Nephrolithaisis Evaluation in Family Practice

Risk of developing kidney stones 10-15% Prevalence increasing in women & with age Kids
more likely to have anatomic & metabolic abnormalites vs control Kids with cystinuria & other hereditary kidney stones at increased risk of decline in renal function, although progression to ESRD uncommon.

 Likelihood of forming a second stone 25- 40% after 5 yrs, 50 % at 10 yrs

Men more likely to recur vs women.

Patients with recurrent stones

97% of patients have identifiable cause medical therapy can significantly reduce the risk of recurrence in majority

 Patients with kidney stones should increase fluid intake to at least 2 L per 24 hours - LEVEL B evidence Kidney stone type should be identified when possible, even on initial stone occurrence - LEVEL C Urine characteristics (e.g., urine pH) should be obtained in patients with kidney stones to guide treatment and prevention LEVEL C Patients with kidney stones should be counseled on stonespecific dietary interventions- LEVEL C Patients with kidney stones should be assessed for risk of chronic kidney disease- LEVEL C To prevent kidney stones, medication use should be evaluated and modified as needed LEVEL C

Calcium oxalate: Calcium phosphate Cystine Struvite Uric acid Other

Children (%) 45- 65 24 - 30 5 to 8 7 - 13 2-4 4

Adult (%) 56 - 61 8 - 18[*] 1 2-4 9 - 17 2

conservative approach to patient with first symptomatic kidney stone:

Increasing fluid intake to produce at least 2L of urine per day
increases urine flow rate & lowers urine solute concentration Only rec with level B evidence (others = level C)

History to assess dietary & behavioral habits that can contribute to stone disease & provoke future stone formation. U/A & culture:
pH > 7.5 & positive urine culture compatible with infection lithiasis
struvite, Ca-phosphate stones

pH < 5.5 favors uric acid stones

cystine, Ca-oxalate

Subsequent monitoring with KUB or U/S for detection of new stones. Monitor initially at 1 yr &, if negative, every 2-4 yrs thereafter. Available stones analyzed to determine crystalline composition.

Risk-based approach Moderate Risk for Future Stones..

Obesity, DM, chronic diarrheal state or other predisposing medical condition, black race, +FH stone disease, or cystine, struvite, or uric acid stone 1. serum chem panel to help identify certain associated disorders
primary hyper-PTH (hypercalcemia) hyperuricemia distal RTA search for residual stones within urinary tract.

2. 3.

non-contrast CT at 5 mm cuts

two 24-hour urine collections in outpatient setting

patient to follow usual diet, fluid intake, physical activity assessment of urine composition to identify metabolic abnormalities that could contribute to nephrolithiasis & guide therapy.

Medical History certain conditions have increased risk kidney stones:

IBD, bowel surgery Gout diabetes mellitus Obesity recommend weight loss and promote low glycemic diet
Body fat hydrophobic so proportion of body water decreases with increasing obesity Decrease surface area to body volume complicates heat exchange and metabolic rate

recent weight changes, metabolic syndromes hyperparathyroidism-associated conditions frequent UTIs, CKD

Medication history
Allopurinol uricosuric Laxative overuse (ammonium urate stones) Antibiotics (Sulfonamides, ampicillin, amoxicillin, ceftriaxone, quinolones, furans, pyridines) increase urine oxalte by reducing intestinal bacterial that break oxalte down Carbonic anhydrase inhibitors (Acetazolamide, topiramate): Ca Phosphate stones Cause mild systemic acidosis and paradoxically high urine pH, hypercalciuria, & low urine citrate Ephedra alkaloids (banned in US) Potassium channel blockers (Amiodarone, sotalol dalfampridine) Potassium-sparing diuretic (Triamterene) Reverse transcriptase inhibitors & protease inhibitors Sulfonylurea

Management all stone types:

Fasting serum glucose > 105 mg/dL, random level > 140 mg/dL Suggestive of insulin resistance or early DM Alkalinize Serum Ca > 10 mg/ dl Consider primary hyperparathyroidism: check intact PTH level Potassium citrate: 10 to 20 mEq orally with meals (rx required) Alkaline Urine pH Acidify urine (pH <7): cranberry juice (16 oz/day) or betaine (650 mg TID) Acidic Urine pH Alkalinize urine (pH 6.5-7) with diet changes or oral supplement, or until 24-hr urine citrate levels in normal range Calcium citrate or potassium citrate

