Nephrolithiasis (Kidney & Ureteric Stones)

Meet the patient

A 38-year-old man is brought to the emergency department writhing on the trolley, unable to get comfortable, clutching his loin and groin in waves. He is pale, sweaty, nauseated, and tries every position — side, knees up, pacing — none of it helps. Dipstick urine shows microscopic haematuria. Between the spasms he looks entirely well.^[1]

Two bedside judgements decide his next hour, and they decide every renal colic you will ever see. Is he writhing or still? — the writhing patient has visceral ureteric colic; the motionless patient who refuses to move has a peritoneal or vascular emergency. And is this a complicated stone? — because fever, sepsis, a solitary kidney, or acute kidney injury convert "colic" into "decompress now, analgesia later". Hold those two questions and the whole topic slots into place.^[1]

What a stone is — and why a first stone is never the last

A stone is not a foreign body. It is a biomineral your patient's own urine precipitated. Nephrolithiasis (literally "stone in the kidney") and the broader urolithiasis ("stone in the urinary tract") describe solid crystalline calculi forming anywhere along the tract — renal parenchyma or calices, ureter, or bladder. Urine normally holds stone-forming ions in metastable solution; when supersaturation overwhelms the inhibitors that keep them dissolved, crystals nucleate, grow, aggregate, and anchor to the renal papilla.^[1]

The disease matters for four reasons an examiner will credit. An acute episode produces pain patients rank among the worst humans experience. An obstructing stone can destroy a kidney — acutely when combined with infection (pyonephrosis, urosepsis), chronically through hydronephrosis and atrophy. Stones are relentlessly recurrent: about half of untreated first-time formers stone again within ten years, so the clinician's job is to prevent the next one, not only relieve this one. And stones are an independent risk factor for chronic kidney disease, hypertension and cardiovascular disease.^[1]

The clinical task is therefore layered, in this order: control pain, decide whether the stone is complicated (infection, AKI, solitary or transplanted kidney, bilateral obstruction, pregnancy) — complicated stones are emergencies — image and locate the stone, choose a modality to clear it (conservative passage, ESWL, ureteroscopy, PCNL), and initiate prevention through metabolic work-up and long-term therapy.^[2][4]

The four stones — COMUS

Stones are classified by mineral composition, which predicts the radiographic appearance, the underlying metabolic defect, and the preventive therapy. The four classical types account for over 95 percent of all stones — remember them as COMUS.^[1]

• Calcium stones (80 to 85 percent) — predominantly calcium oxalate (the commonest), a minority calcium phosphate (brushite). Radio-opaque. Driven by hypercalciuria, hyperoxaluria, hypocitraturia; the calcium-phosphate subgroup favours a high urine pH.
• Uric acid stones (5 to 10 percent) — radio-lucent on plain film (low attenuation, about 150 to 300 Hounsfield units on CT). Form in persistently acidic urine (pH under 5.5); associate with gout, myeloproliferative disease, chronic diarrhoea and ileostomy, metabolic syndrome. The one stone you can dissolve by alkalinising the urine — a perennial exam point.
• Struvite stones (10 to 15 percent) — magnesium ammonium phosphate, made when urease-splitting organisms (Proteus, Klebsiella, Providencia, Pseudomonas, Staphylococcus saprophyticus) hydrolyse urea to ammonia and push urine pH above 7.2. Grow into staghorn calculi filling the renal pelvis and calices; common in women and recurrent-UTI patients.
• Cystine stones (about 1 percent) — hexagonal crystals, semi-opaque ("ground-glass") on plain film, from autosomal-recessive cystinuria (defect in the renal and intestinal dibasic-amino-acid transporter, genes SLC3A1 and SLC7A9). Present from childhood; the cyanide-nitroprusside test is positive.
• Miscellaneous — drug stones (indinavir, triamterene, sulfadiazine, topiramate), excess vitamin C driving oxalate, excess vitamin D and calcium driving hypercalciuria, and rare matrix stones.^[1]

The classic trap: E. coli does NOT produce urease. Only Proteus, Klebsiella, Providencia, Pseudomonas and Staph saprophyticus do. A "struvite stone with E. coli on culture" is a question designed to catch you — look again.^[1]

