RENAL CALCULI—NEPHROLITHIASIS
I. Definition
A. Condition in which one or more stones are present in the pelvis or calyces of the kidney or in the ureter
B. Calculi may be composed of calcium oxalate, calcium phosphate, uric acid, struvite, or cystine.
II. Etiology
A. Approximately 10% of the population will develop urinary calculi during their lifetime.
1. More common in men
2. Usual age of onset is in the 30s.
3. Approximately 50% of patients will have a recurrence within 10 years.
B. Dehydration: occurs more frequently in hot, arid environments
C. Life stress
D. Supersaturation of urine with stone-forming salts
1. Overexcretion of salt or reduced urine excretion
2. May occur as a result of dietary overindulgence
E. Decreased stone inhibitors in urine (e.g., citrate, magnesium, pyrophosphate)
III. Risk factors
A. Gender/age
B. Family history
C. Geography
D. Certain types of food
E. Obesity
F. Stress
H. Bedridden
I. Gout
J. Low citrate levels
K. Irritable bowel syndrome (IBS)
L. AIDS medications
M. Urinary tract infections (UTIs)
N. Other medications (e.g., chemo, thyroid)
O. Drugs associated with stone formation:
1. Triamterene (Dyrenium)
2. Sulfonamides
3. Calcium/vitamin D supplements
4. Carbonic anhydrous inhibitors
5. Indinavir (Crixivan): protease inhibitor
P. Dietary influences
1. ↓renal acid excretion, precursor of uric acid→hyperuricosuria, ↓calcium oxalate solubility
2. Sodium ingestion: ↑Na excretion→↑Ca excretion and Ca mobilization from bone
3. Foods high in oxalate: ↑urinary oxalate excretion (e.g., nuts, chocolate, dark green leafy vegetables, rhubarb, beets, okra)
IV. Types
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A. Calcium stones constitute 80% of renal calculi.
B. Hypercalciuric calcium nephrolithiasis
1. Can be caused by absorptive, reabsorptive, and renal disorders
2. Absorptive (types I, II, and III)
a. Caused by increased absorption of calcium at the level of the small bowel (i.e., jejunum)
b. Treatment is focused on decreasing bowel absorption of calcium.
c. Type I is independent of calcium intake. Urine calcium is increased on a regular or even a low-calcium diet. Cellulose phosphate, 10-15 g 3 times a day with meals, binds to calcium and impedes bowel absorption.
i. Use cautiously in postmenopausal women because it can cause negative calcium balance and osteoporosis.
ii. May also result in hypomagnesemia
iii. Follow-up every 6 to 8 months for metabolic studies
iv. Thiazide therapy is an alternative to the preceding in the treatment of type I absorptive hypercalciuria.
(a) Decreases renal excretion of calcium
(b) Increases bone density by 1%/year
(c) Has limited long-term (less than 5 years) use
d. Type II is diet dependent. Decreasing dietary calcium by 50% (i.e., by 400 mg/day) decreases hypercalciuria. No specific medical therapy is available.
3. Resorptive
a. Because of hyperparathyroidism
b. Hypercalcemia, hypophosphatemia, and elevated levels of parathyroid hormones are present.
c. Surgical resection of the adenoma, which leads to hyperparathyroidism, cures the disease and the stones.
4. Renal hypercalciuria
a. Renal tubules are unable to reabsorb filtered calcium efficiently, and hypercalciuria occurs.
b. Hydrochlorothiazides (HCTZs) are effective as long-term therapy.
C. Hyperuricosuric calcium nephrolithiasis
1. Caused by dietary excess or uric acid metabolic defects
2. Treat with purine dietary restrictions or allopurinol or both
3. In contrast to uric acid calculi, these patients will maintain a urinary pH greater than 5.5.
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