Acute kidney injury UK Medical PG Practice Questions and MCQs
Practice UK Medical PG questions for Acute kidney injury. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Acute kidney injury UK Medical PG Question 1: A 65-year-old man presents with painless hematuria. Cystoscopy shows a bladder tumor. Histology confirms transitional cell carcinoma. What is the most important risk factor for this condition?
- A. Alcohol consumption
- B. Smoking (Correct Answer)
- C. High-fat diet
- D. Sedentary lifestyle
- E. Family history
Acute kidney injury Explanation: ***Smoking***- **Smoking** is by far the most significant and prevalent risk factor for urothelial (transitional cell) carcinoma, contributing to approximately 50-70% of all cases.- Tobacco smoke contains **aromatic amines** and other carcinogens that are metabolized, excreted in urine, and concentrate in the bladder, leading to **DNA damage** and tumor formation.*Alcohol consumption*- Alcohol consumption is not considered a primary or independent risk factor specifically for **urothelial carcinoma**.- While excessive alcohol intake is linked to other cancers, its direct association with bladder cancer is not robust.*High-fat diet*- High-fat diets are generally associated with an increased risk of certain cancers, such as **colorectal** and **prostate** cancer.- However, dietary factors do not represent the primary pathogenic mechanism for transitional cell carcinoma, which is predominantly driven by urinary carcinogens.*Sedentary lifestyle*- A sedentary lifestyle is a generalized risk factor for several cancers, particularly those linked to **obesity** and metabolic syndromes (e.g., endometrial, breast).- There is no strong, direct, or specific mechanistic link between a sedentary lifestyle and the development of **urothelial carcinoma** compared to chemical exposures.*Family history*- While a small proportion of bladder cancers may show some familial clustering, **environmental exposures** like smoking and occupational chemicals are the overwhelming etiologic factors.- Familial predisposition is a minor risk factor and is considerably less important than direct carcinogenic exposure from **smoking**.
Acute kidney injury UK Medical PG Question 2: A 29-year-old woman at 32 weeks gestation presents to the obstetric assessment unit with headache and right upper quadrant pain. She has no significant past medical history. Blood pressure is 168/112 mmHg. Blood tests show: haemoglobin 102 g/L, platelets 88 × 10^9/L, ALT 245 U/L, AST 312 U/L, bilirubin 34 μmol/L, creatinine 145 μmol/L (booking creatinine was 68 μmol/L), LDH 680 U/L. Urinalysis shows protein 3+. Peripheral blood film shows schistocytes. What is the most appropriate immediate management?
- A. Commence IV magnesium sulphate and plan delivery within 24-48 hours
- B. Commence IV labetalol, IV magnesium sulphate, and arrange immediate delivery (Correct Answer)
- C. Commence plasma exchange for thrombotic thrombocytopenic purpura
- D. Commence high-dose corticosteroids for HELLP syndrome
- E. Transfuse platelets and arrange delivery once platelets >100 × 10^9/L
Acute kidney injury Explanation: ***Commence IV labetalol, IV magnesium sulphate, and arrange immediate delivery***
- The patient's presentation with headache, right upper quadrant pain, severe hypertension (168/112 mmHg), proteinuria, thrombocytopenia (platelets 88 × 10^9/L), elevated liver enzymes (ALT 245 U/L, AST 312 U/L), elevated LDH, elevated bilirubin, and **schistocytes** on peripheral blood film is highly indicative of **HELLP syndrome** (Hemolysis, Elevated Liver enzymes, Low Platelets) with severe pre-eclampsia and acute kidney injury.
- **Immediate delivery** is the definitive and most appropriate management for HELLP syndrome, especially given the severity and multi-organ involvement. **IV labetalol** is crucial for managing severe hypertension to prevent maternal stroke, and **IV magnesium sulphate** is essential for seizure prophylaxis in severe pre-eclampsia/HELLP.
