Stone Diseases Flashcards
nephrolithiasis - overview
*the presence of calculi (stones) in the kidney
*calculi are hard deposits of minerals and acid salts originated in the kidneys blocking the ureter making it painful when they pass
*sx typically include acute unilateral, colicky flank pain radiating to the groin, hematuria, and nausea or vomiting
multigenic vs. monogenic nephrolithiasis
*multigenic: result from environment and small contributions of many different genes that just tilt a little towards stone formation
*monogenic: a single-gene pathogenic cause of kidneys stones
demographic risk factors for multigenic nephrolithiasis
*middle aged
*white
*males
*sedentary
*American diet
*lives in stone belt (southeastern US)
*stones increasing in frequency due to poor dietary choices & obesity
pathophysiology of nephrolithiasis - chemical equilibrium (supersaturation)
*concentration of stone constituents, amount of water, and pH
*the major determinant of the concentration of stone constituents in the urine is the amount of water in the urine
*increased water intake and urine output is simply the most important treatment for ALL TYPES of nephrolithiasis
pathophysiology of nephrolithiasis - biochemical equilibrium
*urine is frequently supersaturated with stone constituents (promoters and inhibitors)
*the absolute concentration of stone constituents (e.g. calcium & oxalate) is NOT the sole determinant of stones
*many people with stones have normal urinary parameters, and many people without stones have abnormal parameters
inhibitors - substances that INHIBIT stone formation in the urine
- CITRATE: citrate binds to oxalate and prevents further deposition of calcium oxalate; covers site of crystal growth
- magnesium
- uromodulin
- glycosaminoglycans
- urinary prothrombin fragment 1
promoters - substances that PROMOTE stone formation in the urine
*stents in the GU tract are a nidus for precipitation
*other urinary tract proteins
calcium oxalate stones - overview
*MOST COMMON FORM OF KIDNEY STONE
*most important factors are:
-urine volume
-URINE CALCIUM
-urine sodium (increases urine calcium)
-urine oxalate
-urine pH
-other
*urine crystal: shaped like envelope or dumbbell
role of HYPERCALCIURIA → calcium oxalate kidney stones
*usually idiopathic (may be related to excess GI absorption or increased urinary calcium excretion; may be an autosomal dominant trait)
*secondary causes of hypercalciuria:
-hyperparathyroidism
-sarcoidosis
-excess vitamin D intake
role of increased urinary SODIUM → calcium oxalate kidney stones
*increased urinary sodium → INCREASED URINARY CALCIUM
*this is exaggerated in kidney stone formers
role of hyperoxaluria → calcium oxalate kidney stones
*dietary calcium binds dietary oxalate, so a low calcium diet can increase urinary oxalate
*dietary oxalate is found in: leafy greens, spinach, tea, cocoa, chocolate, high dose vitamin C
*metabolic disorders can play a role in oxalate metabolism
other factors that increase risk of developing calcium oxalate kidney stones
- a HIGH-PROTEIN, MEAT-CONTAINING DIET → increased risk
-this diet is acidic & high in sodium
-sodium → increased urinary calcium, decreased citrate (stone inhibitor), increased urine acid (stone promoter), and low dietary calcium increases oxalate absorption - DISTAL RENAL TUBULAR ACIDOSIS → increased risk
citrate as an inhibitor of calcium oxalate kidney stones
*citrate binds to oxalate and prevents further deposition of calcium oxalate
*covers sites of crystal growth
*important INHIBITOR of stone formation
*renal handling of citrate:
-most citrate is reabsorbed proximally
-an acidic environment favors citrate reabsorption
-hypokalemia favors citrate reabsorption
high protein, high meat diet → increased risk of calcium oxalate kidney stones
*increased urine acid excretion
*increased sodium excretion → increased calcium excretion
*increased uric acid excretion
*decreased citrate excretion
*decreased potassium content
low calcium diet → increased or decreased risk of calcium oxalate kidney stones ??
*low calcium diet → INCREASED risk of stone formation
dietary treatment of calcium oxalate stones
*increase fluid intake
*decrease sodium intake
*eat less protein, more vegetables
*potassium citrate if urinary citrate is low
*decrease sugar intake
calcium phosphate stones - overview
*associated with elevated urine pH > 6 (ALKALINE urine)
*seen in RENAL TUBULAR ACIDOSIS
*more common in WOMEN:
-women generally have a higher urinary pH
*urine crystal: wedge-shaped prism
calcium phosphate stones - dietary treatment
*low sodium intake (decreases urinary calcium)
*increase urine output to 2.5 liters
uric acid stones - overview
*2 common causes:
1. LOW URINARY OUTPUT
2. LOW URINARY pH
*urine crystal: rhomboid shape
note - high urinary uric acid excretion is NOT a predominant cause of uric acid nephrolithiasis
uric acid stones - treatment
*increase the urine pH (alkalinize the urine)
cystinuria - overview
*associated with INABILITY TO REABSORB:
-Cystine
-Ornithine
-Arginine
-Lysine
*NOT the same as cystinosis or homocystinuria
cystine stones - overview
*hereditary condition in which Cystine-reabsorbing PCT transporter loses function, causing cystinuria
*this transporter defect results in poor reabsorption of Cystine, Ornithine, Lysine, and Arginine
*cystine is poorly soluble and thus leads to stones
*urine crystal: hexagonal (“Sixtine” stones have SIX SIDES - see image)
struvite stones - overview
*frequently causes staghorn calculi
*magnesium ammonium phosphate
*bacteria containing urease metabolize urea into ammonium carbonate, and this leads to a very high urinary pH
*seen in setting of chronic UTI
*urine crystal: coffin lid (sarcophagus)
outcomes of kidney stones
*anatomic activity: stones move through GU tract
*metabolic activity: stones grow in size
*calculi may stay in one position and cause no problems
*passage may lead to renal colic
*obstruction may occur
