01-27 Nephrolithiasis Flashcards
Define nephrocalcinosis
– Calcification within the renal parenchyma
– Uncommon, usually bilateral, rarely involves cortex
Bladder stones
– Rare in the Western world, but the most common stone in underdeveloped countries
Five major types of stones?
- Calcium oxalate (80% of U.S. stones)
- Calcium phosphate
- Cystine
- Struvite
- Struvite
What drives phases changes of stone-ogenic compounds and what’s an easy way to prevent phase changes?
supersaturation (SS)
—increase PO h2o intake
4 theories of stone formation
- Matrix Theory
–Organic matrix compounds present in all stones are causally related to stone formation - Inhibitor Theory
–Deficiency in the urine of substrates which normally inhibit crystallization and growth - Crystalloid or Precipitation-Crystallization Theory
–Supersaturation with respect to the stone-forming constituents
Reality: likely due to a combination of these theories
Randall’s plaque hypothesis
nephrocalcinosis causes a focal deposit along papilla which is exposed with loss of urothelium
—this becomes nidus for stone formation
Individual risk factors for stone development
—Family history (RTA, cystinuria) —Medications (chemotherapy; vitamin C) —pH —GI diseases: IBD, gastric bypass —Hyperoxaluria —Hyperuricosuria (gout) —Hypercalciuria
DIET-SPECIFIC Water intake: dilution prevents stones —hard water (calcium sulfate) —soft water (sodium carbonate) Gluttony —purines (meat lovers) —oxalates (coffee, tea, cola, nuts, cranberry juice, rhubarb, strawberry) —calcium
GEOGRAPHIC
—U.S. stone belt in south
– warmer temperature, summer
– sunlight (Vit D increases urinary Ca)
Calcium Oxalate Stones
—Specific Risks
—Tx
RISKS Metabolic defects —Hypercalciuria: most common; ? cause —Hyperoxaluria —Hyperuricosuria Family history Dehydration Diet or medications —High protein diet —Vitamin C, D —Antacid abuse Inhibitor deficiencies —Hypocitraturia —Hypomagnesuria
TX
—for hyperoxaluria due to increased intestinal absorption: diet ∆s and paradoxical Ca or Mg supplementation (binds Oxalate and prevents absorption)
How does high animal protein diet cause stones?
Acid generation from metabolism of sulfur- containing amino acids
—Uric acid generation from metabolism of purines (associated with protein)
—Bone buffering of acids
—Hypercalciuria from bone release of calcium
Calcium Phosphate Stones
—Specific Risks
—Prevention
RISKS Again, hypercalciuria – Vitamin D intoxication – Hyperparathyroidism – Sarcoid
But also alkaline urine
– Urinary acidification defect RTA (esp w/ distal)
– Acetazolamide
– Milk-alkali syndrome
PREVENTION
—HyperPTH: Surgery
—Diet
—Idiopathic hypercalciuria: thiazides; dietary Na+ restriction
—Hyperuricosuria: allopurinol
—Hyperoxaluria: reduce dietary oxalate; calcium and mag for enteric hyperoxaluria
—Specific measures based on 24-hour urine: magnesium, citrate
Uric acid stones —Prevalence —Dx —Tx —Prevention
PREVALENCE
– 5-10% of all stones
DX
– Stone analysis
– Uric acid crystals in the urine NOT diagnostic
– 24 hour urine studies; low pH, hyperuricosuria
TX
– Very susceptible to solubility conditions
– Alkalinization to reach urinary pH 6.5-7.0
– Fluids, treat underlying condition, education
PREVENTION —Hydration —Urinary alkalization w/ K+ citrate —Avoid purine gluttony —Allupurinol if hyperuricosuria
When is alkaline urine preventative of kidney stones vs. causative?
—causative: calcium phosphate stones
—preventative: uric acid & cystine stones
**Acidification almost never indicated
Struvite stones —Prevalence —Etiology —Dx —Tx
PREVALENCE
—Relatively common: ~10% of all stones
—Commonest cause of stones in ♀ & paraplegics
—Most common cause of staghorn caliculi
ETIOLOGY Form in presence of urinary tract infection with urea-splitting organism —Proteus - most common —Klebsiella —Serratia —Enterobacter
DX
—Suspect if recurrent UTIs as bacteria live inside & struvite crystals but this is NOT dx of stones themselves
—Suspect if urine pH > 8
TX —Antibiotics —Urease inhibitors —Percutaneous surgery/lithotripsy —Fluids, treat underlying disease, education
Cystine Stones
—Prevalence
—Etiology
—Dx
PREVALENCE
—Rare, ~1%
ETIOLOGY
—A.R. genetic defect in dibasic amino acid transport in renal tubule and gastric mucosa
—COLA=cystine, ornithine, lysine, arginine
—Only AA to cause clinical disease
DX
—Stone Analysis
—Cystine crystalluria – Hexagonal crystals
—Cyanide-nitroprusside test – Qualitative
—24 hr urine = Quant: Homozy vs heterozy
TX
—High fluid intake (4L/day)
—Urinary alkalinization
—Meds – D-Penicillamine (*tiopronin fewer ADRs)
–— Disrupts disulfide bonds in cysteine, increasing solubility
–— Great concept, but ADRs cause most pts to stop
Staghorn caliculi
Usually struvite,
could be cystine
