Title: Management of a 43 year old man with a history of recurrent calcium oxalate kidney stones
Key words: calcium oxalate, kidney stones, renal stones, calcium oxalate stones, renal damage, hyperoxaluria, oxalate excretion, citrate, calcium, pH, milk, dairy foods, malabsorption, hyperuricosuria, bile secretion, urinary, allopurinol, urate levels, chelator, alkalising effect, sedimentation rate, potassium citrate, animal protein, red meat, salt, refined sugars, rhubarb, strawberries, beans, spinach, peanuts, beetroot, chocolate, cocoa, black tea, low oxalate diet, herbal tea, cranberry juice, hypercalciuria, dehydration, purine, thiazides, magnesium, supplementation, electrolytes, urinary,
Date: Oct 2006
Author: Morgan, G
Management of a 43 year old man with a history of recurrent calcium oxalate kidney stones
Recurrent stone formation in the urinary tract is a relatively common clinical problem affecting around 10% of the population, of which some 67% are classified as calcium oxalate stones with a high 60% recurrence rate (Lapsley 2004). The incidence is higher in men and, untreated, the associated biochemical disturbances are progressive with age (Yagisawa 1999). Dietary and medical intervention measures are indicated given the associated morbidity and the possible long-term repercussions of renal damage.
Calcium oxalate stone formation has been linked to a number of abnormalities of renal function, notably low urinary output and pH, excessive calcium, urate and oxalate excretion, and low citrate excretion. Sedimentation of calcium oxalate crystals is a function of elevated calcium and oxalate concentrations and reduced levels of citrate, pH and urinary volume (Cupisti 1992). In the case under discussion, the rate of hyperoxaluria in men under 60 years old, for example, has been found to be around 56% (Yagisawa (1999). The high content of oxalates in certain foods point to a link to diet, a fact rendered more important by the increased intestinal absorption of oxalate shown by recurrent stone formers (Hesse 1999).
Calcium, taken in the form of milk, dairy products or supplements, is known to bind oxalates in the gut and prevent absorption (Smith 1991). Malabsorption with impaired bile secretion interferes with this ligating function of calcium resulting in increased urinary oxalate excretion and stone formation (Emmett 2003). A higher incidence of hyperuricosuria seen in recurrent stone formers is associated with oxalate stone formation (Yagisawa 1999). The formation of urate seeds may serve to catalyse this process (Grover 1994). Amongst this group, allopurinol has been found to be helpful in both reducing urinary urate levels and the formation of oxalate stones (Ettinger 1986, Sarig 1987). Oxalate stones are also frequently associated with a high urinary calcium to citrate ratio (Berg 1992). Increasing the excretion of citrate by oral supplementation has been shown to dramatically reduce oxalate stone formation by as much as 85% (Ettinger 1997). Citrate may act as a chelator here but, more likely, its efficacy is due to its alkalising effect, raising the urinary pH above the oxalate sedimentation pH of 4.5-5.5 dramatically reducing the rate of stone formation (Berg 1990). Urinary pH plays a critical role in oxalate stone formation. Formation of these types of stone is maximal during the night and early morning when the urinary pH is at its lowest (Robert 1994, Murayama 2001). Concomitantly, alkalising the urine at night with potassium citrate has been shown to lower oxalate stone formation by up to 75%, being more effective than spaced doses (Berg 1992).
High protein diets, along with salt and refined carbohydrates, as well as increasing calcium excretion, also lower urinary pH (Fellstrom 1984, Lapsely 2004). In one series (Fellstrom 1984), a high protein diet led to reductions in urinary pH, an increased calcium excretion of 35% and a lowering of citrate excretion by 25%. Such a picture is highly promotary of stone formation. Against this background, dietary measures are essential in the management of a 43 year old man with a history of recurrent oxalate stone formation. This involves the institution of a more alkalising diet with a reduction in the consumption of animal protein, especially red meat, salt and refined sugars, and an increase in the consumption of low-oxalate containing fruit and vegetables. Rhubarb, strawberries, beans, spinach, beetroot, peanuts, chocolate, cocoa and black tea are examples of high-oxalate containing foods. Low-oxalate diet sheets should be made available. Substitution with herbal teas and cranberry juice, and increasing the daily fluid intake to over 2L/day to prevent nighttime and summer time dehydration is recommended. Other measures are best managed according to the results of 24 hour urinary analyses.
Hypercalciuria would contraindicate the increased consumption of milk, dairy products and calcium. Otherwise a supplement of 500mgs. of calcium a day is recommended. Hyper-uricosuria is a further indication for reducing the intake of high purine foods such as meat and an indication for a trial of allopurinol. Thiazides have been used owing to their renal effects but the evidence for their efficacy is slight (Wolf 1983). Likewise magnesium supplementation in cases of hypomagnesiuria has been suggested, on account of the associated low urinary citrate levels, but with little supporting evidence (Schwartz 2001). An increased daily citrate intake of 3.75-5G at night remains the best-proven prophylactic measure, as described (Berg 1992). Monitoring the effect of these measures on urinary electrolyte composition is recommended to assess progress.
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