser, where it flows on one side of a semi-permeable membrane while dialysate flows on the other [1]. Urea is highly concentrated in the blood and almost absent from the dialysate, so urea diffuses across the membrane down its concentration gradient from blood into dialysate; the membrane's pore size allows small wastes (urea, K⁺, creatinine) through while retaining large proteins and blood cells [2]. The dialysate flows counter-current (opposite direction) to the blood, which maintains a steep concentration gradient for urea along the entire length of the membrane — if it flowed in the same direction, the gradient would equalise partway and removal would be less efficient [1].
SA2 (5 marks): Effectiveness: haemodialysis removes wastes only ~3×/week (not continuous), whereas a transplant restores continuous, near-complete kidney function [1]. Quality of life: HD is centre-based (~12 h/week) and causes fatigue; a successful transplant allows a near-normal lifestyle after recovery [1]. Longevity: average ESRD survival on dialysis is ~5–10 years; median graft survival is 12–15 years with superior patient survival [1]. Risk: HD risks access-site infection, hypotension and clotting (reversible, no surgery); transplant carries surgical risk, lifelong immunosuppression (↑ infection/cancer risk) and possible rejection, and is irreversible [1]. Recommendation: for a 35-year-old otherwise healthy patient, transplantation is preferred — it offers the best longevity and quality of life and the surgical/immunosuppression risks are well-tolerated at this age; haemodialysis is appropriate as a bridge while awaiting a suitable donor (3–5 year wait) [1].
SA3 (6 marks): Glomerulus/Bowman's capsule: blood is filtered under pressure — water, glucose, urea and ions pass into the filtrate while proteins and cells are retained [1.5]. Proximal convoluted tubule (PCT): bulk reabsorption returns ~65% of water, all glucose, and most ions to the blood, conserving essential substances [1.5]. Loop of Henle: the counter-current multiplier (descending limb permeable to water, ascending limb actively pumping out Na⁺/Cl⁻) establishes a high salt concentration gradient in the medulla [1]. Collecting duct (with DCT): under ADH (antidiuretic hormone), aquaporin channels are inserted, increasing water reabsorption from the filtrate into the hyperosmotic medulla — producing concentrated urine; aldosterone regulates Na⁺ reabsorption and K⁺ secretion in the DCT/collecting duct. Together, filtration plus selective reabsorption and ADH/aldosterone-controlled water and ion handling let the kidney excrete concentrated waste while retaining glucose, proteins and needed ions [2 — 6 marks total].
Five timed questions on the nephron, causes of kidney failure, dialysis and transplantation. Beat the boss to bank a tier — gold (perfect + fast), silver (80%+), or bronze (cleared).
⚔ Enter the arenaAnswer questions on the nephron, dialysis (haemo + peritoneal) and transplantation. Pool: lessons 1–20.
Compare dialysis and kidney transplant across cost, quality of life, survival rate, and eligibility criteria — and see why transplant is generally preferred but not available to all patients.
Return to your Think First response about Aisha's choice between dialysis and a transplant.
- Factors: effectiveness (transplant is continuous; dialysis intermittent), quality of life (transplant near-normal; HD centre-based ~12 h/week), longevity (graft 12–15 yr, superior survival), risk (transplant surgery + lifelong immunosuppression vs dialysis access infections), availability (3–5 year transplant wait) and reversibility.
- For Aisha at 42, transplantation generally offers the best long-term outcome — but she must weigh the wait time and immunosuppression. Haemodialysis (or home peritoneal dialysis) bridges the gap while she waits.