• Types of Renal Stones:
o Calcium oxalate (∼75%): most common; radio-opaque
Risk factors: hypercalciuria, hyperoxaluria, low citrate, dehydration
o Uric acid: radiolucent on plain X-ray (visible on CT); acidic urine favours formation
Seen in gout, high cell turnover (e.g. tumour lysis)
o Struvite (magnesium ammonium phosphate): staghorn calculi
Alkaline urine; associated with Proteus, Klebsiella (urease-producing organisms)
o Cystine: rare, seen in inherited cystinuria; faintly radio-opaque
• Clinical Features:
o Renal colic: sudden onset, severe colicky flank pain radiating to groin
o Haematuria: microscopic or macroscopic
o Nausea, vomiting
o Frequency, dysuria if stone is in distal ureter
o Infection signs: fever, pyuria, sepsis if obstructed infected system
• Diagnosis:
o First-line: non-contrast CT KUB (high sensitivity/specificity)
o Ultrasound: alternative in pregnancy; may detect hydronephrosis
o Urinalysis: haematuria, crystals, signs of infection
o Serum calcium, urate, and PTH levels; 24-hour urine in recurrent cases
• Management:
o Conservative (most <5 mm pass spontaneously):
High fluid intake
NSAIDs (e.g. diclofenac) for pain
Alpha-blockers (e.g. tamsulosin) to aid passage
o Referral to urology if:
Obstruction with infection (urological emergency)
Persistent pain
Stone >6 mm or failed conservative management
o Surgical options:
ESWL (extracorporeal shockwave lithotripsy)
Ureteroscopy ± laser
Percutaneous nephrolithotomy (for large/staghorn calculi)
• Definition: Diffuse calcium deposition in the renal parenchyma, most often in the renal medulla
• Causes:
o Hyperparathyroidism (primary or tertiary)
o Renal tubular acidosis (type 1)
o Hypervitaminosis D (excess supplementation or granulomatous disease)
o Medullary sponge kidney
o Sarcoidosis
o Hypercalcaemia of malignancy
• Clinical Features:
o Often asymptomatic; detected incidentally on imaging
o May cause nephrolithiasis, CKD over time
• Diagnosis:
o Renal ultrasound: echogenic pyramids
o CT scan: shows medullary calcification more clearly
• Management:
o Treat underlying cause (e.g. control PTH, correct acidosis)
o Hydration, thiazides may reduce urinary calcium excretion
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Author & Educational Disclaimer
Author:
Dr Phillip Cockrell BM FRCP DipClinEd
Dr Phillip Cockrell is a UK Consultant Physician in Internal Medicine, currently working at Queen Alexandra Hospital, Portsmouth University Hospitals NHS Trust. He has previously worked as a registrar across Intensive Care Medicine, Gastroenterology, Cardiology, Stroke Medicine, Acute Medicine, and Respiratory Medicine.
He has held senior leadership roles including Associate Clinical Director of the Acute Medical Unit, Clinical Director of Internal Medicine, and Chief of Medicine. Dr Cockrell has over 15 years’ experience in postgraduate medical education, having lectured extensively across the MRCP syllabus and contributed to MRCP revision teaching and course development.
Dr Cockrell holds a Bachelor of Medicine (BM), Fellowship of the Royal College of Physicians (FRCP), and a Diploma in Clinical Education (DipClinEd). His teaching approach is based on structured consolidation of complex medical topics to support efficient and effective revision for postgraduate examinations.
Purpose of this content:
The material on this page is intended solely for educational purposes to support revision for the MRCP (UK) Part 1 examination. It reflects examination-relevant principles of internal medicine and is designed to aid learning and pattern recognition.
Medical disclaimer:
This content is designed for postgraduate medical examination revision and does not constitute medical advice, diagnosis, or treatment guidance and must not be used as a substitute for professional clinical judgement, local guidelines, or specialist consultation. Clinical decisions should always be made in the context of individual patient circumstances and current national guidance.
