Skip to learning content
CLINORA
More
MRCP PART 1 · RENAL MEDICINE

Renal medicine questions
for MRCP Part 1.

Clinora has 356 renal medicine single best answer questions covering 349 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

Practise renal medicine free →Other specialties →
FREE SAMPLE QUESTIONS

Try 5 renal medicine questions

Choose your answer, then open the explanation.

Question 1AKI stagingEasy

An adult has a baseline creatinine of 80 micromol/L. Five days later it is 125 micromol/L, with no evidence that a higher stage criterion is met. How should this kidney injury be staged?

  1. AStage 1 acute kidney injury
  2. BStage 2 acute kidney injury
  3. CStage 3 acute kidney injury
  4. DChronic kidney disease G2
  5. ENo acute kidney injury
Show answer and explanation

Answer: A Stage 1 acute kidney injury

NICE uses KDIGO criteria to define and stage AKI. AKI is present if serum creatinine rises by 26 µmol/L or more within 48 hours, or rises by 50% or more (1.5 times baseline) within 7 days, or urine output falls below 0.5 mL/kg/hour for more than 6 hours. Stage by the highest criterion met. Stage 1: creatinine 1.5–1.9 times baseline, or a rise of 26 µmol/L or more, or urine output below 0.5 mL/kg/hour for 6–12 hours. Stage 2: 2.0–2.9 times baseline, or urine output below 0.5 mL/kg/hour for 12 hours or more. Stage 3: 3 times baseline or more, a creatinine of 354 µmol/L or more with an acute rise, starting renal replacement therapy, or urine output below 0.3 mL/kg/hour for 24 hours or no urine for 12 hours. Here 125 ÷ 80 = 1.56 within 7 days, so this is stage 1. Even stage 1 AKI calls for the same response: find the cause, review nephrotoxic drugs, assess fluid status, and monitor creatinine and urine output.

Key clue
An adult has a baseline creatinine of 80 micromol/L. Five days later it is 125 micromol/L, with no evidence that a higher stage criterion is met. How should this kidney injury be staged
What it means
The creatinine has risen 1.56-fold within seven days, meeting NICE/KDIGO stage 1 AKI without a stage 2 or 3 criterion.
What to do
Stage 1 acute kidney injury

Why the other options are less appropriate

  • B Stage 2 needs creatinine at least twice baseline (160 µmol/L here) or prolonged oliguria.
  • C Stage 3 needs a threefold rise, a creatinine of 354 µmol/L or more with an acute rise, renal replacement therapy, or severe oliguria or anuria.
  • D CKD needs abnormal kidney function for more than 3 months. A rise over 5 days is acute.
  • E A rise of 50% or more within 7 days meets the definition of AKI.

Source: NICE NG148: Acute kidney injury recommendations

Question 2Acute tubular injuryMedium

A patient develops AKI after prolonged septic shock. Which urinary sediment finding most strongly supports acute tubular injury?

  1. ADysmorphic erythrocytes and erythrocyte casts
  2. BOval fat bodies and fatty casts
  3. CMuddy-brown granular casts containing tubular epithelial debris
  4. DIsolated hyaline casts after exercise
  5. EHexagonal cystine crystals
Show answer and explanation

Answer: C Muddy-brown granular casts containing tubular epithelial debris

Prolonged septic shock reduces blood flow to the kidney, and the tubular cells of the proximal tubule and thick ascending limb are very sensitive to ischaemia. Injured cells die and slough into the tubular lumen, where they mix with Tamm-Horsfall protein to form coarse, pigmented granular casts, often called muddy-brown casts. Renal tubular epithelial cells may also be seen. Finding these on urine microscopy strongly supports acute tubular injury (acute tubular necrosis) rather than a pre-renal cause, which usually shows only hyaline casts. Damaged tubules also lose the ability to reabsorb sodium and concentrate urine, so the fractional excretion of sodium is usually above 2% and urine osmolality is low. In sepsis these indices are less reliable. Management follows NICE NG148 and KDIGO principles: treat the sepsis, restore perfusion, avoid nephrotoxins such as NSAIDs and aminoglycosides, review drug doses, and monitor fluid balance, potassium and acidosis. Renal replacement therapy is needed for refractory hyperkalaemia, acidosis, fluid overload or uraemic complications.

