Nephrolithiasis Flashcards
(30 cards)
What do “metabolic activity” and “anatomic activity” refer to with regard to kidney stones?
Metabolic: growth of new stones.
Anatomic: movement of stones causing symptoms.
Do people normally get fevers when passing stones?
Nope. If they do, there may be an infection… which is an emergency.
4 most common types of kidney stones?
Calcium oxalate / calcium phosphate. (most common)
Uric acid.
Struvite (infection-related).
Cystine.
What’s an initial lesion that often precedes the development of calcium oxalate kidney stones?
Randall’s plaques - depositions of calcium phosphate.
Most of us have super-saturated urine. Why don’t we all have stones?
Inhibitors of stone formation, such as citrate, are present.
Two inhibitors of stone precipitation?
Citrate.
Tamm-Horsfall protein.
3 categories of physiologic risk factors for stone formation?
Increased crystalloid concentration.
Increased promoters (of stone precipitation).
Decreased inhibitors.
3 factors that increase risk for stones by increasing cystalloid concentration?
Hypercalciuria.
Hyperoxalaturia.
Low urine volume. (drink more water!)
3 factors that increase risk for stone formation by “promoting” stone formation?
Hyper uricemia.
Akaline urine pH -> risk for calcium oxalate stones.
Acid urine pH -> risk for uric acid stones.
95% of kidney stone patients with hypercalciuria have what condition?
Idiopathic hypercalciuria (most don't have hypoPTH). This has similar risk factors to those for cardiovascular disease.
3 common ways to have more Ca++ end up in the urine?
Increased calcitriol -> increased intestinal absorption.
Increased PTH -> increased Ca++ release from bone.
Impaired renal *reabsorption.
*corrected (but impaired excretion wouldn’t make sense anyway)
Effect of high Na+ diet on urine calcium levels? How?
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)
Does restricting Ca++ in diet help prevent stone formation?
Nope, increased Ca++ consumption usually reduces stone risk.
Ca++ supplements, though, can be a problem.
What’s a condition that would cause you to absorb more oxalate than usual?
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)
How does Ca++ intake affect the amount of oxalate excreted in urine?
Low Ca++ intake -> increased oxalate in urine. (part of the reason it’s not helpful to restrict Ca++ intake to prevent stone formation)
Common cause of hypocitraturia?
Acidosis. which increaseds renal citrate catabolism.
5 causes of acidosis associated with hypocitraturia?
High protein diet.
Distal RTA. (and carbonic anhydrase inhibitors)
K+ depletion (-> intracellular acidosis).
Renal insufficiency.
Diarrhea (loss of alkali)
What’s an outcome of chronic hypercalciuria from distal RTA that you could see on an x-ray?
Medullary nephrocalcinosis
2 main physiologic risk factors for uric acid stones? Which is much more common?
Persistently acid urine (often due to ammonia production defect) - 80% of cases.
Hyperuricosuria. - 20% of cases.
Why is obesity associated with persistently acid urine (and thus uric acid stones)?
Insulin resistance -> impaired ammonia synthesis -> acid urine
Why does acid urine promote uric acid stone formation?
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.
Treatment for uric acid stones?
Potassium citrate.
Allopurinol if the cause is from hyperuricosuria.
In what setting would you typically see a staghorn calculus?
Infection, perinephric abscess, renal failure.
What’s the mechanism for infection stone formation?
Infection with urease-positive bacteria (eg. Proteus) -> extremely alkaline urine -> struvite deposition.
