6 Types of Kidney Stones—Causes, Symptoms and Care Options 

That excruciating bolt in your side isn’t always caused by the same culprit. Kidney stones come in six chemically distinct varieties – calcium oxalate, calcium phosphate, uric acid, struvite, cystine and a cluster of drug-induced or rarer stones – each with its own triggers, warning signs and management rules. This article sets out exactly what separates them, so you can recognise the type you’re facing and understand the safest, fastest route to relief.

Around one in ten people will develop a renal calculus in their lifetime, yet many never discover its chemical makeup. That knowledge matters: prevention plans and treatments such as shock-wave lithotripsy, laser ureterorenoscopy or robotic removal rise or fall with stone composition. Most stones pass with pain control and fluids, but complicated cases need prompt input from a specialist urologist like Mr Ashwin Sridhar. Let’s examine each stone before moving on to diagnosis, prevention, and when to seek expert care.

1. Calcium Oxalate Stones: The Common Culprit

Roughly three-quarters of all renal calculi found in UK emergency departments are made of calcium oxalate, so when clinicians talk about the “typical” stone, this is the one they mean. It forms when everyday calcium in the urine binds to oxalate, an organic acid derived from food and cell metabolism, and the pair crystallise faster than the kidneys can flush them away.

What calcium oxalate stones are

Chemically, the stones come in two flavours:

• Calcium oxalate monohydrate (COM) – hard, dense and less amenable to shock-wave fragmentation.
• Calcium oxalate dihydrate (COD) – a little softer and usually breaks up more readily in ESWL.

Both sub-types appear bright white (radio-opaque) on plain X-ray, helping differentiate them from other types of kidney stones.

Causes and risk factors

Anything that tips the balance towards higher urinary oxalate or lower urinary volume fosters stone growth:

• Diet rich in spinach, rhubarb, beetroot, nuts, dark chocolate or high-dose vitamin C
• Chronically low fluid intake or profuse sweating without rehydration
• Low dietary calcium – paradoxically allows more free oxalate to be absorbed from the gut
• Gastro-intestinal conditions (Crohn’s, ulcerative colitis, bariatric surgery) that increase oxalate absorption
• Hyperparathyroidism and other causes of hypercalciuria
• Low urine citrate or persistently acidic urine (pH < 6), both natural crystal inhibitors

Typical symptoms and warning signs

The headline symptom is renal colic: sudden, sharp flank pain radiating towards the groin, often accompanied by nausea, sweating and restlessness. Visible or microscopic blood in the urine is common. Tiny calculi may be silent and first picked up on a “red-flag” haematuria screen.

Diagnosis pointers

• Non-contrast CT KUB: Gold-standard; COM stones look dense (high Hounsfield units).
• Plain KUB X-ray: usually visible thanks to calcium content.
• Urine microscopy: characteristic envelope- or dumb-bell-shaped crystals.
• 24-hour urine profile: raised oxalate, low citrate, high calcium or low volume confirm risk milieu.

Care and treatment options

Acute management aims to control pain and encourage spontaneous passage:

1. NSAID suppository or intravenous diclofenac
2. Oral fluids ± intravenous crystalloid if vomiting
3. A four-week course of an α-blocker such as tamsulosin to relax the ureter

Intervention is considered when the stone is ≥ 6 mm, obstructing, infected or simply too painful:

• ESWL for most upper-tract stones under 1 cm (less effective for COM)
• Semi-rigid or flexible ureterorenoscopy (URS/FURS) with Holmium:YAG laser dusting
• Percutaneous nephrolithotomy (standard or mini-PCNL) for burdens > 2 cm

Prevention is lifelong and evidence-based:

Following these measures slashes the risk of recurrence by up to 50 %, keeping you out of A&E and away from the operating theatre.

2. Calcium Phosphate Stones: The Alkaline Builders

While they account for only a fraction of cases, calcium phosphate stones deserve special attention because their behaviour, imaging appearance and response to treatment differ from their oxalate cousins. They thrive in alkaline urine, often crop up in metabolic disorders, and can grow into stubborn “plate-like” aggregates that challenge conventional shock-wave therapy.

What calcium phosphate stones are

Chemically, these calculi consist of either brushite (calcium hydrogen phosphate) or hydroxyapatite, sometimes layered with a little calcium oxalate. They represent roughly 5–10 % of stones seen in UK stone clinics. Brushite in particular is extremely dense, giving it a high Hounsfield Unit reading on CT and an unfortunate reputation for being “ESWL-resistant”.