*Commence IV magnesium sulphate and plan delivery within 24-48 hours*
- While **magnesium sulphate** is correctly indicated for seizure prophylaxis, delaying delivery for **24-48 hours** in the context of established HELLP syndrome with signs of organ dysfunction (AKI, severe liver dysfunction) is dangerous and can lead to severe maternal and fetal complications, including liver rupture, renal failure, or stroke.
- The critical nature of **HELLP syndrome** often requires delivery within hours of diagnosis and maternal stabilization, not prolonged expectant management.
*Commence plasma exchange for thrombotic thrombocytopenic purpura*
- Although both **TTP** and HELLP syndrome can present with microangiopathic hemolytic anemia and thrombocytopenia, the presence of severe **hypertension** and significant **proteinuria** in a pregnant woman points strongly towards HELLP syndrome.
- Initiating **plasma exchange**, which is the primary treatment for TTP, would be a misdiagnosis and critically delay the definitive treatment for HELLP syndrome, which is delivery, thereby increasing maternal and fetal morbidity and mortality.
*Commence high-dose corticosteroids for HELLP syndrome*
- While corticosteroids (e.g., dexamethasone) are sometimes used as an adjunct in HELLP syndrome to potentially improve platelet counts and liver enzyme levels, they are **not the definitive treatment** and do not replace the need for prompt delivery.
- The primary management for HELLP syndrome focuses on stabilizing the mother and then delivering the fetus and placenta; corticosteroids for maternal benefit are secondary and should not delay the primary intervention, though steroids for fetal lung maturity might be considered if time permits for delivery within 24-48 hours (which is not the case here given the severity).
*Transfuse platelets and arrange delivery once platelets >100 × 10^9/L*
- **Platelet transfusion** is generally reserved for platelet counts below 20-50 × 10^9/L, active bleeding, or prior to invasive procedures/delivery, rather than as a routine measure for a count of 88 × 10^9/L.
- Delaying delivery to achieve an arbitrary platelet count threshold of **>100 × 10^9/L** is inappropriate and unsafe in HELLP syndrome; the platelet count often only improves significantly post-delivery, and such a delay puts the mother at increased risk of complications like intracranial hemorrhage or abruptio placentae.
Acute kidney injury UK Medical PG Question 3: A 38-year-old man with chronic kidney disease stage 5 (eGFR 10 mL/min/1.73m²) secondary to focal segmental glomerulosclerosis is being prepared for renal replacement therapy. He has preserved urine output of approximately 1500 mL per day. He works full-time as a teacher and wishes to minimize time spent on dialysis. Blood tests show: haemoglobin 108 g/L, potassium 5.1 mmol/L, phosphate 1.72 mmol/L, albumin 36 g/L. He has good manual dexterity and lives with his partner. Which renal replacement modality would be most appropriate to offer first?
- A. Continuous ambulatory peritoneal dialysis (CAPD)
- B. Automated peritoneal dialysis (APD) (Correct Answer)
- C. In-centre haemodialysis three times weekly
- D. Home haemodialysis
- E. Pre-emptive renal transplantation
Acute kidney injury Explanation: ***Automated peritoneal dialysis (APD)***
- **APD** is ideal for a full-time teacher as it allows for **overnight dialysis cycles** while the patient sleeps, freeing up their entire day for work and other activities.
- The patient's **preserved residual urine output** (1500 mL/day) and **good manual dexterity** are strong indicators for successful home-based peritoneal dialysis, minimizing the impact on lifestyle.
*Continuous ambulatory peritoneal dialysis (CAPD)*
- **CAPD** requires several **manual exchanges** throughout the day, which would significantly interrupt a teacher's workday and classroom responsibilities.
- Although home-based, it offers less **lifestyle flexibility** and independence during waking hours compared to automated peritoneal dialysis.
*In-centre haemodialysis three times weekly*
- This option involves regular trips to a clinic for **4-hour sessions** three times a week, directly conflicting with the patient's desire to **minimize time spent on dialysis** and maintain full-time employment.
- **In-centre haemodialysis** is generally associated with a more rapid decline in **residual renal function** compared to peritoneal dialysis.
