Early effects of percutaneous nephrolithotomy on glomerular filtration rate and determining the potential risk factors responsible for acute postoperative renal function impairment

In this study, the early effects of percutaneous nephrolithotomy [PCNL] on glomerular filtration rate [GFR] was assessed in different postoperative times and likewise, we determined the correlation of different variables with significant postoperative GFR drop after PCNL. Patient records of 486 cases that had undergone PCNL from January 2010 to October 2011 were reviewed retrospectively. GFR in six hours, one, two and three days after PCNL and in the discharge day were calculated and then compared with preoperative level. Correlation between different variables [Perioperative hemorrhage, co-morbidities, previous stone surgery, renal anomaly, number of access, stone burden and location] and risk of acute postoperative renal function impairment [GFR drop greater than 25%] were assessed. Mean preoperative GFR was 87.85 +/- 29.41ml/min/1.73m[2] which decreased to 86.18 +/- 28.77, 78.45 +/- 28.74, 78.79 +/- 26.94, 84.24 +/- 29.71 and 86.18 +/- 28.77 in 6, 24, 48 and 72 hours after surgery and discharge day post PCNL, respectively. GFR significantly decreased in one and two days after surgery [p value<0.0001 and p value <0.05] but returned to near preoperative values in 3th post PCNL day. Among different variables, only perioperative bleeding [Cut-off point for serum hemoglobin drop was 2.8 mg/dL] was concomitant with significant postoperative renal function impairment. Our findings revealed that co-morbidities, large or multiple stones, multiple punctures and previous history of stone surgery have no significant impact on surgical outcomes. Postoperative GFR returned to near preoperative values in a few days after operation. Avoidance of significant perioperative bleeding is an important point to prevent post PCNL renal insufficiency

Mutations of RAS gene family in specimens of bladder cancer

Studies have shown different types of RAS mutations in human bladder tumors with a wide range of mutation frequencies in different patient populations. This study aimed to assess the frequency of specific-point mutations in the RAS gene family of a group of Iranian patients with bladder cancer. We examined the tumor specimens of 35 consecutive patients with transitional cell carcinoma. The DNA samples were evaluated for the occurrence of HRAS, KRAS, and NRAS activation using a polymerase chain reaction-restriction fragment length polymorphism technique. None of the patients had mutations in the RAS gene family "hot spots" including codons 12, 13, and 61. We failed to find RAS mutations in our bladder tumor samples. These observations may reflect the involvement of different etiological factors in the induction of bladder tumor of which RAS mutation might not be present in all populations