The author has worked on the problem of urolithiasis (urinary stones) for 35 years, writing 94 articles. He has studied hypocitraturia, hypercalciuria and the links between gouty stones, obesity and insulin resistance. This article reviews progress of the past 35 years. Dr. Pak’s main interests have been the causes of stones and the prevention of the return of stones after treatment.
Much has been discovered about the causes of hypocitraturia. Hypocitraturia is associated with the following problems which cause intracellular acidosis: strenuous exercise, overuse of salt, overuse of animal products, distal renal tubular acidosis, poor potassium intake and chronic diarrhea. Hypocitraturia is common and promotes calcium phosphate crystal formation. Potassium citrate makes urine more alkaline, increases the excretion of citrate and protects from uric acid and calcium stones. Acidity causes hypocitraturia by reducing citrate reabsorption by the kidney.
One study showed that calcium citrate was more soluble and easier to absorb than calcium carbonate. Hypercalciuria can be caused by increased absorption of calcium in the intestine. Reduced parathyroid activity inhibits calcium reabsorption in the kidney and can cause hypercalciuria secondarily.
Gout seems to be a part of the metabolic syndrome, with obesity and insulin resistance. In gout, uric acid stones are formed. Uric acid is poorly soluble in acid urine. A high portion of patients with type II diabetes who are stone formers have uric acid stones. Gout has been found to be related to obesity and insulin resistance.
Dietary variables alter stone formation. Vitamin C consumption has been shown to enhance urine oxalate excretion. High dietary calcium increases urinary saturation of calcium oxalate. Potassium rich orange juice increases urinary pH. Potassium poor lemon and cranberry juice barely change pH. Orange and grapefruit juices are rich in potassium. Dr. Pak asserts that the ability of juices to alter urine pH depends on their potassium contents. Dietary sodium increases urinary calcium and reduces urinary citrate. Excess dietary sodium increases the risk of stone formation.
In 1996, Dr. Pak helped create a list of risks for stone formation, including the following: hypercalciuria, hypocitraturia, hyperoxaluria, hyperuricosuria, low urine pH, high urine pH and cystinuria. Serum calcium and parathyroid hormone tests of the blood help differentiate the causes of hypercalciuria.
Calcium restriction has no effect on urine calcium in people with normal calciuria (urinary calcium). Calcium restriction has a strong effect in hypercalciuria and may be used therapeutically. (Calcium restriction can increase bone loss.) Stones can be treated with hypocalciuric drugs combined with potassium citrate.
A simplified approach to treating urolithiasis is suggested by Dr. Pak. First, separate the patients with moderately-severe hypercalciuria from patients with normal urine calcium and those with mild hypercalciuria by a 24-hour urinary calcium on the patient’s normal diet. The moderately-severe patients are treated with thiazides, potassium citrate and diet adjustments. The dietary changes are restricted calcium, oxalate, sodium and animal protein with high intake of liquids. The rest of the patients get liberal calcium with some diet changes. If the patient has hypocitraturia and acute stone problems, consider potassium citrate.
CONCLUSION: Dr. Pak has had a long career treating urinary stones. He gives a simplified plan for treating stones depending on the severity of the problem. Hypocitraturia plays an important part in stone formation.
NOTE: Hypocitraturia is low urinary citrates. Read about the use of citrus beverages for treatment of hypocitraturia and kidney stones.
Hypercalciuria is high urinary calcium.
To read the author’s abstract of the article click on the link to the author’s title of the article above.