Causes and risk factors

Anything that nudges urine pH above 6.8 promotes precipitation of phosphate with calcium:

• Distal (type 1) renal tubular acidosis – kidneys leak bicarbonate, leaving urine chronically alkaline
• Primary hyperparathyroidism or vitamin D excess – raises serum and urinary calcium
• Prolonged use of calcium-based antacids or over-the-counter phosphate binders
• Recurrent UTIs with urease-negative organisms such as E. coli that produce subtle alkalinisation
• High dietary phosphate from fizzy drinks or processed foods
• Low urinary citrate or low volume, just as with oxalate stones

Symptom profile

Clinical presentation mirrors other renal stones: colicky flank pain, nausea, microscopic or visible haematuria. Because they form rapidly on pre-existing fragments, calcium phosphate stones may enlarge into partial staghorn shapes, producing a dull, nagging ache or recurrent infection rather than classic episodic colic.

Diagnosis clues

• Plain KUB X-ray: clearly radio-opaque, sometimes sheet-like
• Non-contrast CT: dense stone; brushite often > 1,500 HU
• Urinalysis: pH persistently alkaline, occasional amorphous phosphate crystals
• Metabolic screen: check serum calcium, phosphate and parathyroid hormone to unmask endocrine drivers

Treatment and prevention

Acute pain control mirrors the oxalate protocol—NSAIDs, hydration and, where appropriate, tamsulosin. Intervention, however, must respect the stone’s hardness:

• ESWL is less effective for brushite; consider ureterorenoscopy with laser dusting or mini-PCNL for burdens > 15 mm
• Potassium citrate can raise urinary citrate but may push pH even higher; use cautiously and titrate to pH 6.5–7.0
• Thiazide diuretics reduce urinary calcium in hypercalciuria
• Address the root cause: correct renal tubular acidosis with oral bicarbonate, excise a parathyroid adenoma, or shorten courses of high-dose antacids
• Dietary tweaks: limit cola-type drinks and processed meats rich in phosphate, keep salt < 6 g day⁻¹, and drink enough water to maintain pale-yellow urine

Adopting these measures shrinks relapse risk and, crucially, reduces the chance of a brushite “brick” that even the best lithotripter can’t crack.

3. Uric Acid Stones: The Acidic, Invisible Ones

If you have all the hallmarks of renal colic yet the plain X-ray is “normal”, your stone may be made of uric acid. These crystals dissolve on film, so they can lurk undetected until a CT scan tells the real story. Their chemistry also sets them apart from other types of kidney stones: they form only in persistently acidic urine and, unlike calcium-based stones, they can often be melted away with medication rather than blasted or plucked out.

What uric acid stones are

Uric acid is the end-product of purine metabolism. When urine pH falls below about 5.5, the molecule becomes insoluble, precipitating into sandy granules that gradually fuse into stones. Pure uric acid calculi account for roughly 5–10 % of stones seen in UK clinics, but mixed stones containing a urate core overlaid with calcium are also common.

Key causes and risk factors

• Diets high in purines – red meat, offal, shellfish, beer
• Gout or hyperuricaemia
• Obesity, type 2 diabetes and metabolic syndrome (insulin resistance lowers urinary pH)
• Chronic diarrhoea or an ileostomy leading to volume depletion and acidic, concentrated urine
• Rapid cell turnover states: chemotherapy, tumour lysis, psoriasis
• Hot climates, Ramadan fasting or endurance sport without adequate hydration

Symptoms worth noting

Uric acid stones provoke the same knife-like flank pain and haematuria as other calculi, but patients sometimes pass “brick dust” – fine, orange-pink crystals – in the urine. Because stones may be multiple and bilateral, renal colic can switch sides or present with vague lower-abdominal discomfort.

