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Renal Week 2 > Lecture 24: Nephrolithiasis > Flashcards

Lecture 24: Nephrolithiasis Flashcards

1
Q

Why do kidney stones develop?

A

The develop as a result of the cost of excreting insoluble minerals in (aqueous) urine

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2
Q

What is the epidemiology of nephrolithiasis?

A
  1. White and Hispanic predominance
  2. 12% lifetime incidence in men
  3. 7% lifetime incidence in women
  4. Summer and early fall = summer predominance of kidney stone prevalence
  5. recurrence is the rule
    -50% recurrence in 5 years
    -80% recurrence in 30 years
    More common in Middle East and the South of the USA
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3
Q

Why has there been a recent explosion of stone incidence?

A
  1. high protein intake
  2. obesity
  3. diabetes
  4. metabolic syndrome
  5. global warming
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4
Q

What are the clinical features of nephrolithiasis?

A
  1. Renal colic, morbidity, economic cost
  2. hematuria (91% of patients)
  3. fever implies concomitant infection and risk of sepsis
  4. Renal failure is unusual (only occurs with bilateral obstruction)
    • can also occur with renal tubular acidosis, cystinuria and infection stones
  5. Spontaneous passage is the rule
    • 90% spontaneously pass
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5
Q

What is renal colic?

A 
Flank pain that radiates to the lower abdomen and groin
Extreme severity (worse than pregnancy)
Cause of pain is obstruction of urinary tract that then leads to expansion of kidney
What is colic?
Severe, often fluctuating pain in the abdomen caused by intestinal gas, obstruction in intestines or kidney stones
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6
Q

What are the dimensions of stones that pass? That don’t pass?

A

Stones that pass 7mm

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7
Q

What does metabolic activity of nephrolithiasis mean?

A

It means that there was new stone growth, growth of existing stone or “gravel” that ultimately caused the symptoms
In a CT scan, if you see a lot of tiny stones (“gravel”), then it is a sign of fresh stone formation

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8
Q

What does anatomic activity say about nephrolithiasis?

A

Anatomic activity = movement of existing stone to cause symptoms
Important because it means symptoms don’t mean recent stone formation

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9
Q

What are the stone types?

A
  1. Calcium oxalate and calcium phosphate
  2. Uric acid
  3. Infection stones (struvite)
  4. Cystine
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10
Q

What are the characteristics of stones made from calcium oxalate/calcium phosphate?

A

75% of all cases
Male predominance
Looks like the back of an envelope in urine

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11
Q

What are the characteristics of stones made from uric acid?

A

Radiolucent unless secondarily
15% of prevalence
Associated with gout and IBD
Looks like a football in urine

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12
Q

Wha are the characteristics of stones made from struvite?

A

Less than10% of prevalence
Most deadly
Form staghorns (extend from one calyx to another)
Formed from magnesium ammonium and phosphate
In the urine, looks lke coffin lids

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13
Q

What are the characteristics of cysteine stones?

A

Most rare form of stone
1%
Genetic defect in amino acid transport
Look hexagonal in urine

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14
Q

What are the histological features of the different stones?

A

Calcium oxalate stones = look like back of envelope
Uric acid crystals = rhomboid or football shapes
Struvite stones = coffin lids
Cystine stones = hexagonal plates

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15
Q

How do stones get started?

A

Stones must be adherent to somewhere in kidney or else they would just wash away
Anchor point = Randall’s plaques which are attached to the papilla
Formation of Randall’s plaques would account for observation that many calcium oxalate stones have calcium phosphate center
Rate of stone formation correlate with Randall’s plaques

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16
Q

What are Randall’s plaques?

A

Calcium phosphate plaques on external surface of renal papilla where a stone is anchored
Rate of stone formation ~ number of Randall’s plaques

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17
Q

What is the activity product ratio? Significance?

A 
Activity product = Calcium concentration * oxalate concentration
Activity product (the product of the amount of calcium and oxalate in urine) has a saturation point
	-past this saturation point, there exists a metastable regioin, where ions are able to be secreted, but nucleation (precipitation) has not yet begun to happen
	-normally, we are at the metastable region because there are inhibitors in urine that prevent nucleation
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18
Q

What is the formation product?

A

Upper limit of metastability
Determined by dripping one ion of an ion pair (say oxalate) into urine until stone precipitation in solid phase is observed

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19
Q

How do stone formers compare to normal chart above?

A

Stone formers usually have higher activity product (more calcium/oxalate concentration)
As well
As a lower formation product, so it is easier to get into the nucleation range

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20
Q

What prevents stones?

A
  1. Citrate (small)
  2. Magnesium (small)
  3. Tamm-Horsfall protein (large, considered a polyanion)
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21
Q

Why is citrate important in mediating nephrolithiasis?

A

Citrate forms a soluble complex with calcium so keeps calcium ions from participation in nucleation

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22
Q

Why is magnesium important in mediating nephrolithiasis?

A

Mg forms a soluble complex with oxalate so keeps oxalate from participation in nucleation

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23
Q

What are risk factors for calcium stone formation?

