Nephrolithiasis Flashcards

1
Q

Describe the epidemiology of stone disease, and what subpopulations are at high risk for different types of stones.

A
  • 12% of men; 6% of women; increasing rate
  • Less prevalent in African-Americans
  • More common during summer months (hydration related)
  • In U.S. = more common in SE
  • More common in middle age
  • Recurrent: 50-60% within 10 years
  • Both genetic and environmental factors

Most stones:
o Low urine volume
o Low Ca2+ diet

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2
Q

Describe the associated diseases with each type of stone

A
Oxalate stones:
o	Hypertension (especially in women)
o	Associated diseases: inflammatory bowel disease, short bowel syndrome, hyperparathyroidism, polycystic kidney disease, medullary sponge kidney
o	Medications: high dose Vit C and Ca2+ supplements

Calcium stones
o High sodium and protein diet
o Associated diseases: Sarcoid

Uric acid stones
o High sodium and protein diet
o Low urine pH
o Associated diseases: metabolic syndrome

Calcium phosphate
o High urine pH
o Associated diseases: hyperparathryroidism, Type I RTA
o Medications: Carbonic anhydrate inhibitors

Struvite stones
o High urine pH
o UTI’s

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3
Q

Differentiate the fundamental pathologic differences between initiation of calcium oxalate stones and calcium phosphate stones.

A

Calcium oxalate
o May have nidus of uric acid or calcium phosphate
“Randall’s Plaques” = initiators
• White deposits on papillae
• Interstitial deposits of CaP on BM of thin loops of Henle, with thin layers of protein matrix
o Calcium oxalate deposits on plaques = grow
o Penetrate into uroepithelium
o Number of plaques = associated with higher urinary Ca2+ and lower urinary volumes

Calcium phosphate (“brushite” stones)
o Crystals deposit in medullary collecting ducts (“Intratubular” crystals)
o Result: damaged and scarring of the renal papillae

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4
Q

Identify the three major physicochemical factors in stone formation

A
  1. Supersaturation
    a. Changes with pH, presence of inhibitors and promoters in urine
    b. Urine volume is important
  2. Urine pH
    a. Determines solubility
    b. High pH → Calcium phosphate stones
    c. Low pH → Uric acid
  3. Inhibitors:
    a. Citrate: chelates urinary Ca2+ and inhibits Ca2+ crystal growth by aggregation
    b. Pyrophosphate
    c. Proteins
    d. Glycosaminoglycans
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5
Q

Describe calcium oxalate stones

A

o Most common type

Causes:
• Most = idiopathic (30-60%)
• Primary hyperparathyroidism (10%)
• Hypocitraturia
• Hyperoxaluria (primarily genetic; could also be dietary or enteric: short bowel syndrome, IBS causing hyper-absorption)
• Hyperuricosuria (heterotopic calcification)
• Other: ADPKD, medullary sponge kidney, Vitamin C

Oxalate absorption:
• Apical intestine transporter (Slc26a6) regulates serum oxalate and urinary oxalate excretion
Oxalobacter formigenes:
• GN anaerobe in 60-80% adult feces
• Metabolizes oxalate in gut
• Affected by antibiotics and dietary oxalate
• More prevalent in non-stone formers

Dietary oxalate (the 8)
•	Spinach
•	Rhubarb 
•	Beets and beet greens
•	Black and green tea
•	Chocolate/cocoa 
•	Some nuts and seeds
•	Soybeans and soy foods (not processed with Ca2+)
•	Potatoes
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6
Q

Describe calcium phosphate stones

A

o Associated with Type I RTA or hyperparathyroidism

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7
Q

Describe uric acid stones

A

(10% of stones)
o Radiolucent on x-ray

Associated with high uric acid levels, gout
• Xanthine stones = with use of Allopurinol

Associated with metabolic syndrome
• Patients have decreased NH4+ excretion → low urine pH

o Seen with urine pH < 6.0
o Treatment: alkalization of pH with Potassium citrate (goal > 6.5)

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8
Q

Describe struvite stones

A

(AKA “Triple Phosphate”)
o Special type of calcium stones
o Due to UTI with urea splitting organism (ex: Proteus, Providencia, Klebsiella, Pseudomonas, enterococci)
o Grow rapidly = very large stones
o May be asymptomatic or have vague flank pain (no acute renal colic)
o Very alkaline urine: pH >7.0
o Coffin-lid crystals in urine
o Treat: surgical intervention (not respond to metabolic therapies)

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9
Q

Describe cystine stones

A

Uncommon ( female
• 1st stone in 2nd or 3rd decade

Diagnosis:
• Hexagonal crystal appearance
• Cyanide-nitroprusside test (measures urine cysteine excretion; positive if >75 mg/L)