Diagnosis approach

• Non-contrast CT KUB: reveals radiolucent stones that would be invisible on X-ray
• Ultrasound: can show hydronephrosis but may miss small calculi
• Urine dipstick: pH ≤ 5.5 strengthens suspicion
• Microscopy: rhomboid or needle-shaped uric acid crystals
• Serum urate: useful baseline, though levels can be normal during an attack

Care pathways

1. Dissolve first – alkalinise urine to pH 6.5–7.0 with potassium citrate or, if contraindicated, sodium bicarbonate. Repeat imaging in 4–6 weeks; many stones shrink or vanish completely.
2. Address purines – moderate red meat and alcohol, adopt a DASH-style diet, and aim for ≥ 2.5 L clear urine daily.
3. Pharmacotherapy – allopurinol (100–300 mg) or febuxostat if hyperuricaemia or recurrent disease.
4. Intervention – flexible ureterorenoscopy or mini-PCNL for stones > 10 mm, obstruction, infection or failed dissolution.

With judicious urine alkalinisation and lifestyle tweaks, most patients avoid the operating theatre and keep this stealthy stone at bay.

4. Struvite Stones: Infection-Driven and Fast-Growing

Unlike other kidney stones that creep up silently, struvite calculi can appear almost overnight. Fed by chronic urinary infections, they grow into branching “staghorn” casts that fill the renal pelvis and calyces, threatening kidney function if not removed in full.

What struvite stones are

Struvite is a crystal lattice of magnesium, ammonium and phosphate (MgNH₄PO₄·6H₂O). Because ammonia is part of the mix, these stones only form when bacteria split urea in urine—a clue to their infectious origin. They are usually hard enough to show up as chalky white shadows on plain X-ray yet can be surprisingly brittle when handled in theatre.

Underlying causes

• Chronic or recurrent UTIs with urease-producing organisms, classically Proteus mirabilis but also Klebsiella, Pseudomonas and some Staphylococcus species
• Functional or anatomical problems that encourage residual urine: neurogenic bladder, indwelling catheters, vesico-ureteric reflux, urinary diversions
• Pregnancy or post-menopausal oestrogen loss (raises UTI risk)
• Diabetes mellitus and spinal cord injury, both linked to frequent bacteriuria

The key step is the bacterial enzyme urease, which hydrolyses urea to carbon dioxide and ammonia, driving urine pH towards 8; in such an alkaline soup, magnesium and phosphate rapidly precipitate.

Symptom pattern

Because they expand quickly and fill space rather than travel, struvite stones often present differently from the corkscrew agony of a tiny ureteric calculus:

• Recurrent flank discomfort or vague fullness
• Fever, chills and offensive, cloudy urine signalling pyelonephritis
• Lower urinary tract symptoms—urgency, frequency, dysuria—between febrile episodes
• Occasionally, painless gross haematuria or a palpable kidney on examination

Classic colic may be absent until a fragment breaks off and obstructs the ureter.

Diagnostic hallmarks

• Plain KUB film: large, branching, radio-opaque “antler-like” shadow
• CT scan: confirms size and extension; helps surgical planning
• Urine dipstick: alkaline pH (≥ 7.5) with leucocytes and nitrites
• Culture: urease-positive organism—guide antibiotics
• Bloods: raised inflammatory markers, possible reduced eGFR if obstruction is longstanding

Treatment strategy

1. Complete stone clearance is non-negotiable; residual fragments act as bacterial lodgings and quickly reform.
   • First-line: percutaneous nephrolithotomy (PCNL), often in stages for massive staghorns
   • Adjuncts: flexible ureterorenoscopy or mini-PCNL to chase residual tips
2. Peri-operative antibiotics tailored to culture; some centres add acetohydroxamic acid (a urease inhibitor) in stubborn infections, though availability in the UK is limited.
3. Post-operative suppression: 3–6 months of low-dose antibiotics or methenamine hippurate to prevent recolonisation while the urothelium heals.
4. Prevention essentials:
   • Prompt treatment of any future UTI
   • Regular catheter changes or, better, intermittent self-catheterisation
   • Consider urine acidification with vitamin C (ascorbic acid) if pH remains high
   • Twice-yearly ultrasound or low-dose CT for early detection of recurrence

Handled promptly and decisively, even a giant struvite staghorn need not condemn a kidney. Delay, however, risks sepsis, renal impairment and complex open surgery—strong incentives for swift referral to a stone specialist.

5. Cystine Stones: A Genetic Challenge

Most people have never heard of cystine stones until they—or their child—present with them. Although they represent only 1–2 % of adult calculi in the UK (and up to 10 % in paediatrics), these crystals are notorious for recurring and doing so early in life. Their stubborn nature stems from cystinuria, a lifelong genetic transport defect that floods the urine with poorly soluble cystine. Knowing the hallmarks of this specific stone type is crucial, because the usual “drink more water and cut down on salt” mantra alone rarely keeps them at bay.

