Miniaturised percutaneous nephrolithotomy versus flexible ureteropyeloscopy: a systematic review and meta-analysis comparing clinical efficacy and safety profile.

PURPOSE: This study aims to comparatively evaluate clinical outcomes of mini-PCNL and FURS for treating urinary tract calculi in a single session. METHODS: A systematic search using electronic databases was performed for studies comparing mini-PCNL and FURS for the treatment of urinary tract calculi. The primary outcome measurements were stone-free rates (SFRs) and complication rates for both techniques. Secondary outcome measurements were to compare patient demographics, operative duration, and inpatient stay. Meta-analysis was performed with Review Manager version 5.3 software. RESULTS: Sixteen studies on 1598 patients (n = 877 for mini-PCNL and n = 721 for FURS) met inclusion criteria. Demographics including age (p = 0.26), body mass index (BMI) (p = 0.51), and gender ratio (p = 0.6), were similar in both groups. Overall, SFR was significantly greater in the mini-PCNL group compared to the FURS group (n = 763/877, 89.3 ± 8.4% versus n = 559/721, 80.1 ± 13.3% [OR 2.01; 95% CI 1.53-2.64; p < 0.01]). Duration of inpatient stay was significantly greater in the mini-PCNL group compared to the FURS group (n = 877, 4 ± 1.6 days versus n = 721, 2.5 ± 2.2 days, respectively [WMD: 1.77; 95% CI 1.16-2.38, p < 0.01]. Overall complication rates were not significantly different between mini-PCNL and FURS (n = 171/877, 19.5 ± 19.1% versus n = 112/721, 15.5 ± 18.9%, respectively [OR 1.43; 95% CI 0.85-2.4, p = 0.18]). CONCLUSIONS: Mini-PCNL is associated with greater SFRs and longer inpatient stay compared to FURS. Complication rates were similar for both techniques. The advantages and disadvantages of both technologies should be familiar to urologists and conveyed to patients prior to urological intervention for nephrolithiasis.

Effect of chronic tolbutamide administration on normal and obese-hyperglycemic mice: evidence for post-receptor potentiation of insulin action.

Obese-hyperglycemic mice (genotype ob/ob) have hyperglycemia, hyperinsulinemia, increased resistance to insulin action and decreased insulin receptors on their liver, fat cell and muscle plasma membranes. Hypoglycemic sulfonylureas are reported to improve diabetic control by decreasing the insulin resistance of subjects with Type II diabetes mellitus: however, it is not clear if their mechanism is to increase plasma membrane insulin receptors or to decrease post-receptor insulin resistance. In this study we treated obese-hyperglycemic mice and their normal weight litter mates with the oral hypoglycemic sulfonylurea tolbutamide for 28 to 34 weeks. Tolbutamide administration to normal mice resulted in the following changes that were indicative of increased insulin action: (1) increased body weight; (2) increased epididymal fat-pad weight; (3) increased 2-deoxyglucose transport into the intact diaphragm muscle preparation. There was no alteration in plasma glucose, plasma insulin or pancreatic insulin content suggesting that the tolbutamide effect was an extrapancreatic effect that was probably not mediated by increased insulin secretion. There was no change in the insulin receptor number or affinity of liver cell membranes prepared from tolbutamide treated mice supporting the notion that the extrapancreatic effect of tolbutamide may occur at a post-insulin receptor location. In contrast to the normal mice, tolbutamide did not increase the body weight, epididymal fat pad weight, the already increased 2-deoxyglucose transport into diaphragm muscle or the decreased number of insulin receptors on hepatic plasma membranes. The tolbutamide caused a striking decrease in pancreatic insulin concentration and degranulation of the islets in obese but not normal mice. This is compatible with previous information that the obese mice have abnormal islets that are not under the normal feed-back control of ambient insulin concentration as are the islets of normal mice. We conclude that tolbutamide potentiates insulin action in normal, but not obese, mice and that this potentiation may be due to a post-insulin receptor action.