Renal Colic and Urinary Stones: Pain, Passage and Prevention

Job one: break the pain — and why an NSAID beats morphine

The instinct is to reach for the strongest opioid. The evidence says reach for an NSAID. The pain of renal colic is not purely mechanical. When a stone obstructs the ureter, prostaglandins pour out — they drive the kidney to keep filtering against the block (raising pressure in the collecting system) and they whip up ureteric smooth-muscle contraction. Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac attack this at the source: by inhibiting cyclo-oxygenase they cut prostaglandin production, which lowers intraureteric pressure and relaxes that spasming smooth muscle. So an NSAID does not merely mask the pain — it unwinds the mechanism generating it. Head-to-head, NSAIDs give at least as much relief as opioids with less vomiting and less need for rescue analgesia, which is why guidelines make them first-line. The prostaglandin logic here is exactly the one taught in the Inflammation & Joints section — the same cyclo-oxygenase, the same mediators, a different organ.

The NSAID cautions travel with the drug wherever it goes. Prostaglandins protect renal blood flow when the kidney is under stress, so an NSAID is dangerous precisely in the patient who is dehydrated, vomiting, elderly, or already has chronic kidney disease — it can tip a struggling kidney into acute kidney injury. Add the familiar gastrointestinal risk (ulceration and bleeding) and the cardiovascular and fluid-retention concerns, and the rule becomes: excellent first-line drug in a well-hydrated patient with good renal function, but not if there is acute kidney injury, established renal impairment, active peptic ulcer disease, or an obstructed infected kidney that is failing. When an NSAID is unsafe or insufficient, opioids are the second-line choice — and an antiemetic (an anti-sickness drug) is given alongside either, because both the colic itself and the drugs provoke vomiting.

Job two: help it pass — medical expulsive therapy

Most small stones pass by themselves. Some need a chemical nudge. Small stones — a few millimetres — usually pass spontaneously with time, fluids and analgesia. For larger stones sitting lower in the ureter (in the distal third), the smooth muscle of the ureteric wall can grip the stone and hold it up. This is where medical expulsive therapy comes in: an alpha-blocker, classically tamsulosin. The lower ureter and its opening into the bladder are rich in alpha-1 adrenoceptors; blocking them relaxes that smooth muscle, widens the passage and reduces the spasm squeezing the stone, so it is more likely to pass and to pass sooner. This is the same alpha-1 blockade — the same drug, tamsulosin — used to relax the prostate and bladder neck in benign prostatic hyperplasia, covered in the BPH chapter; here the target is the ureter instead. The predictable class effects follow the drug: first-dose orthostatic (postural) hypotension and dizziness, and intraoperative floppy iris syndrome, so any patient on tamsulosin heading for cataract surgery should have the eye surgeon warned in advance.

Job three: prevention depends on chemistry

There is no single "stone drug." What prevents the next stone depends entirely on what the last one was made of. Before any drug, one measure protects against every stone type: a high fluid intake, enough to keep the urine dilute and flowing so crystals never reach saturation. This is the cornerstone, and no tablet replaces it. Beyond that, the pharmacology forks by chemistry, and analysing a passed or retrieved stone is what points the way. The four types worth knowing are calcium (much the commonest), uric acid, cystine, and struvite (infection) stones — and each has its own logic.

Calcium stones — the paradox of the thiazide diuretic. For recurrent calcium stones, the dietary levers come first: keep sodium low (a high salt intake drags calcium into the urine), moderate oxalate, and — counter-intuitively — do not slash dietary calcium, because very low calcium intake lets more oxalate be absorbed and can worsen stones. The signature drug is a thiazide diuretic, and it works by a neat quirk of the nephron: thiazides increase renal calcium reabsorption, so they lower the amount of calcium excreted into the urine — less urinary calcium, fewer crystals. This is the same drug class taught for hypertension in the Cardiovascular / Diuretics section, exploited here for a completely different endpoint: its calcium-sparing side effect becomes the whole point. The second agent is potassium citrate, which raises urinary citrate — and citrate is a natural inhibitor that binds calcium in the urine and keeps it from crystallising. Low urinary citrate is itself a stone risk, so replacing it is protective.

Uric acid stones — the pH story, and a familiar gout drug. Uric acid stones are governed by one dominant variable: urine pH. Uric acid is poorly soluble in acidic urine and dissolves readily in alkaline urine, so the mainstay of prevention — and even of dissolving existing uric acid stones — is urinary alkalinisation with potassium citrate or bicarbonate, aiming to nudge the urine pH up. Raise the pH and the uric acid stays in solution instead of crystallising. Where there is genuine overproduction of uric acid (hyperuricosuria, or a link to gout), add allopurinol, a xanthine oxidase inhibitor that blocks the enzyme making uric acid and lowers the load in the first place — the very same drug, and the very same enzyme, met in the gout part of the Inflammation & Joints section. Two mechanisms, one goal: keep uric acid dissolved (alkalinise) and make less of it (allopurinol).

Cystine and struvite — the rarer two, each with its own trick. Cystine stones arise from an inherited defect that leaks cystine into the urine, and cystine — like uric acid — is more soluble in alkaline urine. So the approach layers up: very high fluid intake to dilute it, urinary alkalinisation, and when that is not enough, a thiol drug such as tiopronin or penicillamine that chemically converts cystine into a far more soluble compound. Struvite stones are different in kind: they are infection stones, formed when urease-producing bacteria split urea, raise the urine pH and drive precipitation. Here no metabolic tablet fixes the problem — the treatment is to eradicate the underlying urease-producing infection (and, in practice, remove the stone, since these often grow large). The principle is worth holding onto: with struvite you treat the bug, not the chemistry.