*Home haemodialysis*
- **Home haemodialysis** is a more complex and technically demanding modality, requiring **vascular access** (e.g., AV fistula) and extensive patient training, which could delay the initiation of therapy.
- It involves greater equipment setup and ongoing maintenance at home, which can be more **invasive and disruptive** to the patient's living environment than peritoneal dialysis.
*Pre-emptive renal transplantation*
- While **pre-emptive renal transplantation** is the preferred long-term treatment for CKD stage 5, it is contingent on **donor availability** and is not a dialysis modality to be offered as the initial RRT choice.
- The question specifically asks for an appropriate **renal replacement modality** (dialysis) to offer *first* as the patient prepares for RRT.
Acute kidney injury UK Medical PG Question 4: A 71-year-old woman with type 2 diabetes and hypertension is admitted with sepsis secondary to pneumonia. On admission, her creatinine is 156 μmol/L (baseline 98 μmol/L two months ago). She is treated with IV fluids and antibiotics. On day 3, her creatinine rises to 298 μmol/L. Urinalysis shows: protein 2+, blood negative, leucocytes negative. Urine microscopy reveals muddy brown casts. Renal ultrasound shows normal-sized kidneys with no obstruction. What is the most likely diagnosis?
- A. Acute tubular necrosis (Correct Answer)
- B. Contrast-induced nephropathy
- C. Acute interstitial nephritis
- D. Pre-renal acute kidney injury
- E. Atheroembolic renal disease
Acute kidney injury Explanation: ***Acute tubular necrosis***- The presence of **muddy brown casts** on urine microscopy is a pathognomonic finding for **acute tubular necrosis (ATN)**, indicating sloughing of renal tubular epithelial cells.- **Sepsis** is a common cause of **intrinsic AKI** through hypotension and inflammatory mediators, leading to ATN that typically does not resolve immediately with fluid resuscitation.*Contrast-induced nephropathy*- This typically presents as an acute rise in creatinine within **24-48 hours** following the administration of radiocontrast media, which is not mentioned in this patient's history.- While it can cause ATN, the clinical context of **sepsis secondary to pneumonia** provides a more direct etiology for the tubular injury.*Acute interstitial nephritis*- Usually triggered by medications (e.g., NSAIDs, antibiotics) and typically presents with **white cell casts**, pyuria, and sometimes a maculopapular rash or **eosinophilia**.- Urinalysis in this case was **negative for leucocytes**, making an inflammatory interstitial process significantly less likely than ATN.*Pre-renal acute kidney injury*- Pre-renal AKI is characterized by a rapid improvement in renal function following **volume resuscitation** and usually features a normal urinary sediment without casts.- The persistent rise in creatinine despite **IV fluids** and the presence of granular/muddy brown casts indicate progression from pre-renal states to **structural tubular damage**.*Atheroembolic renal disease*- This condition typically occurs after **vascular procedures** or catheterization, resulting in cholesterol emboli that cause livedo reticularis and peripheral eosinophilia.- The onset of renal failure is often more subacute compared to the rapid progression seen in **sepsis-induced ATN**, and muddy brown casts are not a characteristic feature.
Acute kidney injury UK Medical PG Question 5: A 48-year-old woman with no significant past medical history presents to the emergency department with a 6-hour history of severe right loin pain. CT KUB confirms a 5 mm stone at the right pelviureteric junction with mild hydronephrosis. She is afebrile. Blood tests show: white cells 9.2 × 10^9/L, CRP 8 mg/L, creatinine 78 μmol/L. Urinalysis shows blood 3+, leucocytes 1+, nitrites negative. She has been given adequate analgesia with diclofenac and morphine. What is the most appropriate next step in her management?
- A. Discharge with analgesia, alpha-blocker, and follow-up in stone clinic (Correct Answer)
- B. Admit for IV antibiotics due to obstructive pyelonephritis
- C. Arrange urgent ureteroscopy and stone extraction within 48 hours
- D. Insert percutaneous nephrostomy for decompression
- E. Arrange extracorporeal shock wave lithotripsy (ESWL) within one week
Acute kidney injury Explanation: ***Discharge with analgesia, alpha-blocker, and follow-up in stone clinic***
- This patient presents with **uncomplicated renal colic** as evidenced by the 5 mm stone, controlled pain, normal inflammatory markers, and absence of fever or signs of infection (afebrile, negative nitrites).
