Dialysis & transplantation flashcards
28 high-yield MRCP Part 1 cards from the Intellect Medicos Nephrology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Name four indications for urgent dialysis in AKI.
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Refractory acidosis, refractory hyperkalaemia, dialysable intoxication, refractory fluid overload (pulmonary oedema), symptomatic uraemia (pericarditis, encephalopathy).
Why? Dialysis is used when these do not respond to medical treatment.
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Name three drugs or toxins that can be removed by haemodialysis in overdose.
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Any three of: barbiturates, lithium, toxic alcohols (methanol, ethylene glycol), salicylates, theophylline.
Why? Dialysable drugs are small, water-soluble, poorly protein-bound and have a small volume of distribution.
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Haemodialysis removes solutes mainly by ______, whereas haemofiltration removes them mainly by convection.
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diffusion
Why? Dialysis relies on a concentration gradient across the membrane with countercurrent dialysate. Filtration drags water and solutes across with a pressure gradient and then adds replacement fluid; it clears larger molecules better.
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Haemodialysis removes solutes mainly by diffusion, whereas haemofiltration removes them mainly by ______.
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convection
Why? Dialysis relies on a concentration gradient across the membrane with countercurrent dialysate. Filtration drags water and solutes across with a pressure gradient and then adds replacement fluid; it clears larger molecules better.
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Why is continuous renal replacement therapy (CRRT) preferred over intermittent haemodialysis in the critically ill?
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It removes fluid and solutes slowly, so it causes less haemodynamic instability.
Why? Intermittent dialysis removes large volumes quickly and can cause hypotension. CRRT is more costly and usually needs continuous anticoagulation.
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What is the most common organism causing peritoneal dialysis–associated peritonitis?
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Staphylococcus epidermidis (coagulase-negative staphylococci).
Why? Skin organisms contaminate the catheter during exchanges. Staph aureus and Gram-negatives are less common.
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What dialysis effluent finding confirms PD peritonitis?
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White cell count above 100 cells/mm³ with neutrophils predominating (over 50%).
Why? The fluid is typically cloudy, with abdominal pain. Send effluent for Gram stain and culture.
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What is the empirical treatment of peritoneal dialysis–associated peritonitis?
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Intraperitoneal vancomycin (or teicoplanin) plus ceftazidime (an aminoglycoside can replace ceftazidime for Gram-negative cover).
Why? Antibiotics added to the dialysis fluid reach high concentrations in the peritoneum and cover both Gram-positive and Gram-negative organisms.
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What is the first-choice vascular access for long-term haemodialysis?
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An arteriovenous fistula — first choice is radiocephalic (radial artery to cephalic vein at the wrist).
Why? Fistulae have lower infection and thrombosis rates than grafts or tunnelled lines. A brachiocephalic fistula at the elbow is the next option. NICE advises creating the fistula about 6 months before dialysis is expected to start, to allow maturation.
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Dialysis-related amyloidosis is caused by deposition of which protein, and what is a classic presentation?
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β2-microglobulin; carpal tunnel syndrome (and shoulder/large-joint arthropathy).
Why? β2-microglobulin is normally cleared by the kidney but poorly removed by low-flux dialysis, so it accumulates after 5–7 years on haemodialysis.
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HLA genes are encoded on chromosome ______, and in renal transplantation the most important locus to match is HLA-DR.
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6
Why? Order of importance for matching: DR > B > A. Better matching reduces rejection and the build-up of anti-HLA antibodies.
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HLA genes are encoded on chromosome 6, and in renal transplantation the most important locus to match is HLA-______.
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DR
Why? Order of importance for matching: DR > B > A. Better matching reduces rejection and the build-up of anti-HLA antibodies.
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What causes hyperacute renal transplant rejection, and when does it occur?
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Pre-formed recipient antibodies against donor ABO or HLA antigens (type II hypersensitivity); within minutes to hours.
Why? Antibody binding activates complement and causes widespread thrombosis — the graft turns blue on the table. Cross-matching and ABO matching prevent it.
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What is the first-line treatment of acute cellular (T-cell–mediated) renal transplant rejection?
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High-dose IV methylprednisolone; anti-thymocyte globulin if steroid-resistant.
Why? Acute rejection occurs days to months after transplant with a rising creatinine and is confirmed by graft biopsy.
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What is the mechanism of basiliximab, used as induction therapy in renal transplantation?
