Kidney Disorders, Dialysis and Transplantation
In 1943–1945, Willem Kolff built the first dialysis machine from sausage casings, orange juice cans, and a water pump in Nazi-occupied Netherlands. He treated 16 patients; the first successful treatment occurred in September 1945. The first commercial machine arrived in 1950. Now 2.5 million people globally receive dialysis (ANZDATA 2022: 13,000 Australians), at an annual cost of ~$80,000 per patient per year. When kidneys fail, every homeostatic system they regulate, blood volume, osmolality, pH, and waste removal, fails with them.
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
When Willem Kolff's 1943 dialysis machine cleared urea from a patient's blood through sausage-casing membranes, it was mechanically replicating the filtration function of the nephron, the kidney's functional unit, of which each kidney contains approximately 1 million. Kolff's machine could only do what the glomerulus and tubules normally do: filter blood across a semi-permeable membrane. Understanding why dialysis requires 12 hours a week while the kidneys work continuously, and why it can replicate filtration but not the nephron's hormonal functions, requires understanding the nephron's five regions and what each one does.
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
Glomerulus/Bowman's capsule: pressure filtration (small molecules into filtrate; proteins/cells stay in blood). 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.
Pause, copy the highlighted definition into your book before moving on.
The functional unit of the kidney, of which each kidney has about 1 million, is the _____.
From diabetes to genetics, what destroys nephron function
We just saw that ~1 million nephrons per kidney perform filtration, reabsorption, and hormonal fine-tuning. That raises a question: what diseases destroy nephron function, and how do they each attack different parts of the nephron? This card answers it → diabetes (glomerular capillary damage, ~37% of ESRD), hypertension, PKD (genetic), glomerulonephritis (autoimmune), infection, and acute kidney injury.
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.
ESRD = GFR < 15 mL/min; CKD affects ~10% of Australians. Leading causes: diabetes (~37%, glomerular capillary damage), hypertension (~25%), PKD (autosomal dominant genetic), glomerulonephritis (autoimmune), infection, acute kidney injury (sudden, may recover). Dialysis replaces filtration only, NOT hormone production (erythropoietin, active vitamin D) or precise acid-base control.
Add the highlighted point to your notes before the check below.
What is the leading cause of end-stage renal disease (ESRD) in Australia?
Replacing filtration by diffusion across a semi-permeable membrane
We just saw that kidney failure destroys the nephron's ability to filter waste. That raises a question: when the kidney can no longer filter, what technology can replicate that filtration, and on what principle does it work? This card answers it → dialysis uses diffusion across a semi-permeable membrane; haemodialysis uses an external dialyser; peritoneal dialysis uses the body's own peritoneum.
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
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 hours/session. Peritoneal dialysis: peritoneum = membrane; dialysate infused into abdomen; home-based, daily exchanges. Urea diffuses out (high in blood); glucose stays (equal concentration both sides); proteins too large to cross membrane.
Pause, write the highlighted principle into your book.
Dialysis removes urea from the blood by which principle?
Replacing the failed organ, and the immunological challenge
We just saw that dialysis replaces filtration but not the kidney's hormonal functions. That raises a question: is there a technology that actually replaces the whole organ, and what is the immunological challenge that makes it so difficult? This card answers it → kidney transplant: HLA-matched donor organ; lifelong immunosuppression required; three rejection types (hyperacute, acute, chronic).
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 |
Transplant: HLA-matched donor kidney implanted in the pelvis (iliac artery/vein, ureter to bladder). Lifelong immunosuppressants (tacrolimus, mycophenolate, prednisolone) required. Rejection types: hyperacute (pre-formed antibodies, minutes), acute (T-cell mediated, days to weeks), chronic (fibrosis, months to years). Immunosuppression ↑ infection and cancer (skin, lymphoma) risk.
Pause, copy the highlighted definition into your book before moving on.
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
We just saw that transplant restores full kidney function but requires lifelong immunosuppression. That raises a question: when comparing the three options, haemodialysis, peritoneal dialysis, and transplant, how do they actually rank on the criteria that matter for a real patient decision? This card answers it → transplant is best for quality of life and longevity; dialysis is essential when transplant is unavailable; choice depends on patient age, comorbidities, and donor availability.
| 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 |
Transplant: continuous function, best quality of life and longevity (median graft survival 12–15 yr), but surgical risk, immunosuppression complications, organ shortage (3–5 yr wait), irreversible. HD: 3×/week, centre-based, fatigue. PD: home-based, daily exchanges, peritonitis risk. Cost: HD ~$70k/yr, PD ~$55k/yr, transplant ~$100k surgery + $15k/yr drugs (cheaper long-term). Best choice depends on patient age, comorbidities, and donor availability.
Add the highlighted point to your notes before the check below.
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, and consider it in the context of Kolff's 1943 machine and the ANZDATA 2022 data. Kolff's dialysis treated 16 patients over two years with a 1:16 survival rate in the 1940s. By 2022, ANZDATA records 13,000 Australians receiving dialysis at ~$80,000/patient/year, yet dialysis remains a bridge treatment, not a cure. The transplanted kidney restores continuous homeostatic function (osmolality, pH, waste, blood pressure regulation) that Kolff's machine and modern dialysis can only intermittently replicate.
- Factors: effectiveness (transplant is continuous, like the original nephron function Kolff was trying to replace; dialysis intermittent), quality of life (transplant near-normal; HD centre-based ~12 h/week, ANZDATA: 13,000 Australians still on dialysis despite transplant being available), 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, which more closely replicates Kolff's original peritoneal-membrane design) bridges the gap while she waits.