Stone basics

Cystine is the oxidised dimer of the amino acid cysteine. When urinary concentration exceeds its solubility threshold of roughly 250 mg/L—especially at acidic pH—it crystallises into smooth, yellow-tinged calculi that are only faintly radio-opaque. Unlike calcium or infection stones, cystine calculi can form simultaneously in both kidneys and the ureters, leading to bilateral obstruction.

Causes and genetics

Cystinuria is an autosomal-recessive disorder involving mutations in the SLC3A1 or SLC7A9 genes. These code for a renal tubular transporter responsible for reabsorbing four dibasic amino acids:

• Cystine
• Ornithine
• Lysine
• Arginine

Failure of the transporter leaves cystine—alone in being poorly soluble—to precipitate. A positive family history is common, but new (de novo) mutations can arise, so genetic counselling is advised for all diagnosed patients.

Symptom and presentation

Because stone formation begins in childhood, many patients report:

• Recurrent flank or abdominal pain from a young age
• Episodes of haematuria without infection
• Simultaneous pain from both sides when bilateral stones obstruct ureters
• Occasional nausea or vomiting during acute renal colic

Left unchecked, repeated obstruction may damage renal function by early adulthood.

Diagnostic features

• Mid-stream urine microscopy: pathognomonic colourless, hexagonal crystals
• Cyanide-nitroprusside screening test: turns purple if cystine ≥ 250 mg/L
• Imaging: stones are pale on KUB film; non-contrast CT remains the most reliable modality
• 24-hour urine collection: cystine excretion > 300 mg confirms active cystinuria

Management options

Long-term control relies on three pillars:

1. Super-hydration

   • Aim for ≥ 3 L urine output daily, including a late-night glass to dilute nocturnal urine.

2. Alkalinisation

   • Maintain urine pH 7.5–8.0 with potassium citrate or sodium bicarbonate; use pH dipsticks at home.

3. Thiol drugs

   • Tiopronin (preferred) or D-penicillamine forms soluble cystine complexes; start if stones recur despite hydration and pH control.

Interventions follow general stone principles but with lower thresholds:

• Flexible ureterorenoscopy or mini-PCNL for calculi > 6 mm or obstructing fragments
• ESWL is less effective because cystine absorbs shock waves poorly

Regular follow-up with 24-hour urine testing and low-dose CT helps catch regrowth early, turning a genetic curse into a manageable chronic condition.

6. Drug-Induced and Other Rare Stones

Fewer than 2 % of calculi sent for analysis in UK laboratories fall into this grab-bag category, yet recognising them matters: the fix is often as simple as changing a prescription or correcting an enzyme deficiency. Because these stones do not behave like the better-known calcium or uric acid variants, they can escape routine imaging and present late with obstruction or infection.

Examples of uncommon stones

• Antiretroviral: indinavir, atazanavir, darunavir
• Diuretics & antihypertensives: triamterene, furosemide fragments in neonates
• Antibiotics & sulfonamides: sulfadiazine, ciprofloxacin
• Chemotherapy: methotrexate, acyclovir at high intravenous doses
• Metabolic:
  • Xanthine (allopurinol over-activity or hereditary xanthinuria)
  • 2,8-dihydroxyadenine (deficiency of adenine phosphoribosyltransferase)
  • Matrix stones – soft proteinaceous plugs seen in chronic kidney infections

Mechanisms and risk factors

Two broad pathways exist:

1. Drug crystallisation
   • An offending agent reaches supersaturation in the renal tubule, especially when urine is concentrated or acidic. Low solubility drugs (indinavir dissolves only above 100 mg/L) precipitate quickly after excretion.
2. Inborn or acquired enzyme defects
   • Missing enzymes allow insoluble metabolites such as xanthine or 2,8-dihydroxyadenine to accumulate despite generous hydration.

Additional risk modifiers include dehydration, extremes of urinary pH, pre-existing renal impairment, and co-administration of other renally cleared medicines competing for tubular transporters.

