DIET FOR STONE DISEASE REALITY OR MYTH Doddy M. Soebadi DM SOEBADI FIESTA 20151

Introduction The lifetime prevalence of nephrolithiasis has been estimated at 13% among men and at 7% among women (Pearle 2005, Stamateloe 2003) Following an initial stone event, the spontaneous 5- yr recurrence rate is 35–50% (Uribarri 1989) The recurrence rate is reported to be as high as 50% (5 yr) and 80-90% (10 years) Recurrent stone have more significant metabolic abnormalities compare to single stone episode DM SOEBADI FIESTA 20152

Myths Myth: Dietary calcium causes stones Myth: Water is the only liquid that helps prevent stones Myth: Coffee, tea and carbonated drinks cause stones Myth: Alcohol causes stones Myth: Vitamin C is bad DM SOEBADI FIESTA 20153

Chronic Metabolic Condition Systemic DisorderUrinary Stone DiseaseAcute Episode DM SOEBADI FIESTA 20154

Multifactorial Cause of Urolithiasis DM SOEBADI FIESTA 20155

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Nutrition Therapy: Goals Reduction of Lithogenic Factors Urine Supersaturation Reduce Promoters Increase Inhibitors Combination with Pharmacotherapy? DM SOEBADI FIESTA 20157

Stone Analysis Wet chemical analysisScanning electron microscopy Thermogravimetry(Infra red) spectroscopy Optic polarizing microscopyX ray diffraction Recommendation Infrared spectroscopy X ray diffraction DM SOEBADI FIESTA 20158

Nutrition Therapy Assess nutritional status Risk factors Develop & Apply intervention Empiric vs Tailored Tailor to stone composition DM SOEBADI FIESTA 20159

General Nutrition Recommendations Adequate fluids Eat plenty (>5 servings) fruits & vegetables Eat balanced diet Maintain appropriate weight DM SOEBADI FIESTA

Diet and Stone Disease Low Fluid IntakeUrine Supersaturation Excessive saltHypercalciuria Hypocitraturia High intake of refined carbohydratesHypercalciuria Excessive caffeine/alcoholHypercalciuria Hyperuricosuria Renal Acid LoadHypercalciuria Hypocitraturia Acid Urine Excessive calorie intake - overweightAcid urine, hypocitraturia Excessive calciumHypercalciuria Low fruit/vegetable intakeHypocitraturia Acid Urine High oxalate – Low calcium intakeHyperoxaluria Excessive vitamin CHyperoxaluria DM SOEBADI FIESTA

Diet associated with Low risk Low Salt Adequate calcium Moderate protein Diet for hypertensive (DASH) Vegetarian DM SOEBADI FIESTA

Urinary parameters associated with Lithogenesis Urine Acidity (pH) Urine volume Calcium Oxalate Uric acid Phosphate Citrate Magnesium High urea level – high intake of animal protein Specific crystaloid supersaturation Cystinuria Urinary phytate DM SOEBADI FIESTA

Nutritional sodium sources Source% contribution to intake Processed meat14 Pastry / Baked goods14 Added salt & spices containing salt14 Canned foods9 Sauces & salad dressing8 Homemade cooking7 Cheese7 Pizza & fast food6 Pasta5 Breakfast cereal5 Milk, yogurt, frozen dairy3 DM SOEBADI FIESTA

Acid load of diet Increase calcium in urine Reduced tubular reabsorption Increase GF Increase bone mineral mobilization Increase intestinal absorption DM SOEBADI FIESTA

Food with High Acid Load Increase Acid LoadAlkaline load All food of flesh origin Cheese Eggs mostly from yellow yolk High quantity of grain Fruits Vegetables DM SOEBADI FIESTA

Investigating patient with stone of unknown composition DM SOEBADI FIESTA

General preventive measures DM SOEBADI FIESTA

Hypercalciuria DM SOEBADI FIESTA

Hyperoxaluria DM SOEBADI FIESTA

Hypocitraturia DM SOEBADI FIESTA

DM SOEBADI FIESTA

General metabolic considerations for patient workup and recurrence prevention High-risk stone formers → spesific metabolic evaluation (two consecutive 24 hour urine samples) Initial spesific metabolic workup → should be stone- free (min. 20 day between stone expulsion/removal and 24-h urine collection) Follow-up for patients receiving recurrent stone prophylaxis (24 hour urine measurements) 1 st follow-up → 8–12 week after starting pharmacological prevention If urinary parameters have been normalized → perform evaluation every 12 month Evaluation of patient risk DM SOEBADI FIESTA

General metabolic considerations for patient workup and recurrence prevention All stone formers should follow the preventive measures General considerations for recurrence prevention DM SOEBADI FIESTA

General metabolic considerations for patient workup and recurrence prevention General considerations for recurrence prevention DM SOEBADI FIESTA

General considerations for pharmacological treatment The ideal drug Halt stone formation Side Effects (-) Easy to administer. DM SOEBADI FIESTA

DM SOEBADI FIESTA

Stone specific diagnostic and therapeutic algorithms DM SOEBADI FIESTA

Calcium stones Diagnosis Blood analysis Creatinine Sodium Potassium Chloride ionized calcium (or total calcium + albumin) Uric acid Parathyroid hormone (PTH) Calcium oxalate stone Diagnosis Urinalysis Urine volume Urine pH profile Specific weight Sodium Calcium Oxalate Uric acid Citrate Magnesium DM SOEBADI FIESTA