Treatment:
• High fluid intake → Decrease urinary cystine concentration to 7
• Moderate sodium and protein restriction
• Cysteine-binding drugs (Tiopronin, D-penicillamine Captopril) but side effects

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10
Q

Diagnosis for kidney stones

A

Labs: electrolytes (K+, HCO3-, Ca2+, PO4) to rule out RTA type I or hyperkalemia (hyperparathyroidism); CBC for infection

Urinalysis: microhematuria (gross hematuria may occur); crystal appearance

Differential: pyelonephritis (also have pyuria and fever, not sudden onset), renal papillary necrosis, renal artery or vein occlusions

Imaging:
• X-ray may show stone (only if radiopaque)
• CT scan with contrast (definitive study; 98% PPV, 95% NPV)

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11
Q

Prognosis for stone passage:

A

o less than 0.5 cm: almost always pass
o 0.5-1.0 cm: may pass (50% spontaneously pass)
o greater than 1 cm do not pass, need intervention to eliminate

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12
Q

Stone treatment

A

If likely to pass:
• Hydration with IV fluids
• At home: oral fluids (>2 L/day), pain medications, strain urine for stone

Medical expulsive therapy (MET)
• Medications dilate ureter to help stones pass
• Uses alpha-blockers (tamsulosin)
• Side effect: lower BP

Hospitalization:
o Coexistent UTI with obstruction
o Stones > 1 cm if require intervention
o Obstruction of both kidneys or unilaterally functioning kidney resulting in kidney failure
o If patient can’t tolerate pain or keep fluids down

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13
Q

Describe the diagnostic tests for recurrent calcium stone disease

A

o Stone analysis
o Bicarbonate, phosphorus, calcium, uric acid levels
o Intact PTH level, vitamin D level

UroRisk profile:
• 24 hr urine collection measuring urine concentrations of Na+, Ca2+, phosphorus, uric acid, oxalate, citrate, creatinine, pH and urine volume
• Defines which solutes are high = could be contributing
• Sees if lack of inhibitor present
• Checks acid-base status

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14
Q

Describe the specific therapies for recurrent calcium stone disease, uric acid stones, cystine stones, and struvite stones

A

Calcium stones:
• Hypercalciuria; sodium restriction, thiazide diuretics (increases Ca2+ reabsorption)
• Hypocitraturia: potassium citrate
• Hyperoxaluria: oxalate restriction
• Nidus of uric acid: allopurinol (lowers serum uric acid)
• ***Important not to restrict dietary Ca2+ because it binds oxalate in gut, preventing absorption

Uric acid stones:
• Urine alkalinization (K+ citrate) → increase urine pH >6.0
• Low purine diet
• Allopurinol

Cysteine stones:
• Increase fluids (Goal >3L) → decrease cysteine in urine to 7.0
• Cysteine-binding drugs (Penicillamine, Thiola, Captapril)

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15
Q

Surgical therapies for stones

A

Indications:
• Struvite (infection) stones
• Stones that don’t pass in ureter = cause persistent obstruction

Methods:
Ureteroscopy (URS) = destroys stones in ureter
• YAG laser
• Ultrasonic
• Electrohydraulic lithotripsy
Extracorporeal shock wave lithotripsy (ESWL) = pulverizes stones in upper tracts; also pelvocalcyceal stones
Percutaneous nephrolithotomy (PCNL) = pelvocalcyceal stones

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16
Q

List nutritional adjustments recommended for patients with nephrolithiasis.

A

Prevention:
o Adequate fluid intake: minimum 2 L/day

Calcium:
• Low Ca2+ diet not effective; may contribute to more stones
• Increases oxalate absorption → increased excretion in urine → increased risk of calcium oxalate formation
• Meet DRI for Ca2+ (1000 mg/day for ages 19-50; 1200 mg/day for >50)
• Citric acid in fruits and vegetables → increases citrate excretion
• Complexes with Ca2+ = Ca2+ can’t bind with oxalate or phosphate → Inhibits growth of Ca2+ stones

Protein
• Moderate protein intake recommended
• Because high protein diet increases Ca2+ excretion, acidifies urine

Oxalate
• If make Calcium oxalate stones, can limit oxalate intake
• Foods high in oxalate: spinach/leafy greens, rhubarb, beets, nuts, chocolate
• Most patients benefit from normal Ca2+ intake timed with meals to enhance oxalate binding in GI tract
• Other strategies to decrease oxalate: fish oil, pyridoxine, elimination of excessive ascorbic acid intake from supplements

Sodium
• Limit to 2-3 g/day (DRI is lower = 1.5 g/day)
• Higher Na+ decreases renal tubular Ca2+ reabsorption → increased Ca2+ excretion