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Classify renal calculi. Describe their pathogenesis and complications.

Pathology · 2nd Professional — Para-Clinical

Types and Composition

Urolithiasis is the formation of calculi anywhere in the urinary tract; about 80% form in the kidney.

Type	Share	Radiology	Associations
Calcium oxalate and phosphate	75–80% — commonest	Radio-opaque	Hypercalciuria (idiopathic, hyperparathyroidism, immobilisation, excess vitamin D), hyperoxaluria (excess spinach, tea, ileal disease), hypocitraturia
Struvite (triple phosphate: magnesium ammonium phosphate)	10–15%	Radio-opaque	Infection with urease-producing organisms — proteus, Klebsiella; urea is split to ammonia, alkalinising the urine. Form large branched "staghorn" calculi filling the pelvicalyceal system
Uric acid	5–10%	Radiolucent — invisible on a plain film	Acid and concentrated urine; gout, high purine intake, myeloproliferative disease and tumour lysis; more than half have normal serum urate
Cystine	1–2%	Faintly opaque	Cystinuria — an inherited defect of dibasic amino acid transport; presents in childhood; hexagonal crystals in the urine

Pathogenesis

Supersaturation of urine with the stone-forming salt — the essential requirement; promoted by low urine volume
Nucleation and crystal growth on a matrix or on randall plaques (calcium phosphate deposits in the renal papilla)
Deficiency of inhibitors — citrate, magnesium, pyrophosphate, nephrocalcin, Tamm–Horsfall protein
Urinary pH — alkaline urine favours calcium phosphate and struvite; acid urine favours uric acid and cystine
Stasis and infection — obstruction, anatomical abnormality

CLINICAL PEARL

Struvite stones are made by bacteria, which is why they cannot be dissolved away. Urease-producing organisms split urea to ammonia, raising urine pH and precipitating magnesium ammonium phosphate. The stone then harbours the organisms within it, so the infection cannot be cleared while the stone remains, and the stone grows while the infection persists. Complete surgical removal is essential — antibiotics alone always fail.

Clinical Features and Complications

Renal colic — severe colicky pain radiating from loin to groin, with restlessness (unlike peritonitis, where the patient lies still), nausea and vomiting
Haematuria, usually microscopic; dysuria and frequency when the stone reaches the vesicoureteric junction
Sites of impaction — pelviureteric junction, where the ureter crosses the pelvic brim, and the vesicoureteric junction (the narrowest point)
Complications — obstruction with hydronephrosis, infection and pyonephrosis, recurrent pyelonephritis, renal failure if bilateral, and squamous cell carcinoma of the renal pelvis from chronic irritation
A large stone may be silent — staghorn calculi often cause no colic at all, and are found only when infection or renal impairment supervenes

Applied Aspects

Non-contrast CT of the kidneys, ureters and bladder is the investigation of choice, detecting essentially all stones including radiolucent uric acid stones; ultrasound is used in pregnancy and children
Most stones under 5 mm pass spontaneously; management is analgesia (NSAIDs are highly effective), fluids and medical expulsive therapy with an alpha-blocker
An obstructed, infected kidney is a urological emergency — fever with obstruction requires urgent drainage by nephrostomy or stent, not just antibiotics
Prevention is by high fluid intake above 2.5 litres a day, and by analysing the stone and treating the specific abnormality — citrate for calcium stones, allopurinol and urinary alkalinisation for uric acid stones
India lies in the "stone belt", with high prevalence in the north and west; heat, dehydration and diet contribute, and recurrence is common
Screen for hyperparathyroidism in recurrent calcium stones by measuring serum calcium and PTH

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