Nephrolithiasis

Question 1

What do “metabolic activity” and “anatomic activity” refer to with regard to kidney stones?

Answer 1

Metabolic: growth of new stones.
Anatomic: movement of stones causing symptoms.

Question 2

Do people normally get fevers when passing stones?

Answer 2

Nope. If they do, there may be an infection… which is an emergency.

Question 3

4 most common types of kidney stones?

Answer 3

Calcium oxalate / calcium phosphate. (most common)
Uric acid.
Struvite (infection-related).
Cystine.

Question 4

What’s an initial lesion that often precedes the development of calcium oxalate kidney stones?

Answer 4

Randall’s plaques - depositions of calcium phosphate.

Question 5

Most of us have super-saturated urine. Why don’t we all have stones?

Answer 5

Inhibitors of stone formation, such as citrate, are present.

Question 6

Two inhibitors of stone precipitation?

Answer 6

Citrate.

Tamm-Horsfall protein.

Question 7

3 categories of physiologic risk factors for stone formation?

Answer 7

Increased crystalloid concentration.
Increased promoters (of stone precipitation).
Decreased inhibitors.

Question 8

3 factors that increase risk for stones by increasing cystalloid concentration?

Answer 8

Hypercalciuria.
Hyperoxalaturia.
Low urine volume. (drink more water!)

Question 9

3 factors that increase risk for stone formation by “promoting” stone formation?

Answer 9

Hyper uricemia.
Akaline urine pH -> risk for calcium oxalate stones.
Acid urine pH -> risk for uric acid stones.

Question 10

95% of kidney stone patients with hypercalciuria have what condition?

Answer 10

Idiopathic hypercalciuria (most don't have hypoPTH).
This has similar risk factors to those for cardiovascular disease.

Question 11

3 common ways to have more Ca++ end up in the urine?

Answer 11

Increased calcitriol -> increased intestinal absorption.
Increased PTH -> increased Ca++ release from bone.
Impaired renal *reabsorption.
*corrected (but impaired excretion wouldn’t make sense anyway)

Question 12

Effect of high Na+ diet on urine calcium levels? How?

Answer 12

High Na+ diet leads to reduced Na+ reabsorption in the proximal tubule.
Reduced Na+ reabsorption -> reduced Ca++ reabsorption -> hypercalciuria.
(salt restriction often improves idiopathic hypercalciuria)

Question 13

Does restricting Ca++ in diet help prevent stone formation?

Answer 13

Nope, increased Ca++ consumption usually reduces stone risk.

Ca++ supplements, though, can be a problem.

Question 14

What’s a condition that would cause you to absorb more oxalate than usual?

Answer 14

Fat malabsorption -> oxalate hyperabsorption.
“enteric hyperoxaluria”
(the free fatty acids in the lumen actually chelate Ca++, preventing Ca++ from chelating oxalate… or it might have something to do with bacteria not metabolizing oxalate)

Question 15

How does Ca++ intake affect the amount of oxalate excreted in urine?

Answer 15

Low Ca++ intake -> increased oxalate in urine. (part of the reason it’s not helpful to restrict Ca++ intake to prevent stone formation)

Question 16

Common cause of hypocitraturia?

Answer 16

Acidosis. which increaseds renal citrate catabolism.

Question 17

5 causes of acidosis associated with hypocitraturia?

Answer 17

High protein diet.
Distal RTA. (and carbonic anhydrase inhibitors)
K+ depletion (-> intracellular acidosis).
Renal insufficiency.
Diarrhea (loss of alkali)

Question 18

What’s an outcome of chronic hypercalciuria from distal RTA that you could see on an x-ray?

Answer 18

Medullary nephrocalcinosis

Question 19

2 main physiologic risk factors for uric acid stones? Which is much more common?

Answer 19

Persistently acid urine (often due to ammonia production defect) - 80% of cases.
Hyperuricosuria. - 20% of cases.

Question 20

Why is obesity associated with persistently acid urine (and thus uric acid stones)?

Answer 20

Insulin resistance -> impaired ammonia synthesis -> acid urine

Question 21

Why does acid urine promote uric acid stone formation?

Answer 21

Henderson-Hasselbalch stuff: The lower the pH, the more uric acid and the less urate.
Urate, being charged, is wayy more soluble than uric acid.

Question 22

Treatment for uric acid stones?

Answer 22

Potassium citrate.

Allopurinol if the cause is from hyperuricosuria.

Question 23

In what setting would you typically see a staghorn calculus?

Answer 23

Infection, perinephric abscess, renal failure.

Question 24

What’s the mechanism for infection stone formation?

Answer 24

Infection with urease-positive bacteria (eg. Proteus) -> extremely alkaline urine -> struvite deposition.

Question 25

Probably not important to know but… what’s struvite?

Answer 25

“Triple phosphate”: Calcium, ammonium, and magnesium phosphate.

Question 26

Cause of cysteine stones?

Answer 26

Inherited defect in cysteine reabsorption via a transporter that handles cysteine, ornithine, arginine, and lysine (COAL).

Question 27

3 treatments for cysteine stones?

Answer 27

High fluids
Alkali (K citrate)
Penacillamine, tiopronin (to break sulfide bonds, form adjuncts, makings stuff more soluble)

Question 28

Which diuretic could you give to help someone with stones caused by hypercalciuria?

Answer 28

A thiazide. (recall that thiazides predisopose to hypercalcemia… due to less output in urine)

Question 29

3 urological stone removal techniques?

Answer 29

Ureteroscopy with basket or laser.
Percutaneous nephrolithotomy.
Extracorporeal shock wave lithotripsy.

Question 30

If you see a patient with recurrent stones, should you make sure that they get treatment / counseling to help prevent more stones in the future?

Answer 30

Yes, you should.