Key clue
A patient develops AKI after prolonged septic shock. Which urinary sediment finding most strongly supports acute tubular injury
What it means
Ischaemic acute tubular injury sheds tubular epithelial cells and pigmented granular debris, producing classic muddy-brown casts.
What to do
Muddy-brown granular casts containing tubular epithelial debris

Why the other options are less appropriate

  • A Dysmorphic red cells and red-cell casts mean bleeding from the glomerulus, as in glomerulonephritis, not tubular injury.
  • B Oval fat bodies and fatty casts come from heavy proteinuria in nephrotic syndrome, not ischaemic tubular damage.
  • D Hyaline casts are non-specific and appear with dehydration or exercise. They suggest a pre-renal state rather than tubular injury.
  • E Hexagonal crystals indicate cystinuria, an inherited cause of kidney stones. They do not explain AKI after septic shock.

Source: NCBI Bookshelf: Acute Renal Tubular Necrosis

Question 3Anti-GBM diseaseMedium

A patient has rapidly progressive glomerulonephritis, pulmonary haemorrhage and circulating anti-GBM antibodies. What induction strategy is most appropriate?

  1. AGlucocorticoids, cyclophosphamide and therapeutic plasma exchange started urgently
  2. BSupportive blood-pressure control alone while awaiting spontaneous recovery
  3. CRituximab monotherapy without glucocorticoids or plasma exchange
  4. DMycophenolate mofetil alone for six months
  5. EAntibiotics and delayed biopsy review before any immunotherapy
Show answer and explanation

Answer: A Glucocorticoids, cyclophosphamide and therapeutic plasma exchange started urgently

Rapidly progressive glomerulonephritis with pulmonary haemorrhage and circulating anti-GBM antibodies is anti-GBM disease (Goodpasture disease). Autoantibodies against the alpha-3 chain of type IV collagen attack the glomerular and alveolar basement membranes. KDIGO 2021 recommends starting treatment without delay when the diagnosis is strongly suspected, even before biopsy: plasma exchange to remove circulating antibody, with cyclophosphamide and glucocorticoids to stop further production. Plasma exchange is usually daily for about 14 days or until antibodies are undetectable, with fresh frozen plasma given at the end of sessions when there is pulmonary haemorrhage or a recent biopsy, to limit bleeding. Glucocorticoids usually start with IV methylprednisolone, then oral prednisolone at about 1 mg/kg/day, with oral cyclophosphamide for about 3 months. Treatment is offered to all except those who are dialysis-dependent with 100% crescents and no pulmonary haemorrhage. Check ANCA, because double-positive patients can relapse and need maintenance therapy.

Key clue
A patient has rapidly progressive glomerulonephritis, pulmonary haemorrhage and circulating anti-GBM antibodies. What induction strategy is most appropriate
What it means
Pulmonary haemorrhage with anti-GBM glomerulonephritis warrants urgent glucocorticoids, cyclophosphamide and plasma exchange.
What to do
Glucocorticoids, cyclophosphamide and therapeutic plasma exchange started urgently

Why the other options are less appropriate

  • B Anti-GBM disease with lung haemorrhage does not remit in time on its own. Delay risks dialysis dependence and fatal bleeding.
  • C Rituximab has been used for refractory disease or cyclophosphamide intolerance, but it is not standard first-line induction and does not remove existing antibody.
  • D Mycophenolate alone is slow and unproven for anti-GBM induction, and it does not remove circulating antibody.
  • E Treatment should start on strong suspicion. Waiting for biopsy review allows irreversible glomerular and lung damage.