- Stones **less than 10 mm** (especially 5 mm) have a high rate of spontaneous passage, and **medical expulsive therapy (MET)** with an alpha-blocker like tamsulosin is recommended to facilitate this process.
*Admit for IV antibiotics due to obstructive pyelonephritis*
- There is no evidence of infection; the patient is **afebrile**, and **blood tests** (WBC 9.2, CRP 8) do not indicate significant systemic inflammation.
- **Obstructive pyelonephritis** is a medical emergency characterized by fever, flank pain, and signs of infection with obstruction, which are absent here.
*Arrange urgent ureteroscopy and stone extraction within 48 hours*
- Urgent invasive procedures like **ureteroscopy** are typically reserved for patients with **intractable pain**, signs of infection, acute kidney injury, or stones unlikely to pass spontaneously (e.g., larger stones).
- Given the small size of the stone (5 mm) and controlled pain, a trial of conservative management is more appropriate before considering invasive intervention.
*Insert percutaneous nephrostomy for decompression*
- **Percutaneous nephrostomy** is an invasive procedure indicated for urgent drainage of an **infected obstructed kidney**, severe hydronephrosis with renal impairment, or in patients with a solitary kidney.
- The patient has only **mild hydronephrosis** and no signs of infection or acute kidney injury, thus immediate decompression is not warranted.
*Arrange extracorporeal shock wave lithotripsy (ESWL) within one week*
- **ESWL** is an appropriate treatment for certain stone types and sizes, but for a small 5 mm stone, the chance of **spontaneous passage** with MET is high, making it the preferred initial approach.
- Proceeding directly to ESWL for a small, uncomplicated stone bypasses less invasive and potentially successful conservative management, incurring unnecessary costs and risks.
Acute kidney injury UK Medical PG Question 6: A 52-year-old woman presents to the emergency department with confusion and agitation. Her husband reports she has had watery diarrhoea for 5 days. She has a history of bipolar disorder treated with lithium for 15 years. Blood tests show: sodium 128 mmol/L, potassium 3.2 mmol/L, creatinine 245 μmol/L (baseline 85 μmol/L), lithium level 2.8 mmol/L (therapeutic range 0.6-1.0). ECG shows sinus tachycardia at 105 bpm. What is the most appropriate immediate management?
- A. Stop lithium, give IV 0.9% saline, and arrange urgent haemodialysis (Correct Answer)
- B. Stop lithium, give IV 0.9% saline, and recheck lithium level in 12 hours
- C. Continue lithium, correct dehydration, and arrange gastroenterology review
- D. Stop lithium, give hypertonic saline for hyponatraemia, then arrange dialysis
- E. Stop lithium, give IV fluids, and start haemofiltration
Acute kidney injury Explanation: ***Stop lithium, give IV 0.9% saline, and arrange urgent haemodialysis***- The patient presents with **severe lithium toxicity** (level 2.8 mmol/L) complicated by **Acute Kidney Injury (AKI)** and neurological symptoms like confusion and agitation.- **Haemodialysis** is indicated when lithium levels exceed 2.5 mmol/L in the presence of renal impairment or severe clinical toxicity, as it is the most efficient method for rapid clearance.*Stop lithium, give IV 0.9% saline, and recheck lithium level in 12 hours*- Waiting 12 hours to recheck levels is dangerous in a patient with **neurological symptoms** and **renal impairment**, as toxicity can be life-threatening.- While **IV normal saline** helps correct hypovolaemic hyponatraemia and promotes renal lithium excretion, it is insufficient as monotherapy for severe toxicity.*Continue lithium, correct dehydration, and arrange gastroenterology review*- **Lithium** must be stopped immediately; continuing it would worsen the toxic accumulation and risk permanent **neurotoxicity** or cardiac arrest.- Focusing on a gastroenterology review ignores the acute medical emergency of **lithium-induced encephalopathy** and renal failure.*Stop lithium, give hypertonic saline for hyponatraemia, then arrange dialysis*- **Hypertonic saline** is generally reserved for severe, symptomatic hyponatraemia with risk of cerebral oedema, whereas this patient’s sodium level will likely correct with **volume resuscitation**.- Delaying dialysis to manage mild-to-moderate hyponatraemia first is inappropriate when the primary threat is the high **lithium concentration**.*Stop lithium, give IV fluids, and start haemofiltration*- **Haemofiltration** is significantly less effective than **haemodialysis** for removing lithium because lithium is a small ion that is best cleared via diffusion.- Rapid clearance of high lithium levels in an emergency setting is the standard of care, making **intermittent haemodialysis** the preferred modality.
