Kidney Stones - Wesson Flashcards

1
Q

Sponge Kidney Disease typically features calcifications where?

A

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

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2
Q

Where does nephrocalcinosis typically appear?

A

tubules and interstitial spaces

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3
Q

What is the typical etiology kidney stone disease?

A

idiopathic

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4
Q

What is the most common composition of a kidney stone?

A

Calcium-oxalate or Calcium-phosphate

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5
Q

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

A

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

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6
Q

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

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

A

5-15% (annual incidence 1:1000)

men > women (2:1)

whites > other races

peak incidence in middle age

**also: substantial regional variation (diet?)

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7
Q

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

A
  • indinavir
  • acyclovir
  • triamterene
  • sulfamethoxazole
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8
Q

What is the etiology of cystinuria?

What is its approximate prevalence in the population?

A

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

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9
Q

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

A
  • 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%)

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10
Q

Describe primary hyperoxalosis/hyperoxaluria

A

Rare genetic liver enzyme disorder leading to excessive endogenous oxalate synthesis

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11
Q

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

A

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
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12
Q

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

A

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

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13
Q

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

A
  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)
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14
Q

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

A

increased risk

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15
Q

Name some common clinical presentations of kidney stones

A
  • Renal colic
  • hematuria
  • fever, chills
  • nausea, vomiting
  • dysuria
  • passed stones (there can be multiples)
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16
Q

Name some common physical exam findings seen with kidney stones

A
  • distress (often pacing around room)
  • CVA/abdominal tenderness
  • fever
  • hematuria
  • elevated WBCs
  • elevated serum creatinine
  • positive findings on imaging studies
17
Q

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

What else might be used (though less effectively)?

A

CT Scan

ultrasound

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

18
Q

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

A

uric acid stones

19
Q

Name the crystal type based on appearance:

  1. round/amorphous
  2. square/rectangular tetrahedal
  3. lemon-shaped
  4. rectangular-euhedral
A
20
Q

Describe the acute treatment of kidney stones

A
  • noninvasive - pain control, fluids, expulsive or dissolution therapy
  • extra-corporeal shock wave therapy (ESWL)
  • Ureteroscopy -> lithotripsy or stone basketing
  • Percutaneous surgical removal
21
Q

Describe the treatment strategy for chronic cystine stones

A
  • dilution of urine
  • alkalinization of urine
  • cystine-binding drugs -> penicillamine, tiopronin, captopril
22
Q

Describe the treatment strategy for chronic uric acid stones

A
  • dilution of urine
  • low-protein/high-fruit diet
  • alkalinize urine (increases solubility of urate)
  • xanthine oxidase inhibitors (allopurinol, febuxostat)
23
Q

Describe the treatment strategy for chronic struvite stones

A
  • Dilution
  • Sterilize urine (eliminate urea-splitting bacteria)
  • surgical removal of residual stone material
  • adjunctive therapies: urease inhibitors (acetohydroxamic acid), chemolysis (hemiacidirin)
24
Q

Describe the treatment strategy for chronic calcium stones

A
  • 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)