Calcium Oxalate Stones

Appropriate protein intake (<30% total caloric intake) Ca supplement (ca citrate if trying to raise urine citrate): >850 mg/day w meals Check serum 25-hydroxyvitamin D levels (<30 ng/mL): 24 hr urine (mg/day): oxalate, calcium, magnesium, citrate, phytates -Mg (<70): increase diet Mg (fish, nuts, grains, yogurt); consider Mg Potassium citrate supplementation -Citrate (<450 M, <550 W): supplement (K-citrate, Ca-citrate, Na-citrate). Add lemon or lime juice in water. - Phytates (<3.9 mg/L inorganic phosphate, <0.4 mg/L per inositol-P6) consider increased fiber intake (whole grains, legumes, seeds, nuts)

Hypercalciuria (> 200-250 mg / 24 hrs)

Ca excretion of
increased diet acid loads & salt intake, inadequate &excessive vit D.

Idipathic hypercalciuria (normal serum Ca)

Dietary Ca should not be restricted in those with normal Ca: pts often w/ negative Ca balance.. Can bone demineralization.

Low salt diet reduce urinary Ca excretion

Promotes increased PT Na reabsorption, increasing passive Ca reabsorption - significantly lowering supsersaturation of Ca oxalate

Thiazides (if diet changes fail)

Cause mild volume depletion, increasing PT sodium and Ca reabsorpion Ineffective in setting of high salt diet & should be stopped b/c of increased risk of hypokalemia (increases stone risk) in absence of benefit Monitoring urinary Na regularly will help avoid inappropriate use of thiazides.

Hyperoxaluria (>40mg/day)
Main source oxalate = dietary
recent study that found little relationship btwn dietary oxalate & urinary oxalate excretion
was association with increased vitamin C ingestion

Common in DM, IBD, chronic diarrhea, other small bowel disease Important to look at balance of oxalate of calcium excretion in urine
Hypocalciuria, while appearing to lower risk of calcium oxalate stones, may be a sign of secondary hyper-PTH due to a negative calcium balance. Ca supplementation should be considered if this is present (will also lower GI oxalate absorption & thus lowering stone risk) Oxalate (>40): encourage moderate vit C intake (limit diet to <1mg/day)

Calcium phosphate Stones

Perform pregnancy test in women: increased risk CaP stones with 2nd and 3rd trimester pregnancy
increased GFR and higher urinary Ca excretion throughout pregnancy, with higher urine pH in second & third trimesters. Increases risk of UTI &preterm delivery ( renal colic ~ double risk)

Acidify urine: cranberry juice or Betaine

Little human data acidifying urine decreases stone formation in genetically predisposed rats

Consider decreasing dietary phosphate dairy products, legumes, chocolate, nuts by ~1/3

Cystine Stones
Alkalinize urine 24 hr urine crystals (>250 mg / day)
Decrease methionine (sulfur) intake: avoid dairy products, eggs, legumes, greens Cystine binding agents: Tioproin, Penicillamine
Dose adjusted to maintain urine free cystine concentration <250 mg / day if possible)

Uric Acid Stones

Decrease protein intake (<30% total caloric intake) Reduce or eliminate alcohol intake If diabetes, increase intake of regular or decaffeinated coffee and tea urinary pH alkalinized to 66.5 to reduce uric acid solubility If alkalinization & diet changes fails to prevent uric acid stone recurrence, allopurinol may have a role in reducing uricosuria Hyperuricosuria also risk factor for Ca-oxalate stones: increases supersaturation, favors precipitation

Struivite Stones
Stone analysis or radiography Acidify urine Avoid supplemental Mg (based on animal studies) Acetohydroxamic acid (urease inhibitor) in patients who cannot tolerate surgery Possible surgical intervention, esp for stones >10 mm or if evidence of ongoing obstruction or infection