Renal Stones

Renal stones (Nephrolithiasis) and ureteric stones (Ureterolithiasis) are common urological emergencies. Approximately 80% of stones are composed of Calcium Oxalate. Other types include Calcium Phosphate, Uric Acid (radiolucent), Struvite (triple phosphate, associated with infection), and Cysteine (associated with a genetic defect). Risk factors include dehydration, high protein/salt intake, and certain medical conditions like primary hyperparathyroidism or gout. The classic presentation is renal colic—agonising, spasmodic pain radiating from the loin to the groin as the stone moves through the ureter. Most stones <5mm will pass spontaneously with conservative management. However, stones >10mm or those causing complications (infection, intractable pain, or obstruction in a solitary kidney) require intervention. For diagnosis, a non-contrast CT KUB (Kidneys, Ureters, Bladder) has high sensitivity and specificity. Management includes NSAIDs for pain (Diclofenac or Ibuprofen), medical expulsive therapy (Tamsulosin), or surgical interventions such as Shockwave Lithotripsy (ESWL) or Ureteroscopy.

Stone formation (lithogenesis) occurs when urine becomes supersaturated with certain minerals, leading to crystal nucleation and growth. This is exacerbated by low urine volume (dehydration) and low levels of stone inhibitors (e.g., Citrate). Calcium stones occur due to hypercalciuria (with or without hypercalcaemia). Uric acid stones form in acidic urine, often in patients with gout or high cell turnover. Struvite stones (Magnesium Ammonium Phosphate) form in alkaline urine caused by urease-producing bacteria like Proteus mirabilis, which split urea into ammonia. These can grow large and fill the renal pelvis (Staghorn calculi). Cysteine stones are rare and due to an autosomal recessive transport defect in the proximal tubule. Once formed, stones cause pain as they transit through narrowings: the pelviureteric junction (PUJ), the pelvic brim (over the iliac vessels), and the vesicoureteric junction (VUJ).

The typical patient is 'pacing' the room, unable to find a comfortable position. The pain is intense, unilateral, and colicky. Nausea and vomiting are frequent. Visible or non-visible haematuria is present in >90% of cases. Complications are critical: 1. Pyonephrosis: Infection of an obstructed system (presents as sepsis + loin pain)—this is a life-threatening emergency requiring decompression. 2. Post-renal AKI: Especially if there is a 'silent' obstruction or a stone in a patient with a solitary kidney. 3. Ureteric strictures: From chronic irritation. Red flags include fever (suggesting infection), anuria (suggesting bilateral obstruction or solitary kidney), and intractable vomiting.

Bedside: Urinalysis (Non-visible haematuria is common; check for nitrites/leucocytes indicating infection); Pregnancy test in women of childbearing age. Bloods: FBC, CRP, U&Es (renal function), Bone profile (Calcium), Urate. Imaging: Non-contrast CT KUB is the gold standard (perform within 14 hours of presentation). Ultrasound is used in pregnancy or children. Special: Strain urine to catch stone for chemical analysis; 24-hour urine collection for metabolic workup (citrate, oxalate, calcium) for recurrent stone formers.

Acute Management: 1. Analgesia: NSAIDs (IM Diclofenac 75mg or Ibuprofen) are first-line. 2. Hydration: Maintain fluids but avoid 'forced' fluid overload. 3. Emergency: If infection + obstruction, urgent decompression via nephrostomy or retrograde stent is required. Definitive Management: 1. Stones <5mm: Watchful waiting + Tamsulosin (alpha-blocker to relax ureteric muscle). 2. Stones 5mm-20mm: Extracorporeal Shockwave Lithotripsy (ESWL) or Ureteroscopy with laser lithotripsy. 3. Stones >20mm: Percutaneous Nephrolithotomy (PCNL). Prevention: Increase fluid intake (2.5-3L/day), limit salt and animal protein, and maintain normal dietary calcium intake.