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Flashcards in Kidney Stones - Wesson Deck (24):

Sponge Kidney Disease typically features calcifications where?

calcifications along the corticomedullay junction and 'painbrush-like' appearance radiating outward from the calyces


Where does nephrocalcinosis typically appear?

tubules and interstitial spaces


What is the typical etiology kidney stone disease?



What is the most common composition of a kidney stone?

Calcium-oxalate or Calcium-phosphate


kidney stones often show distinct layers - what does this suggest?

This suggests that stones may form/grow due to some (not fully understood) cyclic process

Stones are generally made up of an aggregate - that is, it isn't a continual or 'epitaxial' process of continous organized deposition


What is the approximate lifetime prevalence of kidney stones in the US?

Who is at greater risk? (i.e. gender, race, age)

5-15% (annual incidence 1:1000)

men > women (2:1)

whites > other races

peak incidence in middle age

**also: substantial regional variation (diet?)


Name a few (4, bolded) drugs that can form stones

  • indinavir
  • acyclovir
  • triamterene
  • sulfamethoxazole


What is the etiology of cystinuria?

What is its approximate prevalence in the population?

A genetic defect in PCT amino acid transport (cysteine, arginine, lysine, ornithine), preventing reabsorption of these amino acids in the PCT

fairly rare - 1:10000


Name the two genetic defects (and inheritance pattern) seen in cystinuria

  • Type A: SLC 3A1. Recessive. Defective PCT S3 transporter
  • Type B: SLC 7A9. Incompletely dominant. Defective PCT S1 transporter

Type AB: combination of type A and type B

Type B is more prevalant (47%) than Type A (38%)


Describe primary hyperoxalosis/hyperoxaluria

Rare genetic liver enzyme disorder leading to excessive endogenous oxalate synthesis



What are the key genetic defects (and inheritance pattern) seen in primary hyperoxalosis/hyperoxaluria?

All recessive inheritance

  • PH1 (80%) - AGXT defect. Increased oxalate and glycolate.
  • PH2 (10%) - GRHPR defect. Increased urine glycerate and oxalate.
  • PH3 (10%) - HOGA1 defect. Increased urine oxalate


Why are calcium oxalate crystals so prevalent (what mechanism makes them form so easily)?

Very low Ksp (~4e-8) -> low solubility -> crystals precipitate from solution even at relatively low concentrations

**Note: data has shown a relationship between oxalate excretion and increased risk of stones, but supersaturation alone is not sufficient to cause stone formation


Name (5) general risk factors for formation of kidney stones

  1. Previous renal disease (stones, PCKD, RTA, MSK, ESRD, transplant)
  2. Other past medical issues (IBD/short-gut, hyperparathyroidism, hypercalcemia, gout, HIV)
  3. Family history (multiple family members affected)
  4. Social history (dehydration)
  5. Diet (low fluids, high salt, high protein, low calcium, high oxalate)


Does decreased dietary calcium increase or decrease risk of stone formation?

increased risk


Name some common clinical presentations of kidney stones

  • Renal colic
  • hematuria
  • fever, chills
  • nausea, vomiting
  • dysuria
  • passed stones (there can be multiples)


Name some common physical exam findings seen with kidney stones

  • distress (often pacing around room)
  • CVA/abdominal tenderness
  • fever
  • hematuria
  • elevated WBCs
  • elevated serum creatinine
  • positive findings on imaging studies


What is the gold-standard imaging methodology for identifying kidney stones?

What else might be used (though less effectively)?

CT Scan


IVP and KUB are old methods, mostly fallen out of favor


What major type of kidney stone is radiolucent (i.e. won't be picked up with x-ray imaging)?

uric acid stones


Name the crystal type based on appearance:

  1. round/amorphous
  2. square/rectangular tetrahedal
  3. lemon-shaped
  4. rectangular-euhedral


Describe the acute treatment of kidney stones

  • noninvasive - pain control, fluids, expulsive or dissolution therapy
  • extra-corporeal shock wave therapy (ESWL)
  • Ureteroscopy -> lithotripsy or stone basketing
  • Percutaneous surgical removal


Describe the treatment strategy for chronic cystine stones

  • dilution of urine
  • alkalinization of urine
  • cystine-binding drugs -> penicillamine, tiopronin, captopril


Describe the treatment strategy for chronic uric acid stones

  • dilution of urine
  • low-protein/high-fruit diet
  • alkalinize urine (increases solubility of urate)
  • xanthine oxidase inhibitors (allopurinol, febuxostat)


Describe the treatment strategy for chronic struvite stones

  • Dilution
  • Sterilize urine (eliminate urea-splitting bacteria)
  • surgical removal of residual stone material
  • adjunctive therapies: urease inhibitors (acetohydroxamic acid), chemolysis (hemiacidirin)


Describe the treatment strategy for chronic calcium stones

  • dilution
  • maintenence of calcium intake
  • reduce urine calcium excretion (sodium restriction and thiazide diuretics)
  • reduce urine oxalate excretion (diet oxalate restriction, add pyridoxine)
  • increase urine citrate (diet: decrease protein and increase fruit, add citrate or bicarb supplements)

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