Exam 2: Urolithiasis DSA

Question 1

Nephrolithiasis

Main types of renal calculi

Answer 1

• Approximately 75% of stones are Ca-based
  
  • the majority Ca oxalate, associated with
    
    • hypercalciuria and/or hyperoxaluria
  • also Ca phosphate and other mixed stones
• 15% struvite
  
  • magnesium-ammonium-phosphate
• 5% uric acid
• 1% cystine

Question 2

Nephrolithiasis

Signs and symptoms

Answer 2

• Stones in the renal pelvis may be asymptomatic or cause hematuria
• Obstruction related to the passing of a stone leads to
  
  • severe pain, often radiating to the groin
  • sometimes accompanied by intense visceral symptoms
    
    • i.e., nausea, vomiting, diaphoresis, light-headedness
  • hematuria
  • pyuria
  • urinary tract infection (UTI)
  • and, rarely, hydronephrosis.
• In contrast, staghorn calculi
  
  • associated with recurrent UTI with urea-splitting organisms
    
    • (Proteus, Klebsiella, Providencia, Morganella, and others
  • may be completely asymptomatic
  • presenting with loss of renal function

Question 3

Answer 3

• Calcium oxalate crystals
  
  • Calcium oxalate bihydrate crystals appear as colorless bipyramids of various sizes “envelope form” (left image)
  • Calcium oxalate monohydrate crystals are colorless and can assume several shapes, including ovoids, biconcave disks, rods and dumbbells (right image)
• Most stones are composed of Ca oxalate.
• These may be associated with hypercalciuria and/or hyperoxaluria.
• Hypercalciuria can be seen in association with
  
  • a very high-Na diet
  • loop diuretic therapy
  • distal (type I) renal tubular acidosis (RTA)
  • sarcoidosis
  • Cushing’s syndrome
  • aldosterone excess
  • or conditions associated with hypercalcemia
    
    • e.g., primary hyperparathyroidism, vitamin D excess, milk-alkali syndrome
    • or it may be idiopathic.
• Hyperoxaluria may be seen with
  
  • intestinal (especially ileal) malabsorption syndromes
    
    • e.g., inflammatory bowel disease, pancreatitis
      
      • due to reduced intestinal secretion of oxalate and/or the binding of intestinal Ca by fatty acids within the bowel lumen
      • with enhanced absorption of free oxalate and hyperoxaluria.
• Ca oxalate stones may also form due to
  
  • (1) deficiency of urinary citrate
    
    • an inhibitor of stone formation
      
      • that is underexcreted with metabolic acidosis
  • (2) hyperuricosuria
    
    • presence of excessive amounts of uric acid in the urine

Question 4

Answer 4

• Ca phosphate crystals
• Ca phosphate stones are much less common
• tend to occur in the setting of an abnormally high urinary pH (7–8)
• usually in association with a complete or partial distal RTA.

Question 5

Answer 5

• Struvite stones
  
  • Triple phosphate, or struvite, crystals
    
    • described as having a “coffin-lid”-shaped appearance. (left)
    • microscopy with UTIs may show significant leukocyturia (right)
• Struvite crystals
  
  • are composed of magnesium ammonium phosphate.
  • They are typically seen in alkaline urine, with a urine pH > 7.0.
• Staghorn calculi and obstruction
  
  • Struvite is the most common component
  • Struvite stones form in the collecting system when infection with ureasplitting organisms.
• Risk factors include
  
  • previous UTI
  • nonstruvite stone disease
  • urinary catheters
  • neurogenic bladder
    
    • e.g., with diabetes or multiple sclerosis
  • and instrumentation

Question 6

Answer 6

• Uric acid stones
  
  • Uric acid crystals can vary in both size and shape
    
    • They can look like
      
      • barrels
      • rosettes
      • rhomboids
      • needles
      • hexagonal plates.
    • They are usually amber in color
      
      • However, urate crystals may assume the color of any pigment
• Uric acid stones develop when the urine is saturated with uric acid in the presence of an acid urine pH
• pts typically have
  
  • underlying metabolic syndrome
  • and insulin resistance
  • often with clinical gout
• associated with
  
  • a relative defect in ammoniagenesis
  • and urine pH that is <5.4 and often <5.0.
• Pts with myeloproliferative disorders and other causes of secondary
  hyperuricemiaandhyperuricosuriadue toincreased purine biosynthesisand/orurate production
  
  • are at risk for stones if the urine volume diminishes.
• Hyperuricosuria without hyperuricemia
  
  • may be seen in association with certain drugs
    
    • e.g., probenecid, high-dose salicylates

Question 7

Answer 7

• Cystine stones
  
  • In contrast to polymorphic urate crystals, cystine crystals are monomorphic, colorless hexagonal plates which look similar to benzene rings.
• Cystine stones are the result of a rare inherited defect in renal and intestinal transport of several dibasic amino acids
  
  • the overexcretion of cystine (cysteine disulfide)
    
    • which is relatively insoluble, leads to nephrolithiasis.
• Stones begin in childhood and are a rare cause of staghorn calculi
• they occasionally lead to end-stage renal disease.
• They are found in acidic urine, typically with a urine pH < 6.0

Question 8

Nephrolithiasis tx

general overview

Answer 8

• Treatment of renal calculi is often empirical, based on:
  
  • odds (Ca oxalate stones most common)
  • clinical history
  • and/or the metabolic workup.
• An increase in fluid intake to at least 2.5–3 L/d is perhaps the single
• *most effective intervention**, regardless of the type of stone.
• Conservative recommendations for pts with Ca oxalate stones (i.e., low-salt, low-fat, moderate-protein diet) are thought to be healthful in general and therefore advisable in pts whose condition is otherwise uncomplicated.
• In contrast to prior assumptions, dietary calcium intake does not contribute to stone risk; rather, dietary calcium may help to reduce oxalate absorption and reduce stone risk.

Question 9

workup for an outpatient with a renal stone

Answer 9

Question 10

Specific Therapies For Nephrolithiasis:

Stone type: Calcium oxalate

Answer 10

• Dietary Modifications
  
  • Increase fluid intake
  • Moderate sodium intake
  • Moderate oxalate intake
  • therapy for fat malabsorption
  • Moderate protein intake
  • Moderate fat intake
• Other
  
  • Citrate supplementation (calcium or potassium salts > sodium)
  • Cholestyramine or other therapy for fat malabsorption
  • Thiazides if hypercalciuric
  • Allopurinol if hyperuricosuric

Question 11

Specific Therapies For Nephrolithiasis:

Stone type: Struvite

Answer 11

• Dietary Modifications
  
  • Increase fluid intake
  • same as calcium oxalate if evidence of calcium oxalate nidus for struvite
• Other
  
  • Methenamine and vitamin C
  • or daily suppressive antibiotic therapy
    
    • e.g., trimethoprimsulfamethoxazole

Question 12

Specific Therapies For Nephrolithiasis:

Stone type: Uric acid

Answer 12

• Dietary Modifications
  
  • Increase fluid intake
  • Moderate dietary protein intake
• Other
  
  • Allopurinol
  • Alkali therapy (K+ citrate)
    
    • to raise urine pH to 6.0–6.5

Question 13

Specific Therapies For Nephrolithiasis:

Stone type: Cystine

Answer 13

• Dietary Modifications
  
  • Increase fluid intake
• Other
  
  • Alkali therapy
  • Penicillamine