1/27 Nephrolithiasis - Walker Flashcards
kidney stone risk factors
- previous stone: 30-50% likelihood of second stone, 5-10yr
- family hx: 50% have first-deg relative with stones
- DM (Ca and uric acid): weight gain, obesity, metabolic syndrome
- vasectomy
- beverages
- lower: coffee/tea/beer/wine
- higher: grapefruit juice
- sugar sweetened bevs
- decreased dietary Ca
- urine vol < 2L / 24h
symptoms: nephrolithiasis
- pain/renal colic
- hematuria (but can be absent in up to 30%)
- nausea, vomiting
- urinary urgency
imaging studies: nephrolithiasis
non-contrast helical CT (current gold standard)
- sn, sp > 90%
- detects radiolucent stones (uric acid)
- may require contrast for other “crystaluric” stones
if radiation contraindicated? sonography! (ex. preg)
treatment guidelines: nephrolithiasis
analgesia/expulsion
- NSAIDs/COX2 → narcotics
- tamsulosin → alpha1 receptors in distal ureter
- nifedipine
- corticosteroids
urology consult if stone > 5mm
NEED TO CATCH THE STONE!!! so that you know how to avoid the next stone
- strain urine
- send stone/fragments for analysis
- biochemical eval
formation of a kidney stone
- supersaturable state (supersat, but stable)
- something happens = nucleation occurs
- nidus forms, crystal growth/aggregation occurs
- →→→ STONE
types of kidney stones
“big four”
- calcium oxalate
- uric acid
- struvite
- cystine
also calcium phosphate (uncommon)
calcium oxalate stones
calcium oxalate monohydrate (Whewllite)
- dumbell like shape
calcium oxalate dihydrate (Weddellite)
- pyramid-esque
calcium stones: risk factors
four principle risk factors
- hypercalciuria (w or w/o hypercalcemia)
- hypocitraturia
- hyperoxaluria
- hyperuricosuria
also systemic diseases assoc with Ca stones
- primary hyperparathyroidism
- medullary sponge kidney
- type I (distal) RTA
idiopathic hypercalciuria
features
rat model
treatment
auto dom?
present in approx 50% of Ca stone formers
- excessive intestinal Ca abs
- decr renal Ca abs
- decr bone mineral density
GHS rat model
- intestinal hyperabs of Ca due to incr sensitivity to 1,25(OH)2 D3
- primary defect in renal tubular Ca reabs
- incr bone resorption with incr vitD receptors in osteoblasts
tx: thiazides
thiazides for Ca-based stones
enhance Ca reabs directly in DCT and indirectly in PCT → diminish urinary Ca
distal nephron: block Na/Ca cotransporter (basolateral) → leads to incr in NCX (apical) activity
- overall, moves Ca out of cell
_proximal nephr_on: incr Na reabs → incr Ca reabs
overall: decr in urinary Ca excretion → decr in urinary Ca stone formation!
hypocitraturia
urinary citrate inhibits Ca stone formation
incr proximal tube reabs of citrate → less urinary citrate. occurs due to:
- metabolic acidosis (ex. RTA, diarrhea)
- incr dietary protein
treatment:
- K citrate
- orange juice > lemonade
- grapefruit juice can increase citrate buuuut also incr urine oxalate
- DASH diet
hyperoxaluria
higher levels of Ca oxalate crystals
causes
- increased intestinal absorption:
- low Ca diet
- absorptive hyperCa
- small bowel disease/resection
- decr degradation of oxalate by Oxalobacter formigenes
- incr oxalate production (rare)
- primary hyperoxaliuria
- large doses of ascorbic acid
treatment
- reduce dietary oxalate in pt with high urinary oxalate levels
- pyridoxine? (cofactor for metabolism glyoxylate → glycine)
- Ca supplements with enteric hyperoxaliuria → Ca binds oxalate, less is absorbed!
- trials to try to develop Oxalobacter formulations
hyperuricosuria
creates a nidus upon which Ca salts (CaOxalate, CaPO4) can accrete
high purine diet contributes
tx:
- hydration
- purine-restricted diet
- alkalinization: K citrate (if stone are CaOxalate)
- allopurinol vs. febuxostat
Ca stones:
dietary tx
- HYDRATION
- low Na
- low animal protein (all forms of meat, but not dairy pdts)
**do not restrict DIETARY CALCIUM! need 1000-1200 mg/day
- however, supplemental Ca may incr risk in women
- if taking supplemental Ca, take with food → decr urinary oxalate
pathogenesis of forms
Randall’s plaques
3 pathways
Randall’s plaques: deposits of CaPO4 found in interstitium of kidney → can serve as an anchor for deposition/stone formation
3 postulated pathways:
- “free particle” formation (either in collection system of kidney or along nephron)
- crystal nuclei form in lumen of nephron at sites of cell injury → crystal attachment and growth
- crystals in urine become attached to site of exposed crystaline deposits of interstitial CaPO4 following loss of normal urothelial covering of renal papilla
uric acid stones
characteristics
risk factors
pleomorphic
form multicolored birefringent crystals
radiolucent on xray → visualize on CT
risk factors
- low urine pH
- relative hyperuricemia
- low FEurate
may precede arthritis in 40% of pt with primary gout
marked decr in uric acid solubility as pH falls below 6.5
- H + urate → uric acid
treatment
- hydration
- alkalinization: K citrate, K bicarb
- allopurinol (not firstline tx)
struvite stones
magnesium ammonium phosphate
“coffin lids”
get really big
cause: infection by bacteria that makes urease (E. Coli does NOT)
- urease producing bacteria catabolize urea → ammonia + carbon dioxide
- incr ammonium and decr phosphate solubility (due to incr urine pH) → stone formation
treatment: surgical intervention usually required
- acetohydroxamic acid (urease inhibitor) in pts with residual/recurrent struvite stones, but only after surgical options exhausted
cystine stones
hexagon crystals are pathognomonic
proximal tubule reabs transport defect for: cystine, ornithine, lysine, arginine
- multiple genotypic/phenotypic subtypes
treatment
- hydration (maintain urine cystine conc < 300)
- alkalinization to urine pH >7/7.5
- formation of Cys-drug complexes with captopril, tiopronin, penicillamine
- doesn’t recur in transplanted kidney
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