Source: KDIGO 2021 Clinical Practice Guideline for Glomerular Diseases

Question 4Lupus nephritisHard

A patient with systemic lupus erythematosus has persistent protein excretion of 650 mg/day, microscopic haematuria and no alternative explanation. What is the most appropriate next renal step?

  1. AStart lifelong dialysis because proteinuria proves irreversible failure
  2. BObserve without renal assessment until nephrotic-range proteinuria develops
  3. CDiagnose class IV lupus nephritis clinically without tissue confirmation
  4. DTreat with NSAIDs alone and repeat urine testing annually
  5. EArrange kidney biopsy to classify suspected lupus nephritis
Show answer and explanation

Answer: E Arrange kidney biopsy to classify suspected lupus nephritis

Persistent proteinuria above 0.5 g/day with haematuria in SLE, with no other cause, suggests lupus nephritis. The pattern of injury can only be defined on tissue. KDIGO 2024 advises kidney biopsy when proteinuria is at least 0.5 g/day (or the equivalent protein-to-creatinine ratio), especially with active urinary sediment, or when kidney function falls for no clear reason. The biopsy is reported using the ISN/RPS classification (classes I–VI), with activity and chronicity scores. Class III and IV are proliferative and need induction immunosuppression with glucocorticoids plus mycophenolate or low-dose intravenous cyclophosphamide. KDIGO 2024 also supports adding belimumab or a calcineurin inhibitor in selected patients. Class V (membranous) may be treated differently, and class VI (advanced sclerosis) points towards preparing for kidney replacement therapy rather than more immunosuppression. Everyone should take hydroxychloroquine and have blood pressure controlled, with renin-angiotensin blockade for proteinuria.

Key clue
A patient with systemic lupus erythematosus has persistent protein excretion of 650 mg/day, microscopic haematuria and no alternative explanation. What is the most appropriate next renal step
What it means
Persistent proteinuria above 500 mg/day with active urine sediment in SLE warrants kidney biopsy to classify lupus nephritis.
What to do
Arrange kidney biopsy to classify suspected lupus nephritis

Why the other options are less appropriate

  • A Subnephrotic proteinuria with haematuria points to possibly reversible inflammation. It does not show end-stage disease, and dialysis is not indicated.
  • B The 0.5 g/day biopsy threshold is set low so that active nephritis is treated before it scars. Waiting for nephrotic-range loss risks permanent damage.
  • C Clinical findings cannot reliably predict ISN/RPS class or chronicity, and these determine which immunosuppressive regimen she needs.
  • D NSAIDs reduce glomerular blood flow, can worsen kidney function and do not treat immune-complex nephritis.

Source: KDIGO 2024 Clinical Practice Guideline for Lupus Nephritis

Question 5Glomerular haematuriaEasy

Which urine microscopy finding most strongly localises haematuria to glomerular inflammation?

  1. AErythrocyte casts with dysmorphic erythrocytes
  2. BCalcium oxalate crystals with isomorphic erythrocytes
  3. CHyaline casts alone after exercise
  4. DSquamous epithelial cells with mixed bacteria
  5. EOval fat bodies with Maltese crosses
Show answer and explanation

Answer: A Erythrocyte casts with dysmorphic erythrocytes

Red cells that enter the urine through a damaged glomerular basement membrane are deformed by mechanical stress and by changes in osmolality and pH as they pass along the tubule, so they appear dysmorphic. Acanthocytes, ring-shaped cells with small blebs, are the most specific dysmorphic form, and a proportion of around 5% or more is often used to favour glomerular bleeding. Red-cell casts form when these cells are trapped in a matrix of uromodulin (Tamm–Horsfall protein) inside the tubule, so their presence shows that bleeding arose within the nephron. Together these findings indicate a nephritic process such as IgA nephropathy, ANCA-associated vasculitis, anti-GBM disease, post-infectious glomerulonephritis. Isomorphic red cells, by contrast, suggest bleeding from the urinary tract below the kidney, such as stones, infection or tumour. The next step is to measure blood pressure, eGFR and the urine albumin- or protein-to-creatinine ratio, and to send ANCA, anti-GBM antibodies, complement and ANA. Haematuria with rapidly falling kidney function needs same-day nephrology referral.