Clinical clues

• Recent start or dose escalation of a listed medicine
• Radiolucent or faint stones on X-ray; some (indinavir) are completely CT-invisible and diagnosed only when “sand” is filtered during ureteroscopy
• Passage of soft, yellow-tan plugs rather than hard calculi
• Disproportionate crystalluria on urine microscopy—needle or “shard” crystals that match the shape of the drug molecule
• In metabolic causes: childhood onset, family history, or persistently low serum urate despite gout-like symptoms (xanthinuria)

Treatment principles

1. Withdraw, switch or dose-reduce the culprit drug where clinically feasible; hydration alone rarely suffices if exposure continues.
2. Push diuresis to ≥ 3 L day⁻¹; use intravenous fluids in hospitalised patients on high-dose antivirals or chemotherapy.
3. Manipulate urine pH:
   • Alkalinise to ≥ 7.0 for sulfonamide, methotrexate and 2,8-dihydroxyadenine stones with potassium citrate or bicarbonate.
   • Acidify to pH < 6.5 for triamterene or indinavir using ascorbic acid, though evidence is limited.
4. Endoscopic removal (URS/FURS) is preferred because many of these stones are soft, friable and poorly responsive to shock-wave therapy.
5. In hereditary forms, long-term allopurinol (2,8-dihydroxyadenine) or dietary purine restriction (xanthinuria) complements hydration.

Early recognition and targeted management prevent chronic obstruction, renal scarring and the frustration of multiple negative X-rays in a patient who still feels classic stone pain.

7. Risk Factors That Cut Across All Stone Types

Regardless of the chemical category, every stone begins the same way: urine becomes too concentrated or too chemically favourable for crystals to stay dissolved. The influences that push you into that danger zone fall into two broad camps—modifiable day-to-day habits and background characteristics you cannot change but should still know about. Understanding both helps you stack the odds in your favour and avoid joining the repeat-stone club.

Modifiable risk factors

A handful of lifestyle tweaks can slash recurrence rates for all six types of kidney stones:

• Chronically low fluid intake or long gaps between drinks
• High dietary sodium (≥ 6 g salt/day) which drags calcium into the urine
• Excess animal protein and added sugars that acidify urine and deplete citrate
• Sparse fruit and vegetable intake—fewer alkaline, citrate-rich foods
• Sugary fizzy drinks and energy drinks (loaded with phosphate or fructose)
• Obesity and prolonged sitting that concentrate urine and alter acid–base balance

Non-modifiable risk factors

Some factors are baked in but still guide surveillance frequency and preventive intensity:

• Age over 40 and male sex (except infection stones, commoner in women)
• First-degree relative with nephrolithiasis
• Congenital urinary tract abnormalities or medullary sponge kidney
• Chronic diseases: gout, inflammatory bowel disease, metabolic syndrome, spinal cord injury

Practical prevention checklist

Aim for pale-yellow urine and follow the quick-reference plan below:

Additional pointers:

• Use a urine colour chart—anything darker than straw means drink.
• Season food after cooking to curb hidden salt.
• Follow a DASH-style plate (vegetables, whole grains, modest meat).
• Move every hour; even a brisk five-minute walk improves renal perfusion.
  Keeping these fundamentals tight works hand-in-hand with any stone-specific measures your urologist recommends.

8. How Doctors Identify Your Stone: Tests and Interpretation

Knowing which of the six main types of kidney stones you are harbouring is impossible without a little detective work. Modern urology therefore blends smart imaging with targeted laboratory tests and, wherever possible, direct chemical analysis of a passed or removed stone. The aim is two-fold: confirm the diagnosis quickly (so pain relief and obstruction management aren’t delayed) and uncover the metabolic triggers that need correcting to stop the next stone before it starts.

Imaging modalities

A scan is nearly always the first port of call because it answers three urgent questions: “Where is the stone?”, “How big is it?” and “Is the kidney blocked?”. Each modality has distinct strengths and drawbacks:

Density on CT gives extra clues: >1500 HU suggests brushite; 200–500 HU hints at uric acid; 600–800 HU fits cystine.

