Ureteroscopy is an endoscopic kidney stone removal procedure which increases the internal pressure in the renal pelvis, the kidney’s urinary collecting system. Elevated renal pelvic pressure may result in systemic absorption of irrigation fluid and urine, which can increase the risk of postoperative fever and sepsis. Urologists have investigated the effects of various surgical parameters on the renal pelvic pressure. However, it still remains unknown which surgical parameter has the most dominant effect on the renal pelvic pressure over time. Here we develop a physical model that computes the renal pelvic pressure as a function of time based on parameters that can be varied during ureteroscopy. The model is developed by applying pipe network analysis to the regions of the urinary tract that are involved in a representative ureteroscopic procedure. Our model unifies the findings of the previously published studies on this topic; an ex-vivo porcine study and an in-vivo human study. Furthermore it allows simulation of surgical procedures based on various techniques. Our simulation demonstrates that the two strong regulators of renal pelvis pressure during ureteroscopy are the size of the gap between ureteroscope and ureteral access sheath and the frequency and duration of ureteroscope withdrawal.
Two previous studies (<10 patients each) have demonstrated that alkali therapy may reduce urine calcium excretion in patients with calcium oxalate nephrolithiasis. The hypothesized mechanisms are (1) a decrease in bone turnover due to systemic alkalinization by the medications; (2) binding of calcium by citrate in the gastrointestinal tract; (3) direct effects on TRPV5 activity in the distal tubule. We performed a retrospective review of patients on potassium citrate therapy to evaluate the effects of this medication on urinary calcium excretion. A retrospective review was performed of a metabolic stone database at a tertiary care academic hospital. Patients were identified with a history of calcium oxalate nephrolithiasis and hypocitraturia who were on potassium citrate therapy for a minimum of 3 months. 24-h urine composition was assessed prior to the initiation of potassium citrate therapy and after 3 months of therapy. Patients received 30-60 mEq potassium citrate by mouth daily. Inclusion criterion was a change in urine potassium of 20 mEq/day or greater, which suggests compliance with potassium citrate therapy. Paired t test was used to compare therapeutic effect. Twenty-two patients were evaluated. Mean age was 58.8 years (SD 14.0), mean BMI was 29.6 kg/m(2) (SD 5.9), and gender prevalence was 36.4% female:63.6% male. Mean pre-treatment 24-h urine values were as follows: citrate 280.0 mg/day, potassium 58.7 mEq/day, calcium 216.0 mg/day, pH 5.87. Potassium citrate therapy was associated with statistically significant changes in each of these parameters-citrate increased to 548.4 mg/day (p < 0.0001), potassium increased to 94.1 mEq/day (p < 0.0001), calcium decreased to 156.5 mg/day (p = 0.04), pH increased to 6.47 (p = 0.001). Urine sodium excretion was not different pre- and post-therapy (175 mEq/day pre-therapy versus 201 mEq/day post-therapy, p = NS). Urinary calcium excretion decreased by a mean of 60 mg/day on potassium citrate therapy-a nearly 30 % decrease in urine calcium excretion. These data lend support to the hypothesis that alkali therapy reduces urine calcium excretion.
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