Key clue
Which urine microscopy finding most strongly localises haematuria to glomerular inflammation
What it means
Dysmorphic erythrocytes and erythrocyte casts are highly characteristic of glomerular bleeding and nephritic inflammation.
What to do
Erythrocyte casts with dysmorphic erythrocytes

Why the other options are less appropriate

  • B Calcium oxalate crystals suggest stone disease, and isomorphic red cells point to bleeding from the lower urinary tract rather than the glomerulus.
  • C Hyaline casts are made of uromodulin alone and are nonspecific; they appear in concentrated urine and after exercise in healthy people.
  • D Squamous cells with mixed bacteria indicate contamination from the skin or urethra and say nothing about glomerular disease.
  • E Oval fat bodies with Maltese crosses show lipiduria in nephrotic syndrome, which is non-inflammatory and does not localise haematuria.

Source: NCBI Bookshelf: Gross and Microscopic Hematuria

That is 5 of 356. Carry on with renal medicine in the practice bank, with progress tracking, flashcards and timed sessions.

Practise renal medicine free →

Topics covered

Show all 349 renal medicine topics
  • A 14 mm ureteric stone
  • A high creatinine is not itself a dialysis prescription
  • A large staghorn calculus without sepsis
  • A meaningful creatinine rise hidden by greater-than-90 reporting
  • A new low eGFR needs confirmation
  • A prior resistant urine culture changes empiric choice
  • A small creatinine rise after ACE inhibition
  • A susceptible urine isolate is not enough for renal infection
  • Accurate GFR when treatment margin is narrow
  • ACE inhibitor management before contrast
  • Acquired cystic kidney disease
  • ACR at the high referral threshold
  • Active antibody-mediated rejection
  • Acute cortical necrosis
  • Acute hyperkalaemia
  • Acute interstitial nephritis
  • Acute interstitial nephritis triad
  • Acute phosphate nephropathy
  • Acute T-cell-mediated rejection
  • Acute tubular injury
  • Acute tubular necrosis sediment
  • ADTKD-MUC1
  • ADTKD-UMOD
  • Adynamic bone disease
  • AKI prevention
  • AKI recognition
  • AKI staging
  • Albuminuria confirmation
  • Albuminuria plus haematuria crosses a referral threshold
  • Albuminuria with haematuria referral
  • Albuminuric chronic kidney disease
  • Allowing time for arteriovenous fistula maturation
  • Alport syndrome
  • Alport syndrome clue
  • Aluminium toxicity
  • An incidental small renal calculus
  • An old eGFR after a new acute illness
  • An untargetable ureteric stone
  • Anaemia of CKD
  • Analgesia when NSAIDs are unsuitable
  • ANCA vasculitis renal test
  • ANCA-associated vasculitis
  • Anti-brush-border antibody disease
  • Anti-GBM disease
  • Anti-GBM disease despite dialysis dependence
  • Anticoagulant-related nephropathy
  • APOL1-associated nephropathy
  • Aristolochic acid nephropathy
  • Assessing symptoms during conservative kidney care
  • Atherosclerotic renovascular disease
  • Attributing fatigue before initiating dialysis
  • Autosomal dominant polycystic kidney disease
  • Avoiding routine CKD mineral panels in uncomplicated G3a
  • Avoiding routine loop diuretics in AKI
  • Avoiding transfusion when transplantation remains an option
  • Bartter syndrome
  • Bartter syndrome type 4
  • Bile cast nephropathy
  • BK polyomavirus
  • C3 glomerulopathy
  • Calcineurin-inhibitor toxicity
  • Calciphylaxis
  • Calcium advice after recurrent stones
  • Calcium testing after a first stone
  • Calcium-alkali syndrome