Acute kidney injury UK Medical PG Question 7: A 67-year-old man with chronic kidney disease stage 3a (eGFR 52 mL/min/1.73m²) secondary to diabetic nephropathy attends for annual review. He takes metformin, gliclazide, ramipril, atorvastatin, and aspirin. Blood tests show: HbA1c 64 mmol/mol, creatinine 128 μmol/L (stable from previous), potassium 5.4 mmol/L, bicarbonate 19 mmol/L. Urine albumin:creatinine ratio is 45 mg/mmol. Blood pressure is 138/82 mmHg. What is the most appropriate modification to his management?
- A. Add SGLT2 inhibitor for renoprotection (Correct Answer)
- B. Increase ramipril dose to maximize renoprotection
- C. Stop ramipril due to hyperkalaemia and worsening renal function
- D. Add sodium bicarbonate supplementation for metabolic acidosis
- E. Add spironolactone for additional proteinuria reduction
Acute kidney injury Explanation: ***Add SGLT2 inhibitor for renoprotection***
- **SGLT2 inhibitors** are a cornerstone in managing **diabetic kidney disease** with albuminuria, significantly reducing the risk of **CKD progression** and cardiovascular events, independent of glycemic control.
- The patient's **eGFR (52 mL/min/1.73m²)** and **uACR (45 mg/mmol)** make him an ideal candidate for initiation, offering substantial **renoprotective benefits** with a favorable safety profile regarding potassium.
*Increase ramipril dose to maximize renoprotection*
- The patient already presents with **borderline hyperkalemia (5.4 mmol/L)**; increasing the dose of an **ACE inhibitor** would significantly elevate the risk of developing **clinically significant hyperkalemia**.
- While ACE inhibitors are vital, the current blood pressure is near target, and the addition of an **SGLT2 inhibitor** provides a safer and more evidence-based next step for renoprotection in this context.
*Stop ramipril due to hyperkalaemia and worsening renal function*
- The **creatinine is stable** from previous readings, indicating no acute worsening of renal function, and a potassium of 5.4 mmol/L is manageable, not warranting immediate cessation of **renoprotective therapy**.
- Stopping the ACE inhibitor would eliminate a critical component of **renoprotection** against **proteinuric progression** in diabetic nephropathy, which is generally not recommended unless severe adverse effects occur.
*Add sodium bicarbonate supplementation for metabolic acidosis*
- NICE guidelines typically suggest considering **sodium bicarbonate** supplementation when serum bicarbonate levels are **less than 18 mmol/L**; this patient's level is 19 mmol/L.
- While metabolic acidosis should be monitored, it is not the most urgent or impactful intervention for slowing the **underlying progression of CKD** and reducing cardiovascular risk compared to adding an SGLT2 inhibitor.
*Add spironolactone for additional proteinuria reduction*
- Adding a **mineralocorticoid receptor antagonist (MRA)** like spironolactone to an ACE inhibitor in a patient with an **eGFR of 52 mL/min/1.73m²** and a **potassium of 5.4 mmol/L** carries a very high risk of inducing **severe hyperkalemia**.