The stone belt and the supersaturation story

The lifetime risk of a kidney stone in a developed country is 10 to 15 percent and rising — westernised diet, the obesity and diabetes epidemic, and warming climates all feed it. Peak age is 20 to 50 years, with a male predominance of about 2:1 for calcium stones, though the gap narrows as female obesity and dietary patterns converge. Recurrence is the rule, not the exception: about 15 percent at 1 year, 30 to 40 percent at 5 years, and roughly 50 percent at 10 years in untreated patients — which is why a first stone always earns a preventive plan.^[1]

Geographically, the global "stone belt" runs through hot, arid regions; in India the high-incidence belt spans the north and west (Gujarat, Rajasthan, Punjab, Delhi), driven by heat, dehydration, dietary oxalate and animal protein. Stones cluster in sedentary occupations, drivers, and anyone with limited daytime fluid access.^[1]

^[1]

The dietary and metabolic risks to elicit at the bedside: low fluid intake, high sodium (increases urinary calcium), high animal protein (acid and uric-acid load), high fructose and sucrose, high dietary oxalate (spinach, rhubarb, nuts, chocolate, tea). And — the paradox every examiner loves — a low-calcium diet INCREASES stone risk, because intestinal calcium normally binds oxalate; starve the gut of calcium and free oxalate is absorbed and excreted. Systemic predispositions: obesity and metabolic syndrome, gout and hyperuricaemia, primary hyperparathyroidism, type 2 diabetes, distal (type 1) renal tubular acidosis (calcium phosphate stones), inflammatory bowel disease and intestinal bypass (enteric hyperoxaluria plus low citrate), and cystinuria.^[1]

The mechanism — supersaturation, Randall's plaque, and the wavefront

The unifying mechanism is urinary supersaturation. When the concentration of a stone-forming salt exceeds its formation product, ions leave solution, nucleate a solid crystal, and the crystal grows and aggregates. Healthy urine resists this with inhibitors — citrate (complexes calcium, lowering free ion activity), magnesium (complexes oxalate), pyrophosphate, Tamm-Horsfall protein (uromodulin) and nephrocalcin. Stones form when supersaturation overwhelms them, or when the inhibitors themselves are deficient — notably hypocitraturia.^[1]

Each phenotype is a distinct physicochemical failure:^[1]

• Calcium oxalate — the dominant phenotype. Driven by hypercalciuria (absorptive, resorptive from hyperparathyroidism, or renal-leak), hyperoxaluria (dietary, enteric from fat malabsorption where unabsorbed fatty acids bind luminal calcium and leave oxalate free for absorption, or primary hyperoxaluria, an autosomal-recessive hepatic enzyme defect), and hypocitraturia. In the idiopathic majority, Randall's plaques — deposits of calcium phosphate (apatite) in the renal papillary interstitium — originate in the thin limbs of the loop of Henle, migrate to the papillary surface, erode through the urothelium, and serve as the nidus to which calcium-oxalate crystals adhere.
• Calcium phosphate (brushite) — favours a persistently alkaline urine, as in distal (type 1) renal tubular acidosis and primary hyperparathyroidism; the RTA also causes hypocitraturia, compounding risk.
• Uric acid — uric acid is the protonated, undissociated form of urate below its pKa of 5.5; below this pH it is poorly soluble and precipitates. The driver is persistently acidic urine (pH under 5.5) — gout, chronic diarrhoea and ileostomy (loss of alkali), myeloproliferative disease and tumour lysis, and increasingly metabolic syndrome (insulin resistance cuts renal ammoniagenesis, dropping urine pH). Because solubility rises steeply with pH, uric-acid stones are the one type dissolvable medically by alkalinising to 6.5 to 7.0.
• Struvite (magnesium ammonium phosphate) — strictly an infection phenomenon. Urease-producing bacteria hydrolyse urinary urea into two molecules of ammonia and one of carbon dioxide; the ammonia raises urine pH above 7.2, and at that alkaline pH magnesium, ammonium and phosphate co-precipitate as struvite. The stone grows fast, layers itself around living bacteria, and forms the staghorn — hence the need for complete surgical removal plus culture-directed antibiotics; medical dissolution is impossible.
• Cystine — autosomal-recessive defect in the rBAT and b-zero-plus amino-acid transporter (genes SLC3A1 type A, SLC7A9 type B) of the proximal tubule and small intestine. The result is massive urinary loss of the dibasic amino acids cystine, ornithine, arginine and lysine (mnemonic COAL); cystine is the least soluble, precipitating at physiological pH. Presents in childhood and is relentlessly recurrent.^[1]

