Renal calculi
D E FI N I T ION
Different types include calcium oxalate (65%), calcium phosphate (15%)
magnesium ammonium phosphate (10–15%), uric acid (2–5%), cystine (1%)1.
AE T IOLOGY
Commonly idiopathic or caused by dehydration or urinary tract infections.
Other risk factors are:
Changes in urinary pH: Calcium oxalate, calcium phosphate and magnesium ammonium
phosphate stones arise in alkaline urine, cystine and uric acid stones arise in acid urine.
Hypercalciuria: Usually idiopathic, drug (lithium, thiazides).
Hypercalcaemia: Malignancy, hyperparathyroidism, sarcoidosis, myeloma, " calcium intake
(milk-alkali syndrome).
Hyperoxaluria: Causes: " intake (in rhubarb, spinach, strawberries, tea, tomatoes, beetroots,
beans, chocolate, nuts), " colonic absorption in patients with small bowel disease or
resection, autosomally recessive inherited enzyme deficiency ! " oxalate production
and excretion.
Hyperuricaemia: Tumour lysis syndrome, high cell turnover states.
Cystinuria: Autosomal recessive, defect of renal tubular transport of cystine and dibasic amino
acids.
Anatomical anomalies: e.g. horseshoe kidneys.
E P IDEMIOLOGY
UK prevalence 2%, lifetime incidence up to 12%. Peak age of presentation
20–50 years. <: , 2:1.
H ISTORY AND EXAMI N A T I ON
May be asymptomatic.
Pain: Loin pain (kidney stones). Renal colic radiating from loin ! groin, scrotum, labium
(ureteric stones). Dysuria, frequency, strangury, penile tip pain (bladder stones). Urinary
retention and bladder distension (urethral stones).
Haematuria.
Symptoms of urinary tract infection and obstruction.
INVE S T I G A T IONS
Blood: U&E, calcium, phosphate, albumin.
PTH, vitamin D, urate, bicarbonate, serum ACE, thyroid function.
Urine: Urinalysis (blood, protein, nitrites), microscopy and culture. 24-h collection: creatinine
clearance, calcium, phosphate, oxalate and urate. Random urine for cystine, glyoxolate,
citrate.
Plain radiography (KUB): Shows radio-opaque stones (calcium oxalate stones are radioopaque,
cystine stones are semi-opaque, urate stones are radio-lucent).
Intravenous urograpm (IVU): IV contrast followed by radiographs may show a filling defect in
the urinary outflow.
High resolution helical CT-abdomen: High diagnostic accuracy and can visualise radio-lucent
calculi.
Renal ultrasound: To assess for hydronephrosis or hydroureter.
Chemical analysis of the stone: If passed.
1Appearances of renal calculi depend on composition:
Calcium oxalate: Mulberry stones with spiky surface, dark (covered by blood from the mucosa of the renal
pelvis injured by the sharp projections).
Calcium phosphate and magnesium ammonium phosphate: Smooth, may be large and take the shape of
calyces. Staghorn calculi, dirty white.
Uric acid: Hard, smooth, faceted, yellow/light brown. These are radiolucent.
Cystine: Translucent, white.
Renal calculi (continued)
MANAGEMENT
Medical Expulsive Treatment: Suitable for <10mm calculi.
Opiate and NSAID analgesics.
Rehydration (Oral or IV).
Treat exarcebtaing factors and UTI.
Calcium channel antagonists (e.g. nifedipine) reduce ureteric spasm.
Alpha-antagonists (e.g. tamsulosin) reduce ureteric spasm.
Extracorporeal shockwave lithotripsy (ESWL): Provides non-invasive outpatient treatment and
usually combined with medical treatment. Usually suitable for smaller stones in the
kidneys or ureter.
Cystoscopy: allows visualization of the stone and urinary tract as well as laser to break up the
stone.
Percutaneous nephrolithotomy: May be necessary for calculi >2 cm or not suitable for other
modalities.
Prevention: " Fluid intake (e.g. >3 L/day avoiding high Ca2þ
water).
Calcium stones: # calcium and vitamin D intake.
Oxalate stones: # oxalate-containing foods and vitamin C intake.
Uric acid stones: Allopurinol (inhibits xanthine oxidase and uric acid synthesis), urinary
alkalization (oral sodium bicarbonate).
Cystine stones: D-penicillamine, urinary alkalinization.
COMPL I C A T IONS
Obstruction and hydronephrosis, infection, complications of the cause,
e.g. renal failure in primary hyperoxaluria.
P ROGNOS I S
Approximately 20% of calculi will not pass spontaneously. Up to 50% of
patients may have recurrence within 5 years.
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