A
  1. increased crystalloid concentration
    i. hypercalciuria
    ii. hyperoxaluria
    iii. low urine volume
  2. Increased promoters
    i. hyperuricosuria
    ii. alkaline urine pH which favors calcium phosphate formation
    iii. acid urin pH (uric acid stones)
  3. Decreased inhibitors
    i. Hypocitraturia
24
Q

What is the most important risk factor for kidney stones?

A

Hypercalciuria

Occurs in 50% of calcium stone formers

25
Q

Why does low urine volume increase risk for nephrolithiasis?

A
  1. low urine volume increases crystalloid concentrations
  2. Risk increase sharply at urine volume below 1 L/day
  3. Climate/season, occupation, urological issues, social factors, things that make you sweat a lot!
26
Q

What is the relationship between activity product ratio and urine volume?

A

The higher the urine volume, the lower the activity product ratio

27
Q

Thus what is a treatment for nephrolithiasis?

A

Increase fluid intake inorder to increase urine volume which decreases activity product ratio

28
Q

What are the characteristics of hypercalciuria?

A

95% of hypercalciuria is idiopathic so we don’t know shit!
The 5% have hyperparathyroidism
Patient profile: white, obese and HTN
Polygenic inheritance, so some genetic component
Not helpful to evaluate the cause of hypercalciuria (either increased reabsorption, increased renal “leak,” or increased bone resorption) because patients often have a combination of all 3
Pathogenesis of idiopathic hypercalciuria could be due to increased vitamin D activation or defect in calcium reabsorption in the kidney
-again the emphasis is that the mechanism is unknown

29
Q

What are parts of the diet that contribute to stones?

A
  1. high salt
  2. high protein
  3. calcium (low and high uncertain)
    High salt diet will increase calcium in the urine, so you want to restrict salt in order to enhance Ca uptake
    Do NOT restrict calcium intake because it does not help with hypercalciuria
    i. further more it has been shown that increasing dietary calcium actually decreases stone risk, possibly by binding and getting rid of oxalate
    ii. also, most patients are at increased risk of osteoporosis so need the calcium
    Very few people take in too much calcium (Wasserstein has only seen 5 patients)
30
Q

What are the characteristics of hyperoxaluria?

A

Oxalate is COOH-COOH
A metabolic endproduct without physiological function
Hard to measure
Hard to treat
Role of oxalate in calcium stone formation is equivocal (unknown) because epidemiological studies don’t show it is not as important as citrate/calcium levels

31
Q

What are the causes of hyperoxaluria?

A
  1. Primary hyperoxaluria
    • gene defect that can lead to either kidney failure due to excessive sodium-oxalate accumulation in kidneys or kidney stones later in life (disorder has to be one or the other)
  2. Hyperabsorption from spinach, peanut butter, rhubarb, chocolate
  3. Enteric oxaluria (intestinal malabsorption)
  4. Low dietary calcium = higher urine oxalate
32
Q

How does intestinal malabsorption lead to increase in oxalate in urine?

A

Intestinal malabsorption  increase of FFA in intestinal lumen  FFa binds to Ca in insoluble soaps, thus taking Ca away from oxalate  without Ca to bind to, oxalate becomes absorbable in the lumen of the GI tract, therefore being absorbed
Takehome point: Ca-Oxalate = NOT easily absorbed in GI tract
Oxalate not bound to Ca = easily absorbed in GI tract

33
Q

What is the treatment for hyperoxaluria?

A

Increased calcium intake in order to bind GI lumen oxalate (may be an explanation for why high calcium helps decrease stone formation)
Decreased dietary oxalate
Cholestyramine, something that is used to bind FFAs and decrease FFA-Ca interaction

34
Q

What is the entric oxaluria theory?

A

A theory that oxalobacter, a bacteria that lives in oxalate, could be the key determinant for oxalate absorption in GI tract
Less oxalobacter = more oxalate absorption
Bile salts and antibiotics decrease oxalobacter and therefore may increase oxalate reabsorption and oxaluria
This is NOT PROVEN YET

35
Q

What are the key characteristics of hypocitraturia?

A

Caused by acidosis, which increases renal citrate catabolism
Citrate is used to inhibit nephrolithiasis, specifically by complexing with calcium to prevent Ca-phosphate interaction in urine

36
Q

How does acidosis lead to hypocitraturia?

A

Acidosis leads to renal tubular citrate catabolism by citrate lyase
Breakdown of citrate increases citrate reabsorption in the cell, leaving less citrate in urine to complex with Ca

37
Q

What are the causes of hypocitraturia?

A
  1. high protein diet (acid ash)
  2. Distal renal tubular acidosis (RTA)
    -caused by carbonic anhydrase inhibitors
  3. K depletion (intracellular acidosis by increasing
    H/K ATPase on apical membrane)
  4. Renal insufficiency
  5. Diarrhea (loss of alkali)
    All of these causes acidify the cell
38
Q

What are the risk factors for uric acid stones?

