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San Antonio--Jejuno-ileal bypass (JIB) reversal improves urinary stone risk factors, although preventing stone recurrence may require alkalinization therapy to normalize urinary citrate excretion, according to a study conducted by researchers at The Cleveland Clinic.
To evaluate the effects of JIB reversal on renal function, on the urinary stone milieu, and on the development of recurrent calculi, investigators reviewed clinical and metabolic courses before and after JIB reversal in four females. The primary indication for the reversal procedure in all women was refractory stone disease, which was associated with hyperoxaluria and hypocitraturia in all women.
The reversal procedure was effective in normalizing hyperoxaluria in all four patients, although hypocitraturia improved, but did not normalize. Stone formation rate was less than that recorded before the reversal procedure, but all patients continued to develop stones until urinary alkalinization therapy was increased to address their hypocitraturia. Thereafter, only one patient developed one stone during 47 months of follow-up, reported Nivedita Dhar, MD, a urology resident at The Cleveland Clinic.
"The interrelationships of JIB, enteric hyperoxaluria, nephrolithiasis, and renal insufficiency are complex, but they are well recognized and have been previously reported. However, there is little information in the literature regarding the effects of JIB reversal on renal function, and even less data regarding changes in the metabolic urinary stone environment," she noted.
"We believe JIB reversal is indicated if oxalate-related complications are progressive and are not controlled adequately with medical therapy. However, continued close follow-up with serum electrolyte and 24-hour urine studies is needed because hypocitraturia may persist and may mandate additional treatment to reduce ongoing stone risk and further renal damage," added Dr. Dhar, who collaborated on this study with Sharon Grundfest, MD, and the late Stevan B. Streem, MD.
The four women in the series had a mean age of 48 years and were 2.2 to 9 years post-JIB surgery (mean, 6.3 years) at the time of reversal. Reversal procedures were performed between 1995 and 2003.
Results from urinary metabolic stone studies showed that at 24 months after JIB, and despite attempts at dietary oxalate restriction, 24-hour urinary oxalate levels were markedly elevated in all four subjects (mean, 112.5 mg; range, 80 mg to 160 mg). In addition, in spite attempts at alkalinization therapy, all four women demonstrated abnormally low 24-hour urine citrate levels (mean, 21.5 mg; range, 5 to 62 mg).
At 4 to 6 months after reversal, the urinary oxalate levels normalized in all women, averaging 33.75 mg/24 hours (range, 31 to 36 mg/24 hours). Urinary citrate excretion increased to a mean of 226.5 mg/24 hours (range, 215 to 248 mg/24 hours) but remained below the normal value of >320 mg/24 hours in all patients.
After alkalinization therapy was in- creased, urinary citrate excretion normalized in all women, increasing to a mean of 547.5 mg/24 hours (range, 480 to 660 mg/24 hours).
Following JIB, patients developed their first stone after a mean of 23.5 months (range, 4 to 42 months) and, until they underwent reversal, each patient developed a mean of 3.2 stones per year and required an average of 2.1 surgical interventions per year (range, 1.2 to 6 surgical interventions per year).
After JIB reversal, patients continued to develop renal stones, but at a decreased rate. Time to first stone formation ranged from 5 to 8 months. The mean annual rate was 0.19 stones per year, and patients required an average of 0.1 surgical interventions per year.
Predisposition for stone formation
"Calcium oxalate stones develop in patients who have undergone JIB due, in part, to the high urinary concentration of oxalate: typically, 2 to 3 times normal," Dr. Dhar said. "However, there are other possible contributing factors, including reduced concentrations of citrate in the urine. Jejuno-ileal bypass-associated acidosis is the most important etiologic factor in causing hypocitraturia.