The pain of renal colic is visceral. Ureteric spasm, distension of the renal capsule and pelvis, and rising peristaltic pressure stimulate C-fibre and A-delta visceral afferents that follow the sympathetic chains of T11 to L2. That segmental innervation is why the pain radiates from loin to groin (T11 to L2 dermatomes cover flank, groin and upper thigh) and why a stone nearing the vesico-ureteric junction refers to the scrotum or labia and irritates the trigone (frequency, urgency, strangury).^[1]

Etymology for viva gold: calculus is Latin for "little pebble" — the same word physicians and mathematicians use, because both denote something worked out from small stones. Colic comes from the Greek kolikos, "of the colon", a reminder that flank pain was blamed on the gut for centuries before the ureter was exonerated.^[1]

The writhing patient vs the still patient

The single most useful bedside sign in renal colic is how the patient moves. The classical presentation is acute ureteric colic:^[1]

• Pain — sudden, severe, fluctuating in colicky waves, in the flank or loin radiating to the groin, testicle or labia. As a stone descends, the pain migrates loin to lower abdomen to groin. The patient is writhing, restless, trying every position — the discriminator from peritoneal pain, where the patient lies motionless.
• Gastrointestinal — nausea and vomiting from visceral afferent overlap with the gastric plexus; ileus is common.
• Urinary — macroscopic or microscopic haematuria (about 90 percent), and — when the stone sits at the vesico-ureteric junction — frequency, urgency, dysuria and strangury.
• Systemic — typically afebrile. Fever, rigors or haemodynamic instability signal infection and convert the episode into an emergency.^[1]

^[1]

Atypical presentations are the ones that bite, because they are missed:^[1]

• The elderly — diffuse abdominal pain, confusion, or a fall; an obstructed infected stone may present as delirium and sepsis with no clear pain story. Always image the older patient with unexplained sepsis of urinary origin.
• Diabetic or immunocompromised — blunted symptoms; risk of emphysematous pyelonephritis (gas-forming organisms in necrotic parenchyma), papillary necrosis, and a stone acting as a nidus for fungating infection. Minimal pain with severe systemic illness is the danger signal.
• Pregnant — renal colic is the commonest non-obstetric cause of abdominal pain needing admission in pregnancy; it can mimic labour, trigger preterm contractions, and shows a right-sided predominance (dextrorotation and ureteric compression by the gravid uterus).
• Children — nonspecific abdominal or flank pain, vomiting, isolated microscopic haematuria, or recurrent UTI; a thorough metabolic work-up is mandatory, because cystinuria, primary hyperoxaluria or distal RTA is far more likely than in adults.
• Silent obstruction — a staghorn or pelvic stone may produce no colic and present late with CKD, hypertension or recurrent UTI.^[1]

The killers that mimic colic — exclude the ectopic, the torsion, the AAA

The differential of acute flank and loin pain is broad, and missing a surgical or vascular emergency is the principal danger. Each mimic breaks the pattern of renal colic in a characteristic way:^[1]

^[1]

The non-negotiable rule: in any woman of childbearing age perform a beta-hCG before CT, and in any patient examine the scrotum to exclude torsion. A stone work-up that misses an ectopic or a torsion is a catastrophic, classic error — and an anticoagulated older "colic" may in fact be a rupturing AAA. Exclude these before you reach for the diclofenac.^[1]

CT KUB is the gold standard

The diagnostic standard is non-contrast CT of the kidneys, ureters and bladder (CT KUB) — low-dose where possible. It is 95 to 98 percent sensitive and 96 to 98 percent specific, detects all stone types (including radio-lucent uric acid, seen as a low-attenuation focus rather than missed), defines size, location and degree of obstruction (hydronephrosis), and excludes competing diagnoses (appendicitis, AAA, diverticulitis). It is first-line in adults with uncomplicated flank pain.^[3]

^[3]

Urinalysis and microscopy — dipstick shows haematuria in about 90 percent; urine pH is diagnostic of type (pH under 5.5 points to uric acid; pH over 7.2 with leucocytes and nitrites points to struvite). Crystals on microscopy: envelope or dumbbell (calcium oxalate), coffin-lid (struvite), hexagonal (cystine — pathognomonic), rhomboid or needle (uric acid). Sterile pyuria with a sterile culture raises renal tuberculosis or partially treated infection.^[1]