  • Central diabetes insipidus
  • Cerebral salt wasting
  • Chloride-responsive metabolic alkalosis
  • Cholesterol crystal embolisation
  • Choosing between forms of peritoneal dialysis
  • Chronic active antibody-mediated rejection
  • Citrate for recurrent calcium oxalate stones
  • CKD
  • CKD blood-pressure targets
  • CKD chronicity
  • CKD metabolic acidosis
  • CKD mineral and bone disorder
  • CKD mineral bone disorder
  • CKD, hypertension and A3 albuminuria
  • Cloudy dialysate emergency
  • CMV syndrome
  • Co-amoxiclav is not an unconditional empiric oral choice
  • Collapsing glomerulopathy
  • Confirming albuminuria
  • Confirming isolated invisible haematuria
  • Confirming moderately increased albuminuria
  • Confirming persistent isolated invisible haematuria
  • Considering withdrawal of dialysis with capacity
  • Contrast during time-critical care
  • Contrast-associated AKI
  • Cooked meat as a pre-analytical influence on creatinine
  • Countercurrent multiplication
  • Cranberry claims in an older patient
  • Creatinine estimate in low muscle mass
  • Cryoglobulinaemic glomerulonephritis
  • Crystalglobulinaemia-associated nephropathy
  • Cystic kidneys with aneurysm family history
  • Cystinuria
  • Cytomegalovirus prevention
  • Delayed graft function
  • Delta ratio
  • Dent disease
  • Detecting AKI despite normal-range creatinine
  • Diabetes alters the ACE-inhibitor threshold
  • Diabetic kidney disease histology
  • Dialysis adequacy
  • Dialysis disequilibrium
  • Dialysis disequilibrium syndrome
  • Dialysis modality and maintaining employment
  • Dialysis-associated haemolysis
  • Dialysis-related amyloidosis
  • Distal potassium secretion
  • Distal renal tubular acidosis
  • Do not normalise haemoglobin with an ESA
  • Double-positive anti-GBM and ANCA disease
  • Drug-associated acute interstitial nephritis
  • Dual renin–angiotensin blockade for residual albuminuria
  • Duration of peritoneal dialysis and elective transfer
  • EAST syndrome
  • Emergency hyperkalaemia stabilisation
  • Emergency imaging despite kidney risk
  • Emphysematous pyelonephritis
  • Encapsulating peritoneal sclerosis
  • Enteric hyperoxaluria
  • Erythropoietin deficiency
  • Erythropoietin measurement in CKD anaemia
  • ESA haemoglobin target
  • Ethylene glycol poisoning
  • Fabry disease
  • Failed oral iron in non-dialysis CKD
  • Familial renal glycosuria
  • Fanconi syndrome
  • Fibrillary glomerulonephritis
  • Fibronectin glomerulopathy
  • Filtration fraction
  • Finerenone
  • First procedural option for a small renal calculus
  • First stone and an occult driver
  • Fluoroquinolone restriction is not a footnote
  • Follow-up after negative assessment of isolated haematuria
  • Fractional excretion of urea
  • Functional iron deficiency
  • G2 filtration without kidney-damage markers
  • Gitelman syndrome
  • Glomerular haematuria
  • Goodpasture pulmonary renal
  • Gordon syndrome
  • Haematuria and proteinuria in unexplained AKI
  • Haematuria changes referral threshold
  • Haematuria plus proteinuria
  • Haemodialysis catheter infection
  • Haemodialysis vascular access
  • Heavy albuminuria without diabetes
  • Hepatorenal syndrome-AKI
  • Hereditary renal hypouricaemia
  • High-dose intravenous iron withholding rules
  • High-output heart failure from AV access
  • HIV-associated nephropathy
  • HNF1B-associated disease
  • Hyperacute rejection
  • Hypercalcaemic nephrogenic diabetes insipidus
  • Hyperkalaemia before starting renin–angiotensin blockade
  • Hyperkalaemia ECG sign
