Paeds · nephrology-urology-fluids-and-electrolytes
Nephrolithiasis and nephrocalcinosis
Also known as Kidney stones · Renal calculi · Urolithiasis · Nephrocalcinosis · Medullary nephrocalcinosis · Paediatric stone disease · Hypercalciuria
Fellowship guide to paediatric nephrolithiasis (stones in the collecting system) and nephrocalcinosis (calcium deposits in the renal parenchyma), the rising incidence of childhood stone disease, hypercalciuria as the commonest metabolic risk factor, the stone-composition and nephrocalcinosis-cause classification, the supersaturation-and-inhibitor pathophysiology, the abdominal pain and haematuria presentation, the ultrasound-first imaging strategy, the acute analgesia and hydration pathway, medical expulsive therapy with tamsulosin for distal ureteric stones, the ESWL, ureteroscopy and PCNL surgical ladder, and prevention through fluids, diet, thiazides and potassium citrate.
On this page
Study tools
Your progress
Saved on this device.
Practise this topic
Target exams
Red flags
- A child with a stone and fever, or a solitary kidney with obstruction, is a urological emergency — the fear is an infected obstructed system causing pyonephrosis and sepsis, so seek urgent urological decompression and start antibiotics
- An obstructing stone with rising creatinine or anuria, especially after a single episode, needs immediate decompression — bilateral obstruction or a stone in a solitary kidney can cause acute kidney injury
- Medullary nephrocalcinosis in an infant with failure to thrive, alkaline urine and metabolic acidosis is distal renal tubular acidosis until proven otherwise — untreated it causes growth failure, rickets and progressive kidney damage
- Nephrocalcinosis in a preterm infant is usually furosemide-driven and largely iatrogenic — review the diuretic, because the deposits often regress when the loop diuretic is stopped or thiazide is substituted
- Recurrent stone disease, bilateral stones or nephrocalcinosis in a child warrants a full metabolic and genetic workup, because monogenic causes underlie roughly 20 percent of paediatric stone disease and many are treatable
Life stages
Care settings
Clinical exam formats
Board mappings
- Nephrolithiasis versus nephrocalcinosis: lumen versus parenchyma
- Hypercalciuria as the commonest metabolic risk factor for stones
- Ultrasound as the first-line imaging modality in children
- Metabolic workup: serum and urine biochemistry plus stone analysis
- Medical expulsive therapy with tamsulosin for distal ureteric stones
- Thiazide for hypercalciuria and potassium citrate for hypocitraturia
- Acute management of renal colic and the infected obstructed system
- Surgical ladder: ESWL, ureteroscopy and PCNL
- Medullary nephrocalcinosis differential: distal RTA, Dent disease and primary hyperoxaluria
- Short case: an adolescent with recurrent calcium oxalate stones
- Long case: an infant with medullary nephrocalcinosis from distal RTA
- Communication station explaining stone prevention and fluids to a family
- Nephrology and urology: nephrolithiasis and nephrocalcinosis
- Metabolic evaluation and prevention of recurrent stone disease
- Inherited causes of nephrocalcinosis including tubulopathies
- Stone composition: calcium oxalate, phosphate, struvite, uric acid and cystine
- Supersaturation and inhibitor pathophysiology of crystal formation
- Pharmacology of tamsulosin, thiazides and potassium citrate
- Assessment and imaging of the child with abdominal pain and haematuria
- Communication: explaining stone prevention and fluid targets to a family
- Nephrolithiasis and nephrocalcinosis: causes, evaluation and management
- Hypercalciuria and the metabolic workup of paediatric stones
- Acute management of renal colic and indications for surgery
- Patient Care: evaluation and management of paediatric stone disease
- Medical Knowledge: pathophysiology and metabolic basis of stones
- Systems-Based Practice: radiation-sparing imaging and prevention
- Nephrology and urology: paediatric nephrolithiasis and nephrocalcinosis
- Metabolic and genetic evaluation of recurrent stones
- Management of medullary nephrocalcinosis and its inherited causes
Stone disease in a child is no longer the rare, exotic diagnosis it once was. Over the past two decades the incidence of paediatric nephrolithiasis has climbed steeply in parallel with adult disease, driven by diet, dehydration, rising obesity and better detection, so that a general paediatrician now sees it regularly. [1] [12] What distinguishes the child from the adult is the obligation to find a cause. A first stone in a child is far more likely than in an adult to reflect an underlying metabolic, anatomical or genetic predisposition, and roughly one in five children with stones carries a single-gene cause. [4] [3] Finding that cause is what prevents recurrence, protects kidney function, and occasionally changes a child's entire trajectory — which is why every paediatric stone deserves a metabolic workup.
