Urolithiasis : Metabolic evaluation ,

management and Prevention

Presented by: Dr Charbel DABALModerator: Dr R. El Khoury

The goals of metabolic evaluation are to provide a guide for treatment to reduce the risk of stone

formation and to identify systemic disease presenting as kidney stone disease

Stone Analysis

Specific metabolic evaluation• Serum: Creatinine, sodium, potassium, chloride,

calcium, albumin, uric acid, bicarbonate, PTH (if serum calcium is high), Vitamin D (if low or high serum calcium or elevated PTH)

• collection of two consecutive 24-hour urine samples in special containers

• Spot urine samples are an alternative method of sampling

• self-determined diet, ideally stone free for at least twenty days

Follow up…

• The first follow-up (24-hour urine measurement) is suggested 8-12 weeks after starting pharmacological prevention

• enables drug dosage adjustment• Once yearly• new stones, new evaluation (Stone composition

changed in 21.2%)

General preventive measures

Diet

• mixed balanced diet with contributions from all food groups, without any excesses

• Fruits, vegetables and fibres: should be encouraged, alkaline content of a vegetarian diet also increases urinary pH

• Oxalate: excessive intake of oxalate-rich products should be limited or avoided to prevent high oxalate load

• Vitamin C: it seems wise to advise calcium oxalate stone formers to avoid excessive intake

• Animal protein: limited to 0.8-1.0 g/kg body weight

• Calcium intake: should not be restricted, daily requirement for calcium is 1,000 to 1,200 mg.

• Sodium: the daily sodium (NaCl) intake should not exceed 3-5 g. High intake adversely affects urine composition

• Urate: intake of purine-rich food should be restricted in patients with hyperuricosuric, calcium oxalate and uric acid stones. Intake should not exceed 500 mg/day

Recommendations for recurrence prevention

Pharmacological recurrence prevention

Ideal drug should •halt stone formation•have no side effects•be easy to administer

Calcium oxalate stones

• Diagnosis:• Blood analysis : creatinine, sodium, potassium,

chloride, ionised calcium, uric acid, • PTH and vitamin D in the case of increased

calcium levels.• Urinalysis: urine volume, urine pH, specific

weight, calcium, oxalate, uric acid, citrate, sodium and magnesium.

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• “Acidic arrest” (urine pH constantly < 5.8) may promote co-crystallisation of uric acid and calcium oxalate.

• Similarly, increased uric acid excretion (> 4 mmol/day in adults or > 12 mg/kg/day in children) can act as a promoter.

Recommendations for pharmacological treatment of patients with specific abnormalities in urine composition

Calcium phosphate stones• Two completely different minerals: carbonate

apatite and brushite. • Diagnosis:• Blood analysis : creatinine, sodium, potassium,

chloride, ionised calcium, uric acid, • PTH and vitamin D in the case of increased calcium

levels.• Urinalysis: urine volume, urine pH, specific weight,

calcium, oxalate, uric acid, citrate, sodium and magnesium.

• Urine culture

Ca10(PO4)6.(OH)2Basic calcium phosphate

CaHPO4.2H20 Calcium hydrogen phosphate

Recommendations for the treatment of calcium phosphate stones

Disorders and diseases related to calcium stones

Hyperparathyroidism• 5% of all calcium stone formation• Renal stones 20% of patients with primary HPT• increase calcium turnover-> hypercalcaemia and

hypercalciuria• repeated measurements may be needed• calcium oxalate and calcium phosphate stones• If HPT suspected, neck exploration should be

performed to confirm the diagnosis. Primary HPT can only be cured by surgery.

Granulomatous diseases

• May be complicated by hypercalcaemia and hypercalciuria secondary to increased calcitriol production -> increased calcium absorption in the gastrointestinal tract

• Treatment focusses on the activity of the granulomatous diseases - reserved for the specialist.

Primary hyperoxaluria

• endogenous oxalate production is increased in patients with PH

• Should be referred to specialised centres, as successful management requires an experienced interdisciplinary team.

• Pyridoxine therapy

Enteric hyperoxaluria• intestinal malabsorption of fat• usually present with hypocitraturia due to loss

of alkali • Urine pH is usually low, as are urinary

calcium and urine volume• All these abnormalities contribute to high

levels of supersaturation with calcium oxalate, crystalluria, and stone formation.

Specific preventive measures are:•restricted intake of oxalate-rich food•restricted fat intake•calcium supplementation at meal times to enable calcium oxalate complex formation in the intestine •sufficient fluid intake to balance intestinal loss of water caused by diarrhoea •alkaline citrates to raise urinary pH and citrate.

Renal tubular acidosis• Caused by severe impairment of proton or

bicarbonate handling along the nephron• Distal RTA type I • acquired or inherited • Reasons for acquired: obstructive uropathy,

recurrent pyelonephritis, acute tubular necrosis, renal transplantation, analgesic nephropathy, sarcoidosis, idiopathic hypercalciuria, and primary parathyroidism; it may also be drug-induced

Uric acid and ammonium urate stones

• high risk of recurrence • form under completely different biochemical

conditions

• Blood analysis : creat, potassium, uric acid• Urinalysis: urine volume, urine pH, specific

weight, uric acid.• Urine culture is needed in the case of

ammonium urate stones.

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Struvite and infection stones

• 7%, F>M, high risk of recurrence • may originate de novo or grow on pre-

existing stones• Blood analysis : creat• Urinalysis: urine pH• Urine culture is needed

Predisposing factors to struvite stone formation

Most important species of urease-producing bacteria

Specific treatment

Cystine stones • 1-2% of all urinary stones in adults • high risk of recurrence• Cystinuria is a common genetic disorder • Blood analysis : creat• Urinalysis: urine volume, urine pH, specific weight, cystine

• no role for genotyping patients• Diagnosis is established by stone analysis -

Quantitative 24hour urinary cystine excretion• Levels above 30 mg/day are considered abnormal

• Cystine is poorly soluble in urine and crystallises spontaneously within the physiological urinary pH range.

• Cystine solubility depends strongly on urine pH

Specific treatment• fluid intake high level of diuresis, aiming for a

24-hour urine volume of > 3 L • maintain urine pH > 7.5, to improve cystine

solubility • A diet low in methionine may theoretically reduce

urinary excretion of cystine• Free cystine concentration can be decreased by

reductive substances, which act by splitting the disulphide binding of cysteine:

• Tiopronin

2,8-Dihydroxyadenine stones and xanthine stones

• high risk of recurrence• Both stone types are rare• Diagnosis and specific prevention are similar to

those for uric acid stones. • Pharmacological intervention is difficult• general preventive measures

Drug stones

Induced by pharmacological treatment Two types exist: •stones formed by crystallised compounds of the drug;•stones formed due to unfavourable changes in urine composition under drug therapy.

Radiolucent even on CT

References:

• EAU Guidelines on Urolithiasis 2017• CUA guideline on the evaluation and medical

management of the kidney stone patient – 2016 update

• Evaluation and Medical Management of Urinary Lithiasis – Campbell-Walsh 10th Edition

Thank You