Flashcards in Nephrolithiasis Deck (15):
1. Describe the epidemiology of stone disease.
lithotomy is one of the oldest know operations, described in the ancient world; with the refining of foods such as grains, stones have moved from bladder to the kidney
12% men, 6% women; less prevalent in Af. Am. and more common in summer months and southeaster states (environment and ~56% genetics)
2. Differentiate the fundamental pathologic differences between initiation of calcium oxalate stones and calcium phosphate stones.
Randall's plaques are calcium phosphate deposits in the BM and intersitium of thin loops of Henle --> nidus for CaOx stones grow and penetrate the uropeithelium
CaP (or cystine) form intratubular crystals in the medullary collecting ducts resulting in damage to tubular cell and scarring of the papilla
3. Identify the three major physicochemical factors in stone formation.
level of the solute above the solubility product
inhibitors (citrate, pyrophosphate and proteins)
4. List and describe the types of kidney stones and their relative frequency.
Calcium: either CaP or CaOx (most common) make up the majority of stones (~70%)
uric acid stones (10-15%)
struvite stones (10-15%)
cystine stones (<1%)
5. Describe the clinical presentations and predictors of stone passage.
ureteropelvic junction or upper ureter: sudden onset of unilateral flank pain (renal colic) radiating into the groin, sometimes associated with nausea and vommiting
uretovesical junction (60%): urinary urgency and suprpubic pain
5. Describe diagnostic workup and reasons for hospitalization with stones.
80-90% of stones are calcium stones (radio opaque) the other 10% are radiolucent (uric acid); microhematuria/ gross hematuria, creatinine levels and electrolytes to rule out RTA type 1 or hyperPTH, CBC to look for infection and UA; definitive study is a CT scan without contrast
size of stone is prognostic for passing or requiring surgical intervention (-/+ 0.5cm) >1cm require intervention
reasons for hospitalization: coexistent UTI with obstruction, stone >1 requiring intervention, obstruction leading to kidney failure; patient cannot tolerate pain or keep fluids down
5. Describe therapy for acute stone disease, including preventive therapy for future stones.
acute: control pain and vomitting, try to dilate ureters and hydration/ medical expulsive therapy (tamsulosin, CCB)
6. Describe the diagnostic tests and specific therapies for recurrent calcium stone disease, uric cid stones, cystine stones and struvite stones.
collecting of stone for analysis
drink >2 L fluid/day which reduces recurrence rates by 50%
work up for PTH leaves, 24 urine collection (Na, Mg, K, Ca, P, volume, uric acid, sulfate, ammonium, oxalate, pH and citrate levels) to nail down cause
tx: hypercalciuria: thiazide diuretic (increase Ca reabsorption), reduce sodium for CaOx stones
give inhibitor potassium citrate (prevent new stones); higher pH can cause CaP brushite stone formation
uric acid stones: tx. with allupurinol, also reduces oxalate kidney stones by 50%
can be followed with Xray (unreliable) or CT (radiation)
1. What subpopulations are at high risk for different types of stones?
low urine: most stones
HTN, women: CaOx
low Ca diets
high sodium and protein: Ca and Uric acid stones
low urine pH: uric acid
high urine pH with "struvite" and CaP stones
IBD and short bowel: CaOx
hyperPTH: CaOx, CaP
PKD and medullary sponge kidney: CaOx
meds: high vit. C and Ca supplements: CaOx
carbonic anhydrite inhibitors: CaP stones
80% calcium stones not due to infection are CaOx
pure CaP stones associated with Type I RTA
5% due to hyperparathyrpidism
"struvite" or triple phosphate stones due to urea splitting UTI (very alkaline)
Describe factors that increase CaOx stone formation.
lack of gut pathogen Oxalobacter formigenes which metabolizes oxalate has been associated with increased calcium oxalate stone formation
hyperoxaluria due to genetic defects in metabolism and increased absorption of oxalate in the gut due to inflammatory bowel disease, short bowel syndrome and gastric bypass
What is the role of citrate in inhibiting calcium stones?
citrate works by chelating urinary calcium and inhibits calcium crystal growth
Describe the formation of uric acid stones: associated causes, dx and tx.
associate with metabolic syndrome, decreased renal ammonium execration and low urinary pH
chronic diarrhea also puts at risk for low urinary pH and stones
dx. stone type not identified, 24h urine for solute increased urinary uric acid and low pH and imaging without calcium stones
tx. potassium citrate decreases uric acid stone formation, goal pH >6.5; low protein/purine diet advised; allopurinol not proven, may be helpful
Describe the formation of cystine stones: associated causes, dx and tx.
occur in patients with genetic defects in dibasic amino acid transport in the kidney and gut (caucasian males, first 2 decades)
associated genes AR: SLC3A1 (2) and SLC7A0 (19)
dx. family hx and stone analysis, UA with hexagonal crystals
tx. decrease cystine concentration of urine with high fluid intake, and alkalinizing urine pH>7
cystine binding drugs include Tiopronin, D-penicillamine and catopril
Describe the formation of struvite stones: associated causes, dx and tx.
associated with organisms that split urea (Proteus, PRovidencia, Dlebsiella, Pseudamonas and enterococci)
form a mix of Mg ammonia phosphate and carbonate apatite CaP (triple phosphate) seen with complicated or recurrent UTI
dx: grow very rapidly and very large (asymptomatic or vague flank pain); UA very alkaline urinary pH >7 and coffin lid struvite crystal
tx. removal of stone by extracorporeal shock wave lithotripsy or percutaneous nephrolitotomy
prevent with surveillance of cultures and antibiotics for UTIs