This page treats nephrolithiasis and nephrocalcinosis as one subject with two expressions, because they share the same metabolic roots and the same preventive logic. Stones form in the lumen; calcium deposits form in the parenchyma; both arise when urine is supersaturated with calcium, oxalate or phosphate and the inhibitors of crystallisation fall short. [5] [3] The first half of the page is the acute and surgical management of the stone in the ureter; the second half is the metabolic and genetic detective work that stops the next one.
Overview & Definition
Nephrolithiasis is the presence of one or more stones (calculi) in the renal collecting system — the renal pelvis, calyces, ureter or bladder. Urolithiasis is the broader term that encompasses stones anywhere along the urinary tract. The stones themselves are crystalline aggregates of urinary solutes bound by a protein matrix, and their composition reveals the cause: calcium oxalate is the commonest in children as in adults, followed by calcium phosphate, then struvite (infection) stones, uric acid stones and cystine stones. [1] [3]
Nephrocalcinosis is a different but related entity — microscopic or macroscopic deposits of calcium salts within the renal parenchyma itself, in the tubular epithelium and interstitium rather than the lumen. [5] It is classified by location into medullary (by far the commonest, because the medulla is where calcium concentrates), cortical (rare, seen in cortical necrosis or chronic glomerular disease) and diffuse. The distinction matters at the bedside: a stone causes colic and haematuria by obstructing flow, whereas nephrocalcinosis is often an incidental ultrasound finding that points instead to a tubulopathy, a metabolic disorder or prematurity. [5] [6]
The two conditions overlap because they share risk factors. The same hypercalciuria that grows a calcium oxalate stone in the pelvis also seeds the medulla with calcium, so a child can have both at once. The unifying concept is urinary supersaturation — when the concentration of stone-forming solutes exceeds what the urine can keep dissolved, crystals nucleate, grow and either lodge as a stone or deposit in the tissue. [3] [5]
References12ShowHide
- [1]Cao B; Daniel R; McGregor R; Tasian GE Pediatric Nephrolithiasis. Healthcare (Basel), 2023.PMID 36833086
- [2]Hu J; Zhang J; Wang J; Tan Y; Zhou L; Xu K Global, Regional, and National Epidemiology of Pediatric Urolithiasis (1990-2021) and 2040 Forecast. J Urol, 2025.PMID 40532191
- [3]Singh P; Harris PC; Sas DJ; Lieske JC The genetics of kidney stone disease and nephrocalcinosis. Nat Rev Nephrol, 2022.PMID 34907378
- [4]Halbritter J; Baum M; Hynes AM; Rice SJ; Thwaites DT; Hildebrandt F Fourteen monogenic genes account for 15% of nephrolithiasis/nephrocalcinosis. J Am Soc Nephrol, 2015.PMID 25296721
- [5]Gefen AM; Zaritsky JJ Review of childhood genetic nephrolithiasis and nephrocalcinosis. Front Genet, 2024.PMID 38606357
- [6]Alonso-Varela M; Gil-Pena H; Santos F Incomplete distal renal tubular acidosis in children. Acta Paediatr, 2020.PMID 32212394
- [7]Jackson W; Taylor G; Selewski D; Smith PB; Tolleson-Rinehart S; Laughon MM Association between furosemide in premature infants and sensorineural hearing loss and nephrocalcinosis: a systematic review. Matern Health Neonatol Perinatol, 2018.PMID 30473868
- [8]Hoppe B; Duran I; Martin A; Kribs A; Benz-Bohm G; Roth B Nephrocalcinosis in preterm infants: a single center experience. Pediatr Nephrol, 2002.PMID 11956879
- [9]Soliman MG; El-Gamal O; El-Gamal S; Abdel Raheem A; Abou-Ramadan A; El-Abd A Silodosin versus Tamsulosin as Medical Expulsive Therapy for Children with Lower-Third Ureteric Stones: Prospective Randomised Study. Urol Int, 2021.PMID 33524970
- [10]Aldaqadossi HA; Shaker H; Saifelnasr M; Gaber M Efficacy and safety of tamsulosin as a medical expulsive therapy for stones in children. Arab J Urol, 2015.PMID 26413330
- [11]Medairos R; Paloian NJ; Pan A; Moyer A; Ellison JS Risk factors for subsequent stone events in pediatric nephrolithiasis: A multi-institutional analysis. J Pediatr Urol, 2022.PMID 34980558
- [12]Bonzo JR; Tasian GE The Emergence of Kidney Stone Disease During Childhood-Impact on Adults. Curr Urol Rep, 2017.PMID 28417430