Bloods — urea, electrolytes and creatinine (renal function — essential before contrast and before NSAIDs), full blood count (leucocytosis means infection), CRP, corrected calcium and phosphate (hypercalcaemia means measure PTH), urate, bicarbonate and chloride (hyperchloraemic metabolic acidosis with alkaline urine means distal RTA), and glucose.^[1]

Stone analysis — every passed or retrieved stone goes for infrared spectroscopy or X-ray diffraction, the definitive composition test that anchors preventive therapy. Metabolic work-up is indicated in recurrent formers, a strong family history, children, bilateral or staghorn stones, a solitary kidney, gout, or any systemic predisposition: two 24-hour urine collections (volume, calcium, oxalate, citrate, urate, sodium, phosphate, plus a cystine screen) and serum calcium and PTH. The goal is a biochemical phenotype — hypercalciuric, hypocitraturic, hyperuricosuric — that dictates targeted drug therapy.^[2][3]

The intravenous urogram is now historical, replaced by CT. A plain KUB still follows up known radio-opaque stones and assesses fragmentation after lithotripsy.^[1]

Is this a complicated stone? — the emergency fork

Resuscitation begins with the ABCs and one immediate judgement: is this a complicated stone? The complicated stone is an emergency, defined by any of: fever or sepsis, acute kidney injury, a solitary or transplanted obstructed kidney, bilateral obstruction, intractable pain or vomiting, or pregnancy with obstruction. These patients need admission, antibiotics and decompression — not analgesia and waiting.^[3][4]

^{[3] [4]}

The classic trap: a "stone" patient who is febrile or hypotensive is not routine colic. Reaching for diclofenac and a discharge letter is the recurring trainee error — the kidney is dying. Decompress first, image and definitive-treat later.^[3]

NSAIDs first — and decompress the infected

Pain control — NSAIDs are first-line. In a Cochrane review of 20 randomised trials (1613 patients), patients given NSAIDs had lower pain scores than opioids in 10 of 13 studies, needed rescue analgesia less often (RR 0.75) and vomited less (RR 0.35):^[5]

^{[5] [6] [7]}

Keep an opioid (not pethidine — it causes the most vomiting) in reserve for when NSAIDs are contraindicated or inadequate: both classes provide effective analgesia, but opioids carry a higher rate of adverse events, particularly vomiting, and a greater likelihood of needing further analgesia. Pair it with an anti-emetic. For hydration, give oral fluids if tolerated and IV isotonic crystalloid if the patient is vomiting or dehydrated — the goal is euvolaemia, not forced diuresis.^[5][3]

The obstructed, infected kidney is a urological emergency, and the order of operations is fixed:^[10]

1. Blood and urine cultures, IV broad-spectrum antibiotics per local sepsis policy, and resuscitation.
2. Prompt decompression of the collecting system BEFORE definitive stone treatment — a retrograde JJ stent (cystoscopic, under anaesthetic) or a percutaneous nephrostomy (radiologically guided). Two randomised trials found neither modality clearly superior for resolving sepsis; percutaneous nephrostomy carries an overall major complication rate of about 4 percent. Do not perform ESWL or ureteroscopy in the face of untreated infection.
3. Definitive stone removal once the sepsis has been controlled.^[10]

AKI from bilateral obstruction or a solitary obstructed kidney likewise needs urgent decompression — relief of obstruction is the treatment. Strain all urine through a filter to capture any passed stone for analysis.^[1]

Pass the small, blast or basket the big

Definitive management is decided by stone size, site, composition and patient factors, in three tiers — conservative and medical expulsive therapy, lithotripsy and endoscopy, and percutaneous surgery.^[4]

Passage is size-dependent — memorise these numbers, they decide conservative versus intervene:^[1]

^[1]

For the uncomplicated stone with controlled pain, offer expectant management with adequate analgesia and hydration — the EAU guideline notes that ureteric stones under 6 mm can pass spontaneously in well-controlled patients, and that medical expulsive therapy (MET), usually with an alpha-blocker, can support stone passage and reduce the need for analgesia. The definitive trial (SUSPEND, 1167 adults with a single CT-confirmed ureteric stone) tested tamsulosin 400 mcg or nifedipine 30 mg daily for up to 4 weeks against placebo: about 80 percent needed no further intervention within 4 weeks in every arm (tamsulosin 81 percent vs placebo 80 percent), so neither drug reduced the need for further treatment overall. Strain the urine, review with imaging, and escalate to intervention if the stone fails to pass, pain is uncontrolled, or renal function deteriorates.^[3][7]

