Urinary tract calculi Flashcards
intro to kidney stones
urolithiasis = stones in the lumen of the urinary tract (kidney, ureter, bladder)
nephrolithiasis = stones in the kidneys
peak incidence in
40-60 yo men
non-modifiable risk factors for renal stones
- age
- male gender
- ethnicity (white>black>asians)
- +ve family history
- anatomical anomalies in kidneys and urinary tract - eg. horseshoe kidney, ureteral stricture
- cystinuria (AR condition of reduced citrate in the urine)
- associated disease - gout, hyperPTHism
- metabolic disorders that increase excretion of solutes (chronic metabolic acidosis, hypercalcuria, hyperuricosuria)
- renal tubular acidosis
- medullary sponge kidney, polycystic kidney disease
modifiable risk factors for renal stones
- diet - excess Ca2+, oxalate, urate, Na+, so hypercalciuria, hyperparathyroidism, hypercalcaemia
- chronic dehydration - low urinary output increases urinary solutes, increases renal stones
- hot climates - risk of dehydration
- concentrated urine from dehydration - this chemical composition of urine favours stone crystallisation
- obesity - increased risk of uric/Ca2+ stones in obese people with low urine pH, hypercalciuria, uric acid stones
- hypertension
- drugs (Ca2+, vit D supplements)
- immobilisation
- beryllium or cadmium exposure
risk factors for recurrent stone formation
- +ve family history of stones
- previous stones
- early onset of stones
- type of stone - certain types are more likely to recur eg. Ca2+, uric acid, ammonium urate, infection (struvite)
aetiology (causes) of stone formation
when solute concentrations exceed saturation (exceed solubility in water) and crystallise
how do stones form
urine becomes supersaturated with minerals - leading to CRYSTAL FORMATION
crystals pass out in the urine OR stay in the kidney forming stones
types of stones
- calcium oxalate (MAIN)
- calcium phosphate
- uric acid
- struvite (infection stones)
- cystine
- drug-induced
stone formation is determined by
promoters (increase crystal formation and aggregation)
inhibitors (reduce stone formation, even if urine is plenty saturated with minerals)
promoters of stone formation
- calcium
- urate
- oxalate
- cystine
- low urine pH (uric acid)
- low urine flow (dehydration)
inhibitors of stone formation
- citrate (MAIN)
- magensium
- high urine flow
affects crystal formation and aggregation
to stop stones forming, gotta see me high CMH
calcium oxalate stones (MAIN)
associated with
- low urine volume
- hypercalciuria (high Ca2+) due to
*intestinal hyperabsorption of calcium
*reduced renal tubular Ca2+ absorption
*increased Ca2+ mobilisation from the bone (primary hyperPTHism) - hypocitraturia (low citrate)
*remember citrate is the main inhibitor so these stones are very likely to form - not inhibited - hyperuricosuria (increased uric acid)
*cause formation of uric acid stones
*these easily bind to calcium oxalate
*so promotes calcium oxalate crystallisation (as reduces its solubility) so more calcium stones form - hyperoxaluria (increased oxalate) due to
*hereditary, lots made in the liver
*increased diet intake from spinach, rhubarb, beetroot
*increased intestinal absorption w/ fat malabsorption
calcium phosphate stones are less common but they occur when pt has
- high urine pH (increases saturation of urine with Ca2+ and PO4-)
- renal tubular acidosis
certain drugs can promote calcium stones
- loop diuretics
- antacids
- steroids (glucocorticoids)
- theophylline
- acetazolamide
- vitamins C+D
which drugs prevent calcium stones from forming
- thiazides (increase distal tubular Ca2+ resorption, less excreted in the urine?)
uric acid stones caused by
- hyperuricosuria + hyperuricaemia (high uric acid because insoluble > soluble so crystal precipitates) = commonly seen in increased uric acid conditions:
*gout
*metabolic syndrome
*DM
*myeloproliferative/high cell turnover disorders (tumour lysis syndrome, myelodysplastic syndrome)
*purine overingestion (uric acid is a product of purine metabolism)
*diseases with extensive tissue breakdown eg. malignancy
*common in children with inborn errors of metabolism eg. rare hereditary enzyme deficiencies - low urinary pH (develop in acidic urine)
*ileostomy pts - loss of HCO3- and fluid results in acidic urine, causing precipitation of uric acid - low urine volume (dehydration, seen in hot climates)
certain drugs can promote uric acid stones
- thiazides
- salicylates
struvite (infection stones) caused by
- UTI’s with urease producing bacteria (from proteus, Klebsiella, pseudomonas)
so formed from any chronic infections
*bacterial infection hydrolyses urea to ammonium, which raises the urine pH
*this alkaline urine causes Mg, NH4, PO4- precipitate, forming a stone
- eventually struvite stones can form staghorn calculi which involve the renal pelvis and extend into calyceal spaces, forming kidney abscess, urosepsis and reduced kidney function
cystine stones (very rare, only in kids) caused by
- cystinuria causes cystine to leak through the kidneys into the urine
- due to an inherited AR disorder of a defective cystine (Aa) transporter
- so reduced absorption of cystine from PCT/SI
drug induced stones (very rare too) formed by
- crystallised compounds of drugs eg. amoxicillin/ampicillin are poorly soluble so crystallise in the urine
- unfavourable changes in urine composition eg. due to calcium/Vit D
- amoxicillin, loop diuretics increase calcium stones
- thiazides promote uric acid stones inhibit calcium stones
plain x-ray appearance of urinary stones
RADIOPAQUE (white/light) - main COP
*calcium oxalate
*calcium phosphate
RADIOLUCENT (black/dark) - DUA in the dark
*drug induced - penicillins, erythromycin, oestrogen
*uric acid
*ammonium urate
summary of stones
NON-INFECTION STONES
- calcium oxolate : hypercalciuria, hyperoxaluria, acidic urine,
- calcium phosphate : hypercalciuria, alkaline urine,
- uric acid : hyperuricuria, hyperuricaemia (high uric acid in blood and urine), acidic urine
INFECTION STONES
- struvite : alkalised urine from bacterial UTI - proteus, klebsiella
GENETIC STONES
- cystine : defective transporter
symptoms of urinary stones
most pt are ASYMPTOMATIC
but most common symptoms are:
- renal colic pain
- haematuria
what pain with urinary stones?
sudden, severe unilateral flank pain
intensifies with time
LOIN TO GROIN PAIN
radiates from the flank to the iliac fossa, testis or labia
why is renal colic pain described as loin to groin
radiates anteriorly along the abdomen,
inferiorly to the groin, testicles, labia majora,
as the stone moves towards UVJ
what causes the renal colic pain
when stones enter the kidney, renal pelvis, or ureter
and either obstructs it or causes dilation, stretch and spasm while it passes down the ureter
- obstructs urinary flow
because increased tension in the urinary tract stimulates PG release - VASODILATION - increases diuresis and pressure in the kidney when there’s obstruction
also SMC spasm due to PG acting on the ureter, causing oedema and hyperperistalsis
what makes the pain worse
fluids, diuretics, alcohol - increase peristaltic flow so worse pain if urinary tract is obstructed
exertion - mobile calculi move causing pain and haematuria