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A monoclonal antibody against CD25 (the IL-2 receptor α chain) on activated T cells.
Why? It blocks IL-2–driven T-cell proliferation around the time of transplant.
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What is the usual triple maintenance immunosuppression after kidney transplantation?
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Tacrolimus + mycophenolate mofetil + prednisolone.
Why? This combines a calcineurin inhibitor, an antimetabolite and a corticosteroid. mTOR inhibitors (sirolimus, everolimus) are alternatives.
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What is the mechanism of action of tacrolimus?
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It binds FKBP-12 and inhibits calcineurin, preventing IL-2 transcription and T-cell activation.
Why? Ciclosporin acts the same way but binds cyclophilin. Both are nephrotoxic, so trough levels are monitored.
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Name two side effects more typical of ciclosporin than tacrolimus.
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Gingival hyperplasia and hirsutism (also more hypertension and hyperlipidaemia).
Why? Tacrolimus is more likely to cause post-transplant diabetes, tremor and neurotoxicity. Both cause nephrotoxicity and hyperkalaemia.
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A renal transplant patient on tacrolimus is prescribed clarithromycin. What is the risk?
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Raised tacrolimus levels causing nephrotoxicity (clarithromycin inhibits CYP3A4).
Why? Calcineurin inhibitors are CYP3A4 substrates. Inhibitors (macrolides, azoles, diltiazem, grapefruit) raise levels; inducers (rifampicin, carbamazepine, St John's wort) lower them and risk rejection.
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What is the mechanism of action of mycophenolate mofetil?
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It inhibits inosine monophosphate dehydrogenase (IMPDH), blocking de novo purine (guanine) synthesis.
Why? Lymphocytes depend on the de novo pathway, so T- and B-cell proliferation is selectively reduced.
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A transplant patient on azathioprine is started on allopurinol for gout. What is the danger?
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Severe bone marrow suppression — allopurinol inhibits xanthine oxidase, which breaks down azathioprine.
Why? Avoid the combination or greatly reduce the azathioprine dose. Check TPMT activity before starting azathioprine.
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Which metabolic side effect is characteristic of mTOR inhibitors (sirolimus, everolimus)?
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Hyperlipidaemia.
Why? They also impair wound healing, cause mouth ulcers and proteinuria, so they are often avoided immediately after surgery.
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What is the most common opportunistic infection after renal transplantation, and its first-line treatment?
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Cytomegalovirus (CMV), usually 4–12 weeks post-transplant; treat with IV ganciclovir or oral valganciclovir.
Why? It causes fever, cytopenias, hepatitis and pneumonitis. Foscarnet is used for ganciclovir-resistant CMV.
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Six months after a kidney transplant, creatinine is rising and urine shows 'decoy cells'. Which virus is likely and how is it managed?
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BK polyomavirus nephropathy — reduce immunosuppression.
Why? There is no reliable antiviral, so lowering immunosuppression lets the immune system control the virus.
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Which virus drives post-transplant lymphoproliferative disorder (PTLD), and what drug is used if it develops?
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Epstein–Barr virus; reduce immunosuppression and give rituximab (anti-CD20).
Why? Immunosuppression lets EBV-infected B cells proliferate unchecked.
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What is the most common malignancy after renal transplantation?
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Non-melanoma skin cancer, especially squamous cell carcinoma.
Why? Long-term immunosuppression (especially azathioprine and calcineurin inhibitors) increases skin cancer risk; advise sun protection and skin surveillance.
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Name two glomerular diseases most likely to recur in a renal transplant.
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FSGS, IgA nephropathy and MPGN (any two).
Why? Primary FSGS can recur within days, probably due to a circulating permeability factor.
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What is the most common vascular complication after renal transplantation, typically 3 months to 2 years after surgery?
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Transplant renal artery stenosis.
Why? It presents with resistant hypertension, worsening graft function, a bruit over the graft and flash pulmonary oedema. Doppler ultrasound is the first test.
More Nephrology topics
- Renal physiology, GFR & diuretics
- Acute kidney injury, contrast & TMA
- CKD: staging, management & complications
- Nephrotic syndrome, amyloid & diabetic kidney
- Nephritic syndrome, GN & vasculitis
- RTA & inherited tubular disorders
- Cystic, inherited & renal tumours
- Renal stones
- UTI, prostatitis & incontinence
- Prostate, testis & haematuria
- Sodium, potassium & calcium