Extracorporeal shock-wave lithotripsy (ESWL) focuses external shock waves onto the stone to fragment it; the fragments then pass. Indications: renal stones and proximal or mid-ureteric stones under 20 mm with favourable anatomy. Contraindications: pregnancy, uncorrected bleeding diathesis or anticoagulation, distal obstruction, cystine and calcium-oxalate-monohydrate stones (too hard), calcified AAA, and a long skin-to-stone distance in obesity. Complications: steinstrasse (a column of fragments obstructing the ureter), haematuria, sepsis, perinephric haematoma.^[4]

Ureteroscopy (URS) with Holmium:YAG laser lithotripsy passes a rigid or flexible scope transurethrally to the stone, which is fragmented in situ and basketed. Indications: ureteric stones of any size (especially distal), kidney stones under 20 mm (flexible URS, retrograde intrarenal surgery). Stone-free rates exceed 90 percent for distal-ureteric stones. A JJ stent may be left for 1 to 2 weeks after a difficult procedure. Complications: ureteric injury or stricture, sepsis, stent-related symptoms.^[4]

Percutaneous nephrolithotomy (PCNL) creates a tract through the flank into the kidney and removes the stone directly (often after ultrasonic or pneumatic fragmentation). It is the gold standard for kidney stones over 20 mm and for staghorn calculi, and where ESWL or URS have failed; mini-PCNL is an option for 10 to 20 mm stones. Stone-free rates exceed 90 percent even for large stones. Complications: bleeding (rarely needing renal angiography or embolisation), sepsis, colonic or pleural injury. Laparoscopic or open stone removal is now rare, reserved for complex anatomy.^[4]

Prevent the next one — fluids and normal calcium

Every first-time stone former gets general measures; recurrent or metabolically abnormal formers add targeted drug therapy. Prevention halves recurrence, which is the whole point of follow-up.^[2]

General measures (all stone types):^[8][9]

• Fluids — the single most effective intervention. In randomised trials, a water intake over 2 L/day, or fluid pushed until urine output exceeds 2.5 L/day, cut stone recurrence by about half (RR 0.39); high fluid intake is the one dietary measure with consistent randomised-trial support.^[9]
• Low salt — about 50 mmol of sodium chloride per day in the Borghi randomised trial — sodium and calcium share tubular reabsorption; less sodium means less urinary calcium.
• Reduced animal protein — 52 g per day in the same trial — cuts acid and urate load.
• Normal dietary calcium — 30 mmol (about 1200 mg) per day, NOT a low-calcium diet. In the five-year randomised comparison, the normal-calcium, low-salt, low-protein diet halved recurrence (12/60 vs 23/60 relapses, RR 0.49), while the low-calcium diet raised urinary oxalate — intestinal calcium normally binds dietary oxalate, and starving the gut of calcium frees oxalate for absorption (Borghi, NEJM).^[8]
• Restrict oxalate (spinach, rhubarb, nuts, chocolate, tea, beetroot) in calcium-oxalate formers.

Everyone forgets: telling a calcium-stone former to "avoid dairy" is the opposite of correct. A low-calcium diet frees oxalate for absorption and increases stone risk. Prescribe normal calcium, low salt, low animal protein.^[2]

Targeted therapy by phenotype — match the drug to the biochemical defect:^[2]

^[2]

