Download 126524643053ad303eb2..

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Metabolic Evaluation of
Paediatric Stones
Ahmad Nazran, UMMC
Advanced Urology Course June 2014
Introduction
Increasing global incidence of paediatric urolithiasis
Predisposing factors found in > 75% of children with
urolithiasis
Studies have found a metabolic component in 33 – 95% of
paediatric urolithiasis patients (Bastug et al, Nat Rev Urol 2012)
Non-specific symptoms e.g. irritability, vomiting more
common in very young children
Older children may be able to complain of flank pain or
haematuria
Gross haematuria less common in children; microscopic
haematuria or urinary tract infection may be the only finding
(Tekgul et al, EAU 2013)
Urology International
Metabolic Risk Factors of
paediatric urolithiasis
•
•
Hypercalciuria
• Normocalcaemic hypercalciuria
• Idiopathic hypercalciuria
• Distal renal tubular acidosis
• Diuretic use
• Monogenic disorders
• Hyperalimentation
• Medullary sponge kidney
• Hypercalcaemic hypercalciuria
• Primary hyperparathyroidism
• Hypo / hyperthyroidism
• Immobilization
• Metastatic bone disease
• Cushing syndrome
• Hypervitaminosis D or A
• Adrenal insufficiency or excess
Hypocitraturia
• Hyperchloraemic metabolic
acidosis
• K deficiency
• Infection
•
•
•
•
•
Hyperoxaluria
• Primary hyperoxaluria
• Lack of intestinal oxalatedegrading bacteria
• Dietary excess
• Gut malabsorption
Hyperuricosuria
• High dietary purine
• Purine overproduction
• Renal tubular disorders
• Drugs
Cystinuria
• Hereditary
• Renal tubule immaturity
Xanthinuria
• Allopurinol
• Hereditary
Hypomagnesuria
Bastug et al, Nat Rev Urol 2012
Metabolic Evaluation
All paediatric patients should undergo metabolic evaluation
upon identification of the first urinary stone
Urinary obstruction should be ruled out first and if present,
treated
Bastug et al, Nat Rev Urol 2012
History
Family history of urolithiasis, renal disease or gout
Prematurity
Recurrent skeletal fractures
Immobilization
Malabsorption
Diet
Vitamin D intake
Enteral or parenteral nutrition rich in calcium, oxalate, protein,
sodium and phosphorus
Bastug et al, Nat Rev Urol 2012
Examination
Abdominal / flank pain
Growth retardation
Bone deformities suggestive of rickets
Photophobia due to band keratopathy
Signs of infection
Bastug et al, Nat Rev Urol 2012
Urinalysis
Haematuria
Pyuria
Crystals
Presence of bacteria
Urine pH
C&S
Bastug et al, Nat Rev Urol 2012
Imaging
Ultrasound
X-ray
Non-contrasted CT
IVU / CTU (contrasted)
Bastug et al, Nat Rev Urol 2012
Initial Metabolic Investigations
Serum calcium, phosphorus, uric acid, magnesium, alkaline
phosphatase, pH, bicarbonate, creatinine
If relevant serum PTH, vitamin D metabolites, vitamin A,
plasma oxalate
Urine glycolate, glycerate and glyoxalate concentrations
Genetic testing for primary hyperoxaluria
Bastug et al, Nat Rev Urol 2012
After passage of stone
24 hour urine
Ideally 6 weeks after passage
Calcium, uric acid, oxalate, citrate, creatinine, sodium, cystine
Can calculate ratio to creatinine in random urinary
specimen, but mainly for screening
Urinary calcium : creatinine > 0.2 on 2 samples warrants 24
hour collection
Stop vitamin C supplementation prior to urine collection
Bastug et al, Nat Rev Urol 2012
Stone Chemical Analysis
Best diagnostic evaluation
Can be retrieved either by spontaneous passage or surgery
2/3 of stones consist or more than one substance
Presence or absence of risk factors should be identified even
if the stone is analyzed
Bastug et al, Nat Rev Urol 2012
Bastug et al, Nat Rev Urol 2012
Tegul et al, EAU 2013
Tegul et al, EAU 2013
Thank You
Related documents