Nephrolithiasis and nephrocalcinosis — viva

Opening (must-hit)

"This is an uncomplicated ureteric stone — an 8 mm stone at the right vesicoureteric junction with hydronephrosis but no fever and no signs of sepsis or acute kidney injury. He is stable. My immediate management is analgesia with a non-steroidal anti-inflammatory drug, an antiemetic and hydration to correct dehydration, and I screen for the red flags: fever with obstruction, a solitary kidney, and acute kidney injury, none of which he has. Because the stone is distal and under 10 mm in an afebrile child, I would start medical expulsive therapy with tamsulosin and arrange outpatient review, with urology in reserve if it fails to pass. Once it is passed or removed, I arrange a full metabolic workup — stones in children are rarely a one-off event." [1][10]

Examiner: "What would make this an emergency rather than a routine stone?"

"The emergency is the infected obstructed system. If he developed a fever, or if the urine showed infection with this obstructing stone, the concern is pyonephrosis progressing to urosepsis, and he would need urgent urological decompression with a ureteric stent or nephrostomy, blood and urine cultures, and intravenous antibiotics. The same urgency applies to a stone in a solitary kidney, bilateral obstruction, or any stone with acute kidney injury or anuria — those bypass the conservative pathway and go to urology and theatre. Forced high-volume intravenous hydration does not speed passage and risks overload, so resuscitation is about correcting dehydration and screening for these complications, not flushing the stone." [1][5]

Examiner: "Tell me about tamsulosin — the dose, the evidence and the limits."

"Tamsulosin is a selective alpha-1-blocker that relaxes the smooth muscle of the distal ureter, and I use it off-label for a distal ureteric stone under 10 mm. The Aldaqadossi randomised trial in children with distal ureteric stones under 1 cm used 0.4 mg once daily with ibuprofen, and showed improved spontaneous passage over ibuprofen alone; a later trial found silodosin comparable to tamsulosin. I give it for up to four weeks with a planned review, I monitor blood pressure for hypotension, and I confine it to distal stones in older children. The limits are that the evidence is modest and extrapolated, the dose in smaller children is less certain, and it does not suit proximal or large stones, which go to surgery." [10][9]

Examiner: "Walk me through the surgical ladder and when each applies."

"ESWL — extracorporeal shock wave lithotripsy — fragments upper-tract stones in a single session and suits renal and proximal ureteric stones of moderate size. Ureteroscopy with holmium laser lithotripsy is the workhorse for ureteric and many renal stones, with a high stone-free rate, and it is increasingly first-line for most ureteric stones that fail conservative management. Percutaneous nephrolithotomy is reserved for large stones over 2 cm or staghorn calculi. For a struvite staghorn I prefer PCNL over ESWL because residual fragments harbour infection and regrow, so complete clearance is the goal. For this boy's 8 mm distal stone, ureteroscopy would be the surgical fallback if tamsulosin fails." [1][11]

Examiner: "What metabolic workup, and why in a first stone?"

"Bloods: calcium, phosphate, magnesium, bicarbonate on a venous gas, creatinine, urate, and parathyroid hormone if calcium is high or borderline. Urine: culture to exclude urease-splitting organisms, urinalysis for pH and crystals, a nitroprusside screen for cystine, and stone analysis when retrieved. The urinary metabolic evaluation hinges on calcium — I confirm hypercalciuria with a 24-hour urine calcium above 4 mg per kilogram per day, and use a spot calcium-to-creatinine ratio as the screen, remembering the upper limit falls with age, from about 0.8 mg/mg in infants to below 0.3 mg/mg in older children. I add a 24-hour urine for oxalate, citrate, uric acid and cystine, and a gene panel for recurrent, bilateral or syndromic disease. I do this after a first stone because a metabolic or genetic cause underlies the majority of paediatric stones — monogenic disease alone explains about a fifth — and without prevention roughly half of children recur within three to five years." [3][4]

Examiner: "Now flip it — an infant with medullary nephrocalcinosis. How do you think?"

"Nephrocalcinosis is a tissue problem, not a lumen problem, and medullary disease in an infant redirects me to a focused differential: distal renal tubular acidosis, Dent disease, primary hyperoxaluria, idiopathic hypercalciuria, and prematurity with furosemide. The first test is a venous gas and a urine pH — if the child is acidotic but the urine is alkaline above pH 5.5, that is distal renal tubular acidosis, the cause not to miss, because untreated it causes growth failure, rickets and progressive kidney damage, all preventable with alkali. In a preterm infant the commonest cause is actually furosemide-driven hypercalciuria, which usually regresses when the loop diuretic is stopped or a thiazide is substituted. I would send the full metabolic panel and consider a genetic panel for severe, bilateral or progressive disease, and primary hyperoxaluria must be excluded because it progresses to chronic kidney disease." [6][5]

Closing summary

"In summary: a paediatric stone is ultrasound first, a non-steroidal anti-inflammatory drug for analgesia, and the fever-or-solitary-kidney red flag for emergency decompression. A distal ureteric stone under 10 mm gets tamsulosin, with ureteroscopy as the surgical fallback. Every child gets a metabolic workup after a first stone because hypercalciuria is the commonest cause and monogenic disease explains a fifth. And an infant with medullary nephrocalcinosis and failure to thrive is distal renal tubular acidosis until proven otherwise." [1][6]