CRAM Flashcards
Dietary recommendations: Ca++ stones and high urinary Ca++
Limit Na+
Maintain normal Ca++ (1-2g/day)
Dietary recommendations: Ca++Oxalate stones + high urinary oxalate
Limit oxalate
Maintain normal Ca++ (1-2g/day)
Dietary recommendations: Ca++ stones + low urinary citrate
Limit non-dairy animal protein and increase fruits and veggies
Dietary recommendations: Uric acid or Ca++ stones and high urinary uric acid
Limit non-dairy animal protein
Dietary recommendations: Cystine stones
Limit Na+ and protein intake
Medical therapy:
Recurrent stones + high urinary Ca++
Thiazide diuretic
Medical therapy:
Recurrent Ca++ stones + low urinary citrate
Potassium citrate
Medical therapy:
Recurrent CaOx stones + hyperuricosuria + normal urinary Ca++
Offer urinary allopurinol
If uric acid stones, DON’T offer allopurinol as first-line therapy
Medical therapy:
Recurrent Ca++ stones without other lab abnormalities
Empiric thiazide diuretics and/or K-cit
Medical therapy:
Uric acid and cystine stones
K-cit to raise urinary pH (these stones form in acidic urine)
Medical therapy:
Cystine stones refractory to dietary changes (adequate hydration, limit salt to 2-3 g daily) and urinary alkalinization (pH >7) or large recurrent stone burdens
Offer cysteine-binding thiol drugs (alpha-mercaptopropionylglycine = Thiola = tiopropin), which is better tolerated than D-Penicillinamine
Medical therapy:
Residual/recurrent struvite stones after surgery exhausted
Offer acetohydroxamic acid (AHA = Lithostat; urease inhibitor)
q3month CBC to monitor for hemolytic anemia
This drug decreases stone growth rate, doesn’t change stone recurrence
Renacidin = citric acid glucono-delta-lactone magnesium carbonate
Used for dissolution treatment of residual struvite stones/fragments
Urease-producing organisms
Proteus, klebsiella, staph aureus, pseudomonas, providentia, ureaplasma
Enteric/acquired hyperoxaluria is a/w:
IBD and short-gut syndrome
Unabsorbed fat binds to Ca++ –> oxalate goes unbound until it is reabsorbed in the colon –> high oxalate in the blood and then urine –> treat with Ca++ supplementation to bind oxalate in the gut
Crohn’s stone formation
low urine volume (dehydration) + low urine pH and hypocitraturia (metabolic acidosis) + hyperoxaluria (over absorption of intestinal oxalate –> CaOx stones
Isolated hypomagnesemia
Suggests IBD –> refer to GI
PO Reloxaliase
Recombinant oxalate decarboxylase enzyme derived from B. subtilis and expressed in E. Coli
Degredes oxalate within GI tract –> decreased oxalate absorption and urinary excretion
Lumasiran = Oxlumo
siRNA
decreases glycolate oxidase, which decreases glyoxylate’s conversion to oxalate
Approved for Tx of type 1 primary hyperoxaluria
CF is a/w which urinary abnormalities?
Hyperoxaluria, hypocitraturia (prone to stones)
Prevent stones: Roux-En-Y
Dietary Ca++ at mealtime
Decrease high oxalate foods
Metabolic acidosis –>decreased urinary citrate –> K-Cit
Stones: Colon resection and end ileostomy
Fluid and bicarbonate loss
Concentrated urine with low pH
Increased risk of uric acid stone formation
Lesch-Nyhan Syndrome
Absence of HGPRT
Neuro dysfunction, behavioral disturbances, uric acid overproduction with hyperuricosuria and hyperuricemia
A/w uric acid stones
Patients can get xanthine oxidase stones while on allopurinol –> decrease (don’t stop) allopurinol and start K-cit
Pregnancy and stones
Placental production of VitD –> increases calcium absorption and decreases serum PTH –> physiologic hypercalciuria
BUT
Urine citrate and GAG also increased so stone formation risk is unchanged