Nephrolithiasis (K16)
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Transcript of Nephrolithiasis (K16)
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NEPHROLITHIASISEtiology, stone composition, medical management, and prevention
Urology Division, Surgery DepartmentMedical Faculty, University of Sumatera Utara
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EpidemiologyPrevalence 2-3%, maybe in mountainous, desert & tropical areas: = 3 : 125% stone formers have a family historyUric acid and Ca stones more frequent in, infectious stones more common in The most common kinds of stones are calcium oxalate, uric acid, struvite and cysteine
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Composition of renal stonesCalcium oxalate 36 70%Calcium phosphate (hydroxyapatite) 6 20%Mixed Ca oxalate & Ca phosphate 11 31%Magnesium ammonium phosphate (struvite) 6 20%Uric acid 6 17%Cystine 0.5 3%Miscellaneous (xanthine, silicates & drug metabolites) 1 4%
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Factors influencing stone formationGenetics 1. Idiopathic hypercalciuria 2. Cystinuria 3. Primary hyperoxaluria, type 1 & 2 4. Lesch-Nyhan syndrome is an X-linked disease causing hyperuricemia 5. Familial renal tubular acidosis , Ehlres-Danlos syndrome, Marfans syndrome, Wilsons disease
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Environmental 1. Dietary factors - >> protein & sodium intake risk Ca stone - >> purine diets urine pH hyperuricosuria - B6 deficiency formation & excretion oxalate - dehydration, inadequate fluid intake, vit C excess, Ca supplements, Ca-containing antacids
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2. Geographical factors - higher during summer months - higher in southeast United States and lower in Mid-Atlantic and Northwest regions
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Stone formationCrystallization - stone salts that precipitate out of urine - the point of saturation of a salt in solution is called the solubility product (Ksp) - when the product of the components of a salt (e.g. calcium and oxalate) exceeds Ksp, salt crystals will precipitate out of solution - crystallization is based on Ksp, pH, and the presence of stone inhibitors and promoters
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Nucleation - is the process by which stones form around a core, or nucleus - homogeneous stone nuclei form in solution - heterogeneous stone nuclei form around existing structures, such as cellular debrisAggregation - crystals join together to form larger clumps
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TYPES OF STONE
CALCIUM OXALATERecommended treatment : - absorptive : Ca restriction, sodium cellulose phosphate, thiazides, fluid intake - other types : thiazide & fluid intake
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URIC ACID STONES5-10% of all stoneUrine pH < 5.5Associated with uric acid in urine, not necessarily associated with hyperuricemiaSecondary causes : gout (20%), chemoth/ for myeloproliferative cancerMost common radioluscent
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Th/ : dissolve : - fluids, alkali (citrate th/), allopurinol, protein restriction - aim urine output > 2500 ml/day - potassium citrate or sodium bicarbonate achieve urine pH 6.5-7.0 avoid pH >7.0 can precipitate ca phosphate - if hyperuricemic or hyperuricosuric allupurinol
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STRUVITE STONESComposed of Mg ammonium phosphate crystals= infection stones or triple phosphate stoneStaghorn calculi are typically struvite stoneCaused by infection with urease-producing bacteria : - proteus id the most common - urease hydrolized urea to form ammonia alkalinizes the urine, pH and allows crystals to form
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Urine pH will be >7.2Th/ : - surgery - AB to prevent infection / stone recurrence - irrigation with acidic solution successful but requires lengthy, complicated treatment and costs danger : risk of sepsis, hypermagnesemia - acetohydroxamic acid : inhibit urease; 20-70% severe side effect
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CYSTINE STONES1% of all stonesCongenital disorders, autosomal recessiveCaused by a defect in cystine reabsorption in the proximal tubuleCystine poorly soluble at normal pH (pKa 8.3)Crystal form benzene ring on microscopy
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Th/ : - low methionine / sodium diet - hydrate to 3 L urine output/day - alkalinize urine : potassium citrate complex cystine - ESWL not effective
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CALCIUM PHOSPHATE STONE - urine pH > 5.5 - hypocitraturia - 70% of adults with type 1 Renal Tubular Acidosis have stones - 80% are women - associated with renal cyst
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Inhibitors of CaPO4 crystallization : - Mg- pyrophosphate - citrate- nephrocalcinTh / : - potassium bicarbonate or potassium citrate correct acidosis & urine citrate - fluids - thiazides if hypercalciuric
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OTHER STONESDihydroxyadenine radioluscentXanthine radioluscentMatrix radioluscentAmmonium acid urateTriamtereneIndinavir radioluscent
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MEDICAL MANAGEMENT
DIETARY PREVENTION - fluids : urine output stone formation if possible maintain >2.5 L urine/day - coffee, tea, beer, wine stone risk - lemon juice urinary citrate risk - grapefruit juice risk
PROTEIN - dietary protein urine Ca/uric acid/oxalate & urine citrate low/moderate protein intake is desirable
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CALCIURIA - except in case of absorptive hypercalciuria, Ca binds intestinal oxalate prevent its absorption - unless absorptive hypercalciuria maintain adequate calcium intake
SODIUM - dietary sodium urinary sodium has not been proven to stone risk sodium in moderation
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ASCORBIC ACID (VITAMIN C) - metabolized to oxalate - vit C intake urinary oxalate - advice : vitamin C in moderation
OXALATE - tea, instant coffee, spinach, chocolate, nuts oxalate (+) increase urinary oxalate - high-oxalate foods in moderation for Ca oxalate stone former
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PHARMACOLOGICAL PREVENTIONTHIAZIDES - HCT 25-50 mg or chlorthalidone 12.5-25 mg (up to 100mg) - start with small dose, titrate as needed
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CITRATE - Inhibits Ca oxalate crystallization - effective for hypocitraturic stone disease - potassium citrate 10-20 mEq w/meals - side effects : GI intolerance
ALLOPURINOL - inhibits xanthine oxidase & uric acid prod - use in uric acid & hyperuricosuric Ca oxalate stone - 300 mg/o, max 800 mg - dose in renal failure
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PHOSPHATE (ORTHOPHSOPHATE) - vit D level urinary Ca excretion - urine pyrophosphate & citrate - clinical benefits are uncertain
MAGNESIUM - urinary citrate - clinical benefits uncertain
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SODIUM CELLULOSE PHOSPHATE - binds Ca in the gut and inhibits absorption - indicated for use in absorptive hypercalciuria - 5 g with meals
ANTIBIOTICS - long-term prophylaxis for struvite stone after surgical treatment - drug should be culture specific
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SUMMARYThe most common type is calcium oxalate. Uric acid stones form at pH 7.2. treatment is surgery & antibiotics
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Cystine stones caused by a congenital autosomal recessive disorder. Treatment : urinary alkalinization Calcium phosphate stones associated with type 1 RTADietary interventions to prevent stones include fluid intake, protein intake and sodium intakePharmacological interventions to prevent stones include thiazides, citrate, allopurinol, sodium cellulose phosphate
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