  • Hypernatraemia calculation
  • Hypokalaemic nephropathy
  • Hypovolaemic hyponatraemia
  • Icodextrin and false glucose readings
  • IgA nephropathy
  • IgA nephropathy timing
  • Imaging suspected renal colic
  • Immunotactoid glomerulopathy
  • Improving AKI in a kidney transplant recipient
  • Infected obstructed kidney
  • Infected obstructed urinary system
  • Infection-related glomerulonephritis
  • Information after an unplanned dialysis start
  • Intercourse-associated episodes and a targeted preventive dose
  • Interpreting albuminuria categories
  • Intradialytic hypotension
  • Iron-status testing in CKD with thalassaemia trait
  • KFRE threshold for specialist referral
  • Kidney Failure Risk Equation
  • Kidney replacement therapy initiation
  • Known cause and ultrasound
  • LCAT-deficiency nephropathy
  • Liddle syndrome
  • Light-chain deposition disease
  • Light-chain proximal tubulopathy
  • Liquorice-associated mineralocorticoid excess
  • Lithium-induced nephrogenic diabetes insipidus
  • Loop diuretics as AKI treatment
  • Loop diuretics for overload during renal recovery
  • Lupus nephritis
  • Lysozyme nephropathy
  • Maintaining dietary calcium after calcium oxalate stones
  • Malignant hypertension
  • Medical expulsive therapy
  • Medication review in advanced CKD
  • Medication review in hypovolaemic AKI
  • Medullary sponge kidney
  • Membranous nephropathy
  • Metabolic acidosis compensation
  • Metformin in CKD
  • Microscopy is not required to confirm dipstick blood
  • Minimal change disease
  • Monitoring after ACE inhibitor dose escalation
  • Monoclonal gammopathy of renal significance
  • Myeloma cast nephropathy
  • Nail-patella syndrome
  • Nephritic syndrome clue
  • Nephrogenic diabetes insipidus
  • Nephrogenic systemic fibrosis
  • Nephronophthisis
  • Nephrotic syndrome complications
  • No renal-dose dopamine for AKI
  • Non-diabetic albuminuria without hypertension
  • Non-diabetic CKD with ACR at least 70
  • NSAID exposure in chronic kidney disease
  • Nutcracker syndrome
  • Obesity and kidney transplant assessment
  • Obstructive AKI
  • Oliguria as AKI criterion
  • Oliguria criterion for AKI detection
  • One low eGFR is not chronic disease
  • Osmotic demyelination prevention
  • Osmotic nephrosis
  • Osteitis fibrosa cystica
  • Page kidney
  • Peritoneal dialysis fast transport
  • Peritoneal dialysis peritonitis
  • Persistent colic despite adequate analgesia
  • Persistent hyperkalaemia on an ACE inhibitor
  • Persistent phosphate elevation and binder use
  • Phosphate-binder selection
  • Pigment nephropathy
  • Podocyte foot-process effacement
  • Post-obstructive diuresis
  • Post-renal obstruction
  • Post-streptococcal glomerulonephritis
  • Post-transplant de novo thrombotic microangiopathy
  • Post-transplant erythrocytosis
  • Post-transplant lymphoproliferative disorder
  • Pre-emptive transplantation rather than obligatory dialysis
  • Pre-renal AKI indices
  • Pregnancy changes the disposition discussion
  • Pregnancy planning while receiving dialysis
  • Preoperative vessel assessment for dialysis access
  • Primary hyperaldosteronism
  • Primary hyperoxaluria
  • Primary hyperparathyroidism
  • Primary polydipsia
  • Probiotics are not a proven replacement
  • Procedure for a larger ureteric stone
  • Proton-pump inhibitor hypomagnesaemia
  • Proximal renal tubular acidosis
  • Pseudohyperkalaemia
  • Pseudohyponatraemia
  • Psychological assessment before kidney transplantation
  • Pulmonary oedema in AKI