A
  1. Acidic urine (80%)
    -often due to defect in urinary ammonia production (no ammonia to buffer secreted protons)
  2. Hyperuricosuria (20%)
    Take home point: hyperuricosuria accounts for only a SMALL FRACTION of uric acid stone cases
    Most of the uric acid stones forms with just low pH urine
39
Q

What can cause acidic urine, a risk factor for uric acid stones?

A
  1. insulin resistance
  2. gout
  3. diarrhea/ileostomy
    • enhanced loss of alkali equivalents
40
Q

What is the treatment for uric acid stones?

A
  1. K-citrate is most effective treatment
    -this is a form of alkali treatment
    Helps convert uric acid (pH = 5 and 15% solubility) to urate (pH =7; solubility = 100%)
  2. Allopurinol in hperuricosuria or refractory uric acid stones
41
Q

What is the CT image of struvite stones?

A

Staghorn calculus (infection stones)
Due to infection
Arrows = episodes of separate stone formation
Due to UTI
Stones are connected to one another to look
Like an antler

42
Q

What are the characteristics of infection stones?

A

Most severe form of nephrolithiasis
Can lead to renal failure, sepsis and abscess
Seen in patients with urinary tract or bladder
Abnormality

43
Q

What is the mechanism through which infection stones are formed?

A

Urease positive UTI causes extremely alkaline urine
Infectious agent = Proteus and not E. coli
Urease breaks down urea to ammonia, and ammonia makes urine alkaline
Urine alkalinity  struvite stone formation
Known as a triple phosphate because alkaline urine contains Mg, NH4 and Ca, all of which can complex with phosphate

44
Q

What is struvite made out of?

A

Mg-NH4-PO4

45
Q

What organisms produce struvite stones?

A
  1. proteus
  2. klebsiella
  3. pseudomonas
  4. stah
    NOT E coli
46
Q

What are the characteristics of cystine stones?

A

Autosomal recessive
Increased cysteine excretion due to transporter that handles cysteine, ornithine, arginine and lysine (the COAL transporter)
-only urinary loss of cysteine is significant
Nitroprusside detects cystinuria

47
Q

How does one treat cystine stones?

A

High fluid intake (must drink at midnight and at 6am)
Pencillamine and tiopronin are drugs that make cystine most soluble
Hardest to treat

48
Q

What is the evaluation of nephrolithiasis?

A

Diseases to screen for in stone formers:
i. HTN
ii. diabetes
iii. hyperthyroidism
iv. sarcoid
v. gout
vi. neurogenic bladder
vii. intestinal malabsorption
look for patients who take carbonic anhydrase inhibitors and calcium supplements (former is risk factor, latter is something that is good for preventing stones)
patients who have high protein/weight reducing diets (risk factor)
Look at stone and urine analysis to determine what type of stone
Then look at electrolytes, Cr, Ca, P and PTH levels
24 hour studies

49
Q

What is the treatment of nephrolithiasis?

A
  1. high fluids (2.5 L/day = most important advice
  2. moderate calcium = 2-3 dairy servicings a day
  3. low oxalate diet, fruit and vegetables, lemonade (not proven to work…so why put that on dumbass?)
  4. low salt and low animal protein for hypercalciuria
  5. use of thiazide diuretics
  6. Potassium citrate
50
Q

How does thiazide treat nephrolithiasis?

A

Reduces urine calcium excretion
Increases bone density
Used along with Na restriction

51
Q

What is the mechanism of action for thiazide treatment for hypercalciuria?

A

Thiazide actually has an anticalciuric effect on the PROXIMAL tubule
Does so by increasing sodium excretion in distal tubule and causing volume CONTRACTION at first
-this volume contraction then leads proximal tubule to reabsorb much more sodium/calcium
-thus thiazide decreases Ca urine by inducing a compensatory mechanism for ECF volume depletion
-that is why it is so important to prescribe concomitant Na restriction with thiazide!
No salt restriction = limited effectiveness of thiazide

52
Q

What are indications for thiazides?

A

HTN and hypercalciuria

53
Q

What are the adverse effects of thiazide diuretics?

A

K depletion

54
Q

What is the MoA of K-citrate for nephrolithiasis?

A

Increases urine citrate (alkali effect)
Increase urine pH to help with uric acid stones
Reduces urine calcium by increasing urine pH
Ideal for mixed calcium nd uric acid stones

55
Q

How does K-citrate increase pH in urine?

A

Citrate is metabolized into bicarb

56
Q

What is potassium citrate contraindicated for?

A

Hypercalciuria
Calcium phosphate stones
Both form stones in alkali conditions
Thus only give K-citrate for uric acid stones

57
Q

How are stones removed surgically?

A

Through ureteroscopy with basket
Laser to dissolve the stone
Percutaneous nephrolithotomy
Extracorpreal shock wave lithotripsy
-pass shock wave through liquid medium and focuses on the stone
-converts solid to fluid
However this is costly so better to prevent stones

Renal Week 2 (12 decks)

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