- Although MRAs can reduce proteinuria, **SGLT2 inhibitors** offer superior evidence for long-term **renal outcomes** and a more favorable potassium safety profile in patients with CKD and diabetes.
Acute kidney injury UK Medical PG Question 8: A 34-year-old previously healthy woman presents with oliguria and peripheral oedema. Blood tests show: creatinine 320 μmol/L (baseline 72 μmol/L two weeks ago), urea 22.4 mmol/L, albumin 28 g/L. Urinalysis shows protein 4+, blood 2+, and no leucocytes or nitrites. Urine protein:creatinine ratio is 520 mg/mmol. Renal biopsy shows crescentic glomerulonephritis. Serology shows: ANCA negative, anti-GBM negative, ANA 1:640 (speckled pattern), anti-dsDNA positive, C3 0.42 g/L (normal 0.75-1.65), C4 0.08 g/L (normal 0.14-0.54). What is the most likely diagnosis?
- A. Lupus nephritis class IV (Correct Answer)
- B. Anti-GBM disease (Goodpasture syndrome)
- C. ANCA-associated vasculitis
- D. IgA nephropathy with crescents
- E. Post-streptococcal glomerulonephritis
Acute kidney injury Explanation: ***Lupus nephritis class IV***
- The patient presents with **rapidly progressive glomerulonephritis (RPGN)**, significant **proteinuria**, **positive anti-dsDNA**, high-titre **ANA**, and **hypocomplementemia (low C3 and C4)**, which are hallmark features of **Systemic Lupus Erythematosus (SLE)**.
- **Class IV (Diffuse Proliferative)** is the most common and severe form of lupus nephritis, frequently manifesting with **crescentic glomerulonephritis** on biopsy and a combined nephritic-nephrotic picture.
*Anti-GBM disease (Goodpasture syndrome)*
- This diagnosis is excluded by the **negative anti-GBM serology** results in the patient.
- While it causes **crescentic GN**, it does not typically present with **hypocomplementemia** or positive **anti-dsDNA** antibodies.
*ANCA-associated vasculitis*
- The **negative ANCA** results make this diagnosis highly unlikely in this patient.
- ANCA vasculitis is characterized as a **pauci-immune** glomerulonephritis and would typically present with **normal complement levels**, not the profound **hypocomplementemia** seen here.
*IgA nephropathy with crescents*
- While IgA nephropathy can cause crescentic glomerulonephritis, it typically presents with **normal complement levels**.
- The presence of **positive anti-dsDNA** and **low C3 and C4** strongly rules out IgA nephropathy, which lacks these specific serological markers.
*Post-streptococcal glomerulonephritis*
- Post-streptococcal GN usually shows **low C3 with normal C4** (alternative pathway activation), whereas this patient has both low C3 and **low C4**, indicative of classical pathway activation characteristic of **SLE**.
- This condition is not associated with **positive anti-dsDNA** or a high-titre **ANA**.
Acute kidney injury UK Medical PG Question 9: A 56-year-old woman with chronic kidney disease stage 4 (eGFR 20 mL/min/1.73m²) secondary to IgA nephropathy presents for routine review. She reports increasing fatigue. Blood tests show: haemoglobin 95 g/L, ferritin 280 μg/L, transferrin saturation 28%, PTH 18.5 pmol/L (normal 1.6-6.9), corrected calcium 2.12 mmol/L, phosphate 1.85 mmol/L, 25-hydroxyvitamin D 32 nmol/L. What is the most appropriate initial management of her secondary hyperparathyroidism?
- A. Start alfacalcidol 250 nanograms daily
- B. Start calcium carbonate 1.25 g three times daily with meals
- C. Start cinacalcet 30 mg daily
- D. Arrange parathyroidectomy
- E. Start colecalciferol 20,000 units weekly (Correct Answer)
Acute kidney injury Explanation: ***Start colecalciferol 20,000 units weekly***
- The initial step in managing **secondary hyperparathyroidism** in CKD is to correct **vitamin D deficiency** (defined as <50 nmol/L); this patient's level is 32 nmol/L.
