Abstract-Renin in collecting duct cells is upregulated in chronic angiotensin II-infused rats via angiotensin II type 1 receptors. To determine whether stimulation of collecting duct renin is a blood pressure-dependent effect; changes in collecting duct renin and associated parameters were assessed in both kidneys of 2-kidney, 1-clip Goldblatt hypertensive (2K1C) rats. Renal medullary tissues were used to avoid the contribution of renin from juxtaglomerular cells. Systolic blood pressure increased to 184Ϯ9 mm Hg in 2K1C rats (nϭ19) compared with sham rats (121Ϯ6 mm Hg; nϭ12 T he renin-angiotensin system regulates blood pressure, renal hemodynamics, and tubular sodium reabsorption. During angiotensin II (Ang II)-dependent hypertension, there is an augmentation of intrarenal Ang II levels that is greater than can be explained on the basis of the plasma Ang II concentrations. 1-4 Increased Ang II kidney content results from the combination of uptake of circulating Ang II and local formation of Ang II from enhanced angiotensinogen (AGT) produced and secreted by proximal tubule cells. 2,5,6 Chronic Ang II infusion stimulates proximal tubule AGT production and tubular secretion leading to increased urinary AGT excretion, indicating that the secreted AGT traverses the distal nephron segments. 6,7 In addition to juxtaglomerular (JG) cells, renin is expressed in the principal cells of connecting tubules and cortical and medullary collecting ducts, suggesting angiotensin peptide formation in the distal nephron segments. 8 -10 The upregulation of renin in the collecting ducts (CDs) of Ang II-infused hypertensive rats, along with substantial angiotensinconverting enzyme activity in the late distal tubular fluid and in urine, 11 further support the hypothesis that, in Ang IIdependent hypertension, there is an increased spillover of proximally produced AGT into distal nephron segments leading to augmented Ang II formation and enhanced distal Na ϩ reabsorption. 12,13 In Ang II-infused rats, JG and CD renin are differentially regulated. 13 Treatment with Ang II type 1 (AT 1 ) receptor blockers prevents the stimulation of distal nephron renin mRNA and protein in Ang II-infused rats, 13 a response opposite from the well-known effect of AT 1 receptor blockade on JG renin. Because AT 1 receptor blocker treatment of Ang II-infused rats also prevents the Ang II-mediated increases in arterial blood pressure, an alternative possibility is that the restoration of normal arterial blood pressure was responsible for the reduced responses in CD renin. The present study was performed to elucidate whether the stimu-

Alterations in the balance between ANG II/ACE and ANG 1-7/ACE2 in ANG II-dependent hypertension could reduce the generation of ANG 1-7 and contribute further to increased intrarenal ANG II. Upregulation of collecting duct (CD) renin may lead to increased ANG II formation during ANG II-dependent hypertension, thus contributing to this imbalance. We measured ANG I, ANG II, and ANG 1-7 contents, angiotensin-converting enzyme (ACE) and ACE2 gene expression, and renin activity in the renal cortex and medulla in the clipped kidneys (CK) and nonclipped kidneys (NCK) of 2K1C rats. After 3 wk of unilateral renal clipping, systolic blood pressure and plasma renin activity increased in 2K1C rats (n = 11) compared with sham rats (n = 9). Renal medullary angiotensin peptide levels were increased in 2K1C rats [ANG I: (CK = 171 ± 4; NCK = 251 ± 8 vs. sham = 55 ± 3 pg/g protein; P < 0.05); ANG II: (CK = 558 ± 79; NCK = 328 ± 18 vs. sham = 94 ± 7 pg/g protein; P < 0.001)]; and ANG 1-7 levels decreased (CK = 18 ± 2; NCK = 19 ± 2 pg/g vs. sham = 63 ± 10 pg/g; P < 0.001). In renal medullas of both kidneys of 2K1C rats, ACE mRNA levels and activity increased but ACE2 decreased. In further studies, we compared renal ACE and ACE2 mRNA levels and their activities from chronic ANG II-infused (n = 6) and sham-operated rats (n = 5). Although the ACE mRNA levels did not differ between ANG II rats and sham rats, the ANG II rats exhibited greater ACE activity and reduced ACE2 mRNA levels and activity. Renal medullary renin activity was similar in the CK and NCK of 2K1C rats but higher compared with sham. Thus, the differential regulation of ACE and ACE2 along with the upregulation of CD renin in both the CK and NCK in 2K1C hypertensive rats indicates that they are independent of perfusion pressure and contribute to the altered content of intrarenal ANG II and ANG 1-7.

Background and objectives Little is known regarding whether mortality among ESRD patients with SLE differs between those initiating with peritoneal dialysis (PD) versus hemodialysis (HD). This study compared the mortality risk of ESRD patients with SLE initiating with PD versus HD after matching their baseline sociodemographic and clinical factors.Design, setting, participants, & measurements Of 11,023 ESRD patients with SLE initiating dialysis with PD or HD between 1995 and 2006 with complete records in the US Renal Data System, 1352 pairs were matched on 13 predictors utilizing a predicted probability of group membership into the PD group using propensity score matching. The primary outcome was overall mortality. Secondary outcomes were cardiovascular-related and infection-related mortality. Outcomes were compared between groups with survival statistics. The period of observation ended on December 31, 2009. The median follow-up was 3 years.Results Matched pairs were predominantly women (86%) with a median age of 39 years. Matched pairs had a balance (P$0.05) of all baseline factors. Matched pairs had a similar risk of overall mortality (hazard ratio, 0.96 [95% confidence interval, 0.82 to 1.13]; mortality, 21.4% [290 to 1352] versus 22.5% [304 to 1352] for PD versus HD) within the first 3 years of observation. Matched pairs also had similar cardiovascular-related mortality (10.5% versus 9.5% for PD versus HD) and infection-related mortality (3% versus 4.4% for PD versus HD).Conclusions In ESRD patients with SLE, the mortality was similar among those initiating with PD versus HD after predictors were matched between groups.