The dissolvable stone and the dangerous ones

• Calcium oxalate — radio-opaque, spiky, commonest; work up hypercalciuria, hyperoxaluria, hypocitraturia and hyperparathyroidism; a thiazide plus citrate backbone.
• Calcium phosphate (brushite) — favours alkaline urine; look for distal RTA (metabolic acidosis, alkaline urine, hypocitraturia, nephrocalcinosis) and primary hyperparathyroidism; treat the cause plus citrate.
• Uric acid — the dissolvable stone; alkalinisation to 6.5 to 7.0 can dissolve stones without surgery; check gout, myeloproliferative disease, chronic diarrhoea, metabolic syndrome.
• Struvite or staghorn — infection stone; complete surgical clearance (PCNL, sometimes staged) is the goal because residual fragments harbour bacteria and regrow; long-term antibiotics; almost never ESWL as sole therapy.
• Cystine — childhood onset, hexagonal crystals, positive cyanide-nitroprusside; aggressive fluids plus alkalinisation plus thiol chelators; lifelong; specialist metabolic clinic.
• Drug stones — review the list: indinavir (radio-lucent HIV protease inhibitor), triamterene, sulfadiazine, topiramate or acetazolamide (chronic metabolic acidosis drives calcium phosphate), vitamin C excess (oxalate), vitamin D or calcium excess (hypercalciuria).
• Staghorn calculus — fills the renal pelvis and calices; usually struvite; PCNL is the gold standard; untreated it causes progressive renal failure, xanthogranulomatous pyelonephritis, and squamous-cell carcinoma of the renal pelvis in the long term.
• Nephrocalcinosis — diffuse renal calcification (medullary more than cortical); causes include medullary sponge kidney, distal RTA, hyperparathyroidism, sarcoidosis, milk-alkali syndrome; distinct from discrete stones.^[1]

Pregnancy, children, and the solitary kidney

• Pregnancy — renal colic is the commonest non-obstetric cause of abdominal pain needing admission. Ultrasound is first-line (avoid ionising radiation); a limited low-dose CT is reserved for cases where ultrasound is non-diagnostic and the risk of missing a dangerous stone outweighs the radiation dose. Analgesia: paracetamol first; avoid NSAIDs after 32 weeks (premature closure of the ductus arteriosus and oligohydramnios) and in the third trimester generally; opioids sparingly. ESWL is contraindicated. An obstructed or infected system in pregnancy is decompressed with a temporary JJ stent or percutaneous nephrostomy, definitive therapy deferred to the postpartum period.^[3]
• Children — every child with a stone needs a comprehensive metabolic work-up (cystinuria, primary hyperoxaluria, distal RTA, hypercalciuria). Ultrasound is first-line; CT is minimised. MET (alpha-blockers) is used cautiously. Recurrence over a lifetime is the concern, so preventive habits are installed early.
• Solitary or transplanted kidney — any obstruction is an emergency: urgent decompression to preserve the only functioning renal unit. Transplant patients may stone at the uretero-ureteric anastomosis, and immunosuppression blunts the signs of infection.
• Diabetic or immunocompromised — high risk of emphysematous pyelonephritis and papillary necrosis; a high index of suspicion and early imaging are essential.
• Anticoagulated or bleeding diathesis — NSAIDs are hazardous; assess and reverse coagulopathy before ESWL or PCNL, but never withhold decompression of an obstructed infected system.
• The elderly — atypical pain, comorbidity, polypharmacy (NSAID toxicity), and a higher likelihood that flank pain is not a stone (AAA, mesenteric ischaemia, malignancy, zoster).^[1]

The mantra, and the mnemonic

^[1]

The mantra: decompress the infected obstruction, dissolve the uric acid, pass the small, blast or basket the big, prevent with fluids and normal calcium.^[1][2]

^{[3] [4] [5] [6] [7] [8] [9] [10] [12]}

Ward-round test — three stems, thirty seconds each

Stem 1 — the obstructed, infected stone (answer)ShowHide

A 45-year-old man presents with left loin-to-groin colic, temperature 39 degrees Celsius, rigors, and a tender left kidney. CT KUB shows a 7 mm stone at the left vesico-ureteric junction with marked hydronephrosis. The registrar prescribes diclofenac and plans ureteroscopy in the morning. What is the right sequence? Model: This is an obstructed, infected kidney — a urological emergency, and analgesia plus overnight ureteroscopy is the wrong order. Give IV fluids, take blood and urine cultures, and start IV broad-spectrum antibiotics per local sepsis policy, then promptly decompress with a retrograde JJ stent or percutaneous nephrostomy BEFORE definitive stone treatment — the evidence review of this scenario notes neither decompression modality is clearly superior, and nephrostomy carries a major complication rate of about 4 percent. Ureteroscopy or ESWL in the face of untreated infection seeds sepsis. Definitive removal follows once the patient is afebrile and cultures are clear. The mantra for this stem: decompress the infected obstruction first.^[10][3]