- Replacing **native vitamin D** (colecalciferol) can often lower **PTH levels** significantly before more potent agents are required.
*Start alfacalcidol 250 nanograms daily*
- **Alfacalcidol** is an active vitamin D analogue typically reserved for when PTH remains high despite normal **25-hydroxyvitamin D** levels.
- It carrys a higher risk of **hypercalcaemia** and **hyperphosphataemia** compared to native vitamin D supplementation.
*Start calcium carbonate 1.25 g three times daily with meals*
- While this patient has mild **hyperphosphataemia**, calcium-based **phosphate binders** are generally secondary to addressing the underlying vitamin D status.
- First-line management of moderately elevated phosphate in CKD includes **dietary restriction** and achieving vitamin D sufficiency.
*Start cinacalcet 30 mg daily*
- **Cinacalcet** is a calcimimetic typically used in **dialysis patients** or those with **refractory hyperparathyroidism**.
- It is not indicated as initial therapy when a clear **vitamin D deficiency** is present and untreated.
*Arrange parathyroidectomy*
- This is a definitive surgical treatment for **tertiary hyperparathyroidism** or severe, symptomatic **refractory secondary hyperparathyroidism**.
- It is indicated if PTH is extremely high (often >85 pmol/L) and unresponsive to **medical management**.
Acute kidney injury UK Medical PG Question 10: A 28-year-old man presents to the emergency department with sudden onset severe left-sided loin pain radiating to the groin. He has vomited twice and appears distressed. He has a history of inflammatory bowel disease (Crohn's disease) and has undergone two small bowel resections. CT KUB shows a 7 mm calculus at the left vesicoureteric junction with moderate hydronephrosis. Blood tests show: creatinine 88 μmol/L, calcium 2.35 mmol/L, uric acid 380 μmol/L. What is the most likely stone composition in this patient?
- A. Calcium oxalate (Correct Answer)
- B. Calcium phosphate
- C. Uric acid
- D. Struvite (magnesium ammonium phosphate)
- E. Cystine
Acute kidney injury Explanation: ***Calcium oxalate***- In patients with **Crohn's disease** and a history of **small bowel resections**, **fat malabsorption** is common. Unabsorbed fatty acids in the colon bind to calcium, preventing it from binding to oxalate, thus increasing the absorption of **free oxalate** (enteric hyperoxaluria).- This increased systemic oxalate is excreted in the urine, leading to supersaturation and the formation of **calcium oxalate stones**, which are the most common type of kidney stone in this clinical context.*Calcium phosphate*- These stones are typically associated with conditions such as **renal tubular acidosis (Type 1)** or **primary hyperparathyroidism**, neither of which is indicated by the patient's presentation or blood test results.- They usually form in **alkaline urine**, whereas patients with chronic diarrhea from Crohn's may have acidic urine due to bicarbonate loss, making calcium phosphate less likely.*Uric acid*- While chronic diarrhea can lead to concentrated, acidic urine and potentially **uric acid stone formation**, the patient's serum **uric acid level is normal (380 μmol/L)**, which does not support this as the primary etiology.- Uric acid stones are also often **radiolucent** on plain X-ray, though visible on CT, but the direct metabolic consequence of Crohn's disease points more strongly to oxalate.*Struvite (magnesium ammonium phosphate)*- **Struvite stones** are **infection stones**, formed in the presence of **urease-producing bacteria** (e.g., *Proteus*, *Klebsiella*) that hydrolyze urea to ammonia, raising urine pH and promoting stone formation.- They are often associated with **recurrent urinary tract infections** and can grow to form **staghorn calculi**, neither of which is suggested in this patient's presentation.*Cystine*- **Cystine stones** result from **cystinuria**, an **autosomal recessive genetic disorder** affecting the renal tubular reabsorption of dibasic amino acids.- While typically presenting in younger individuals, there is no history or clinical feature to suggest this rare metabolic disorder, such as characteristic **hexagonal crystals** in urine or a family history.
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