Interpretation of results and etiology. ↑↑↑ Ionized calcium in serum → require assessment of intact PTH (to exclude Hyperparathyroidism) Spesific Treatment General preventive measure (fluid intake and diet) Thiazide and Thiazide-like agents Alkalinizing agents Calcium oxalate stone Calcium stones DM SOEBADI FIESTA

DM SOEBADI FIESTA

DM SOEBADI FIESTA

Mainly appears in two different minerals Carbonate apatite (occurs at pH ≥ 6,8; associated with infection) Brushite (at pH 6,5-6,8) Possible causes → HPT, RTA and UTI. HPT and RTA → common causes Calcium stones Calcium phosphate stone DM SOEBADI FIESTA

Calcium stones Diagnosis Blood analysis Creatinine Sodium Potassium Chloride ionized calcium (or total calcium + albumin) PTH Calcium phosphate stone Diagnosis Urinalysis Urine volume Urine pH profile Specific weight Calcium Phosphate Citrate DM SOEBADI FIESTA

Treatment Specific (fluid intake and diet) Pharmacological → depends on effective reduction of urinary calcium levels using THIAZIDE → L-methionine may be helpful if urine pH constantly >6,2 Calcium stones Calcium phosphate stone DM SOEBADI FIESTA

DM SOEBADI FIESTA

DM SOEBADI FIESTA

Disorders and diseases related to calcium stones HPT Primary HPT → surgery Granulomatous diseases → steroid, hydroxychloroquine or ketoconazole DM SOEBADI FIESTA

Hyperoxaluria Pyridoxine reduces urinary oxalate (one-third patients with primary hyperoxaluria type 1) Urine dilution achieved by adjusting fluid intake L/d (adults) ; 1.5 L/m 2 body surface (children) Calcium oxalate crystallization prevent by Hyperdiuresis, alkaline citrate and magnesium Intestional malabsorption of fat → Enteric Hyperoxaluria Disorders and diseases related to calcium stones DM SOEBADI FIESTA

DM SOEBADI FIESTA

Disorders and diseases related to calcium stones Distal RTA Main therapeutic aim → restore normal acid-base equilibrium Alkaline citrates or sodium bicarbonate is the key Monitored by venous blood gas analysis (base excess ±2.0) Thiazide may lower urinary calcium excretion (if calcium excretion >8 mmol/d) DM SOEBADI FIESTA

DM SOEBADI FIESTA

DM SOEBADI FIESTA

Disorders and diseases related to calcium stones Nephrocalcinosis Associated with metabolic factors Blood analysis (PTH, vitamin D, vitamin A, sodium, potassium, magnesium, chloride and blood gas analysis) Urinalysis (urine pH profile, daily urine volume, specific weight of urine, levels of calcium, oxalate,phosphatee, uric acid, magnesium and citrate) DM SOEBADI FIESTA

Considered to be at high risk of stone recurrence May be a result of Dietary excess, endogenous overproduction, myeloproliferative disorders, tumor lysis syndrome, drugs, gout or catabolism Associated with UTI, malabsorption, malnutrition Form in urine at pH >6.5 Common in urinary bladder Uric acid and ammonium urate stones DM SOEBADI FIESTA

Diagnosis Blood analysis (creatinine and uric acid) Urinalysis (urine volume, urine pH profile, specific weight of urine, and uric acid) Interpretation of results Acidic arrest (pH constantly <6) → crystallization Hyperuricosuria → uric acid excretion 4 mmol/d in adults or >0.12 mmol/kg/d in children Treatment (fluid intake and diet) Uric acid and ammonium urate stones DM SOEBADI FIESTA

DM SOEBADI FIESTA

High risk of recurrence Diagnosis Blood analysis (creatinine) Urinalysis (urine pH profile and urine culture) Interpretation Stone contain struvite and/or carbonate apatite and/or ammonium urate. Culture = urease-producing bacteria (Proteus mirabilis) Treatment Fluid intake and diet, complete surgical stone removal, antibiotics, urinary acidification (using methionine), urease inhibition Struvite and infection stones DM SOEBADI FIESTA

DM SOEBADI FIESTA

DM SOEBADI FIESTA

High risk of stone recurrence Diagnosis Blood analysis (creatinine) Urinalysis ( urine volume, pH profile, specific weight, cystine) Established by stone analysis Interpretation Soluble in urine at pH 6.0 (limit 1.3mmol/L) Only HPLC (high performance liquid chromatography), can differentiates between cystine, cysteine, and drug- cysteine complexes after therapy Cystine stones DM SOEBADI FIESTA

Treatment Spesific fluid intake and diet (minimum of 3.5 L/d in adults, or 1.5L/m 2 body surface in children) restricted sodium intake (not to exceed >2 g/dL) Pharmacological (maintain urine pH >7.5) Tiopronin (drug of choice) → recommended for cystine levels >3.0 mmol/d Ascorbic acid (controversial) → for cystine levels <3.0 mmol/d Captopril → second-line if Tiopronin unsuccessful Cystine stones DM SOEBADI FIESTA

DM SOEBADI FIESTA

DM SOEBADI FIESTA

Your love for leafy greens may increase risk for kidney stones Too little calcium Your salad obsession A salty diet Not enough citrus fruits Too much meat Too much iced tea A can of soda Your parents Living in the South DM SOEBADI FIESTA

DM SOEBADI FIESTA