Stem 2 — the dissolvable stone (answer)ShowHide

A 60-year-old man with gout presents with colic; CT KUB shows a 12 mm stone in the renal pelvis reported as "low-attenuation, around 200 Hounsfield units", and his urine pH is 5.2. What is the stone, and what is the medical treatment? Model: Low attenuation on CT with a persistently acidic urine (pH under 6) and a background of gout is an uric-acid stone — the one stone you can dissolve without surgery, and the EAU guideline names oral chemolysis as an option for uric-acid stones. Alkalinise the urine to a target pH of 6.5 to 7.2 with potassium citrate and/or sodium or magnesium bicarbonate, titrated to serial urine pH. In a 216-patient cohort treated exactly this way, 61 percent of stones dissolved completely and 14 percent partially within 3 months; lower stone density and smaller size predicted success. The patient who fails to dissolve or develops obstruction or infection proceeds to ESWL or ureteroscopy. The mantra: dissolve the uric acid.^[11][3]

Stem 3 — hypercalcaemia and recurrent calcium stones (answer)ShowHide

A 52-year-old woman has passed three calcium-oxalate stones in two years. Her corrected calcium is 2.7 mmol/L, with a low phosphate and a normal renal function. What single test confirms the diagnosis, and what is the curative treatment? Model: Hypercalcaemia with recurrent calcium stones demands a parathyroid hormone (PTH) level — here it will be inappropriately high or non-suppressed, confirming primary hyperparathyroidism (the biochemical pattern is high calcium, low or low-normal phosphate, and high or inappropriately normal PTH). The treatment is parathyroidectomy — the only curative treatment of the metabolic disorder; a systematic review of 13 studies (over 8000 patients) found surgery significantly reduces long-term stone recurrence without eliminating it entirely (in the single randomised trial, 0 percent recurred after surgery versus 4 percent under observation), so follow-up with serum calcium, PTH and 24-hour urine parameters continues. The mantra for this stem: hypercalcaemia plus recurrent calcium stones — check the PTH, then parathyroidectomy.^[12]

References12ShowHide

1. [1]Khan SR, Pearle MS, Robertson WG, et al. Kidney stones Nat Rev Dis Primers, 2016.PMID 27188687
2. [2]Pearle MS, Goldfarb DS, Assimos DG, Curhan G, Denu-Ciocca CJ, Matlaga BR, et al. Medical management of kidney stones: AUA guideline J Urol, 2014.PMID 24857648
3. [3]Türk C, Petřík A, Sarica K, Seitz C, Skolarikos A, Straub M, Knoll T. EAU Guidelines on Diagnosis and Conservative Management of Urolithiasis Eur Urol, 2016.PMID 26318710
4. [4]Türk C, Petřík A, Sarica K, Seitz C, Skolarikos A, Straub M, Knoll T. EAU Guidelines on Interventional Treatment for Urolithiasis Eur Urol, 2016.PMID 26344917
5. [5]Holdgate A, Pollock T. Nonsteroidal anti-inflammatory drugs (NSAIDs) versus opioids for acute renal colic Cochrane Database Syst Rev, 2005.PMID 15846699
6. [6]Yaowalaorng J, Kunthasook W, Lokeskrawee T, et al. Superior efficacy of intramuscular diclofenac compared to intravenous tramadol for acute renal colic in northern Thai patients: a randomised double-blind, sham-controlled trial Emerg Med Australas, 2025.PMID 39763427
7. [7]Pickard R, Starr K, MacLennan G, et al. Medical expulsive therapy in adults with ureteric colic: a multicentre, randomised, placebo-controlled trial Lancet, 2015.PMID 25998582
8. [8]Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria N Engl J Med, 2002.PMID 11784873
9. [9]Fink HA, Akornor JW, Garimella PS, et al. Diet, fluid, or supplements for secondary prevention of nephrolithiasis: a systematic review and meta-analysis of randomized trials Eur Urol, 2009.PMID 19321253
10. [10]Ramsey S, Robertson A, Ablett MJ, et al. Evidence-based drainage of infected hydronephrosis secondary to ureteric calculi J Endourol, 2010.PMID 20063999
11. [11]Tsaturyan A, Bokova E, Bosshard P, et al. Oral chemolysis is an effective, non-invasive therapy for urinary stones suspected of uric acid content Urolithiasis, 2020.PMID 32770255
12. [12]Jahrreiss V, Yurdakul O, Veser J, Seitz C. Effect of parathyroidectomy on stone recurrence in primary hyperparathyroidism: A systematic review Wien Klin Wochenschr, 2026.PMID 41874646