Renal Stone Disease

Prepared and reviewed by the PrepElephant Academic Review Team

First published 8 Oct 2026 · Spot an error?

Reference basis: Harrison's Principles of Internal Medicine; Campbell-Walsh Urology; Davidson's Principles and Practice of Medicine

On this page

Direct answer
What you must remember
From first colic to a metabolic work-up
Where the examiner tries to catch you
Frequently asked questions
Related topics

Direct answer

Renal stone disease is calculus formation in the urinary tract, most often calcium oxalate, driven by urinary supersaturation, low urine volume and metabolic abnormalities. Calcium oxalate and calcium phosphate stones form with hypercalciuria or hyperoxaluria, uric acid stones with persistently acidic urine, and struvite stones with urease-producing infection. Prevention rests on a urine output of about 2.5 litres a day, normal dietary calcium and targeted therapy guided by a 24-hour urine analysis.

What you must remember

Calcium oxalate: the commonest type, linked to hypercalciuria, hyperoxaluria and low urine volume, and radio-opaque on plain film.
Calcium phosphate: seen in hyperparathyroidism, distal renal tubular acidosis and brushite stones, typically with a raised urine pH.
Struvite: magnesium ammonium phosphate, formed in urease-producing infection with Proteus or Klebsiella, and capable of forming staghorn calculi.
Uric acid: radiolucent on plain film, formed when urine is persistently acidic, with gout, diarrhoea and hyperuricosuria as associations.
Cystine: autosomal recessive cystinuria, with hexagonal crystals and a positive cyanide-nitroprusside test, recurring from childhood.
Work-up: non-contrast CT for stone detection and a 24-hour urine collection measuring volume, calcium, oxalate, citrate, urate and sodium.
Prevention: a urine output of about 2.5 litres daily, moderate salt and animal protein, normal dietary calcium, and potassium citrate for hypocitraturia.

From first colic to a metabolic work-up

A 41-year-old man has his first renal colic with a 6 mm stone in the distal ureter, and non-contrast CT confirms the size and position. The table below sets out how each stone type is recognised and what it implies.

Stone type	Associated setting	Key point
Calcium oxalate	Hypercalciuria, hyperoxaluria, low urine volume	Radio-opaque on plain film
Calcium phosphate	Hyperparathyroidism, distal renal tubular acidosis, brushite	Typically raised urine pH
Struvite	Urease-producing Proteus or Klebsiella infection	Can form staghorn calculi
Uric acid	Persistently acidic urine, gout, diarrhoea, hyperuricosuria	Radiolucent on plain film
Cystine	Autosomal recessive cystinuria	Hexagonal crystals, recurs from childhood

Pain is controlled with an NSAID, and because the stone is small and distal, medical expulsive therapy with an alpha blocker may be offered, although its benefit is debated, along with generous fluid intake. Intervention is reserved for infection, obstruction with a deteriorating kidney, uncontrollable pain or failure to pass the stone over a reasonable period.

Once the stone has passed or been removed, a 24-hour urine collection on a normal diet looks for low volume, raised calcium, raised oxalate, low citrate, high urate or high sodium, while serum calcium and parathyroid hormone exclude primary hyperparathyroidism.

Each abnormality has a matched treatment: a thiazide for hypercalciuria, potassium citrate for low citrate, allopurinol for hyperuricosuria with calcium stones, and fluid and salt restriction for all.

Where the examiner tries to catch you

Four traps recur in renal stone questions.

Trap: restricting dietary calcium to prevent stones. Correct: low dietary calcium increases oxalate absorption and worsens calcium oxalate disease, so intake is moderate, not low.
Trap: expecting uric acid stones to show on plain film. Correct: they are radiolucent, so a non-opaque ureteric lesion in a gout patient requires CT.
Trap: using urine alkalinisation or allopurinol loosely for uric acid stones. Correct: alkalinisation to a pH of about 6 to 6.5 dissolves them, whereas allopurinol is used mainly for hyperuricosuria.
Trap: answering with a drug in a hot-climate case. Correct: in parts of India, low fluid intake and dehydration in heat are major contributors, so water is the commonest answer.

Frequently asked questions

What is the commonest type of renal stone and how is it prevented?

Calcium oxalate is the commonest type of renal stone, and it is prevented by a urine output of about 2.5 litres a day, normal dietary calcium and moderate salt and animal protein. Targeted therapy such as thiazides for hypercalciuria or potassium citrate for low citrate follows the 24-hour urine results.

Why do uric acid stones not show on plain radiography?

Uric acid stones do not show on plain radiography because uric acid is radiolucent, so they are missed on plain film but seen on non-contrast CT.

Why is dietary calcium not restricted to prevent calcium oxalate stones?

Dietary calcium is not restricted because calcium in food binds oxalate in the gut, reducing the amount of oxalate absorbed and excreted in the urine. Restricting calcium therefore increases urinary oxalate and worsens calcium oxalate stone formation, which is the reverse of what patients expect.

What is the target urine volume for stone prevention?

The target urine volume for stone prevention is about 2.5 litres a day, which keeps stone-forming salts dilute and below their saturation point. Fluid intake is spread through the day, and extra fluid is needed in hot weather.

Which stones are associated with urease-producing infection?

Struvite stones, made of magnesium ammonium phosphate, are associated with urease-producing infection by organisms such as Proteus, Klebsiella and Pseudomonas. Urease raises the urine pH and promotes crystallisation.