  • Rapid eGFR decline despite a moderate current value
  • Rapidly progressive glomerulonephritis
  • Reassessing diet after a change in dialysis modality
  • Recognising accelerated CKD progression
  • Recurrent calcium oxalate stones
  • Recurrent FSGS after transplantation
  • Reducing the burden of dialysis appointments
  • Refeeding syndrome
  • Reference GFR measurement for potential kidney donation
  • Refractory colic despite a small stone
  • Renal abscess
  • Renal ammonium handling
  • Renal amyloidosis
  • Renal artery fibromuscular dysplasia
  • Renal artery stenosis indication
  • Renal colic in pregnancy
  • Renal fibromuscular dysplasia
  • Renal infarction
  • Renal papillary necrosis
  • Renal response to extrarenal potassium loss
  • Renal sarcoidosis
  • Renal transplant rejection
  • Renal ultrasound in advanced stable CKD
  • Renin–angiotensin blockade in A3 albuminuria
  • Renin–angiotensin system blockade
  • Residual impairment after an AKI episode
  • Resistance matters even when symptoms are easing
  • Revisiting conservative kidney management
  • Route of a short-acting ESA
  • Routine pre-treatment stenting before shockwave lithotripsy
  • Routine stent after uncomplicated ureteroscopy
  • Scleroderma renal crisis
  • Screening before a non-urgent contrast CT
  • Secondary focal segmental glomerulosclerosis
  • Secondary hyperparathyroidism and renal anaemia
  • Secondary hyperparathyroidism in advanced CKD
  • Separating dialysis preparation from automatic initiation
  • Severe hypermagnesaemia
  • Severe symptomatic hyponatraemia
  • SGLT2 inhibitor eGFR dip
  • Slope matters more than a single category
  • Small creatinine rise after ACE inhibitor
  • Sodium reduction before thiazide stone prevention
  • Solitary kidney obstruction
  • Stable A3 albuminuria without diabetes
  • Stenting after uncomplicated ureteroscopy
  • Stenting before shockwave treatment
  • Struvite stone
  • Suspected pyonephrosis
  • Systemic HRT is not UTI prophylaxis
  • Tertiary hyperparathyroidism
  • The 48-hour failure checkpoint
  • The complicated case needs specialist input
  • Thin basement membrane nephropathy
  • Thromboembolism
  • Thrombotic microangiopathy
  • Time-critical drainage of infected obstruction
  • Timing an open surgical peritoneal dialysis catheter
  • Timing iron indices after an intravenous infusion
  • TINU syndrome
  • Toluene-associated acidosis
  • Translocational hyponatraemia
  • Transplant renal artery thrombosis
  • Tubuloglomerular feedback
  • Tumour lysis syndrome
  • Type 1 cardiorenal syndrome
  • Type 4 renal tubular acidosis
  • Ultrasound timing when AKI has no identified cause
  • Unexpected haemoglobin fall during ESA maintenance
  • Uraemic complication despite falling creatinine
  • Uraemic pericarditis
  • Uraemic platelet dysfunction
  • Urgent dialysis indication
  • Urgent referral for renal replacement therapy
  • Uric acid stone
  • Urinary osmolal gap
  • Urine anion gap
  • Urine chloride in metabolic alkalosis
  • Urine–blood carbon dioxide gradient
  • Vasopressin signalling
  • VEGF-inhibitor-associated renal thrombotic microangiopathy
  • Venous air embolism
  • Very high ACR and the need for confirmation
  • Vitamin D deficiency in CKD
  • Volume expansion in high-risk contrast exposure
  • Vomiting makes the oral route unreliable
  • Water advice after recurrent stone formation
  • When routine ultrasound adds little in resolving AKI
  • When to begin renal replacement planning
  • When to investigate anaemia in CKD

Other MRCP Part 1 specialties