Laboratory investigations

Bloods screen for systemic drivers:

• Serum calcium, phosphate, parathyroid hormone (hyperparathyroidism)
• Uric acid (gout or chemotherapy)
• Creatinine/eGFR for renal function

Urine tests dig deeper:

• Dipstick: pH, blood, nitrites, leucocytes
• Microscopy: crystal shape (hexagonal = cystine, envelope = calcium oxalate, rhomboid = uric acid)
• 24-hour urine collection: volume, calcium, oxalate, citrate, urate, sodium—essential for personalised prevention plans

Stone analysis

If you pass a fragment, keep it; if you undergo surgery, ask for analysis. Infra-red spectroscopy or X-ray diffraction confirms composition to within a few percent, settling therapeutic debates (for example, whether alkalinisation alone can dissolve the stone). NHS laboratories usually report results within two weeks, and the findings feed directly into follow-up dietary advice and any need for medications such as thiazides, potassium citrate or allopurinol. Armed with this triad—scan, labs and stone chemistry—your urologist can tailor treatment with much greater precision than the old “one-size-fits-all” approach.

9. Modern Treatment Pathways in the UK

Once the stone has been identified, attention turns to “what next?”. Across the UK, treatment algorithms are guided by National Institute for Health and Care Excellence (NICE) NG118, Royal College of Radiologists imaging standards, and the growing availability of day-case laser technology in both NHS and private units. The overarching aim is to clear the stone swiftly, preserve renal function and nip any metabolic driver in the bud—all while minimising theatre time and radiation dose. Whether you require nothing more than painkillers and patience or a full percutaneous operation hinges on several measurable factors.

Conservative vs. interventional decision-making

NICE thresholds can be boiled down to five Rs—Radius, Region, Ruckus, Risk and Renal numbers:

• Radius (size)

  • ≤ 5 mm: 70 % pass unaided; offer analgesia, anti-emetics and ± tamsulosin 0.4 mg for four weeks.
  • 6–10 mm: trial of medical expulsive therapy, but plan intervention if no progress after 4–6 weeks.

  • 10 mm: elective intervention usually advised.

• Region (location)

  • Distal ureteric stones pass more readily than proximal or renal-pelvic stones.
  • Lower-pole renal stones under 6 mm may be observed; upper-pole stones of similar size often treated earlier.

• Ruckus (symptoms)

  • Uncontrolled pain, persistent vomiting or work-limiting colic all tip the balance toward surgery.

• Risk (infection/sepsis)

  • Any obstructing stone with fever is an emergency—decompression within 12 hours via JJ stent or nephrostomy, followed by definitive clearance once cultures are negative.

• Renal numbers

  • Falling eGFR or a solitary kidney prompts early stone removal, irrespective of size.

Shared decision-making is key; many patients opt for proactive removal to reduce downtime or avoid another A&E visit.

Overview of interventional techniques

Private providers such as Mr Ashwin Sridhar can often schedule URS or mini-PCNL within days, a boon for patients juggling work or travel commitments.

Post-treatment follow-up

Clearance is only half the story; preventing the next episode starts immediately after theatre:

1. Imaging
   • Low-dose CT or ultrasound at 2–3 months to confirm stone-free status (earlier—7 days—if complications occurred).
2. Metabolic work-up
   • 24-hour urine and serum panel six weeks post-op; results feed into a personalised diet and drug plan.
3. Dietary & lifestyle counselling
   • NHS stone clinics and most private practices run dietitian-led sessions covering fluid targets, salt limits and the specific tweaks for each of the six types of kidney stones.
4. Recurrence surveillance
   • Annual ultrasound for low-risk patients; 6-monthly for cystine or recurrent struvite formers.
   • Published UK data show that rigorous follow-up halves the five-year recurrence rate (from ≈50 % to under 25 %).

By marrying evidence-based thresholds with modern laser and robotic tools, UK urologists can now convert a once-terrifying diagnosis into a largely outpatient journey—fast relief today, risk-proofing for tomorrow.

Living Stone-Free Starts Today

Six very different chemistries—calcium oxalate, calcium phosphate, uric acid, struvite, cystine and drug-related stones—cause one very similar agony. Knowing which of the six you have shapes everything from the painkillers you take this afternoon to the diet, tablets or surgery that will stop the next attack. Whatever the flavour, two habits cut risk across the board: drink enough to keep your urine pale and curb excess salt, sugar and animal protein. Layer on stone-specific tweaks—urine alkalinisation for uric acid, antibiotics for struvite, thiol drugs for cystine—and recurrence rates plummet.

Still in pain, worried about a recurrent stone, or simply want a tailored prevention plan? Book a discreet, rapid appointment with Mr Ashwin Sridhar. As a leading London urological surgeon he offers same-week imaging, advanced laser or robotic removal, and personalised metabolic work-ups that keep you stone-free for good. Start the conversation here.