Hypertension, a remediable risk factor for stroke, cardiovascular disease, and renal failure, affects 50 million individuals in the United States alone. African Americans (blacks) have a higher incidence and prevalence of hypertension and hypertension-associated target organ damage compared with Caucasian Americans (whites). Herein, we explored the hypotheses that transforming growth factor-␤1 (TGF-␤1) is hyperexpressed in hypertensives compared with normotensives and that TGF-␤1 overexpression is more frequent in blacks compared with whites. These hypotheses were stimulated by our recent demonstration that TGF-␤1 is hyperexpressed in blacks with end-stage renal disease compared with white end-stage renal disease patients and by the biological attributes of TGF-␤1, which include induction of endothelin-1 expression, stimulation of renin release, and promotion of vascular and renal disease when TGF-␤ 1 is produced in excess. TGF-␤1 profiles were determined in black and white hypertensive subjects and normotensive controls and included circulating protein concentrations, mRNA steady-state levels, and codon 10 genotype. Our investigation demonstrated that TGF-␤1 protein levels are highest in black hypertensives, and TGF-␤1 protein as well as TGF-␤1 mRNA levels are higher in hypertensives compared with normotensives. The proline allele at codon 10 (Pro 10 ) was more frequent in blacks compared with whites, and its presence was associated with higher levels of TGF-␤1 mRNA and protein. Our findings support the idea that TGF-␤ 1 hyperexpression is a risk factor for hypertension and hypertensive complications and provides a mechanism for the excess burden of hypertension in blacks.

Objective To evaluate the effect of a modified method of percutaneous catheter placement without a break-in procedure on the development of catheter-related complications in patients on continuous ambulatory peritoneal dialysis (CAPD). Design A prospective, observational clinical study. Setting Peritoneal dialysis (PD) units of two university-based hospitals. Patients and Methods This study included 51 consecutive patients on CAPD. A straight double-cuffed Tenckhoff catheter with a straight intraperitoneal segment was used, and all catheters were inserted using a modified percutaneous placement method under local anesthesia. The catheter was introduced directly into the deep pelvis through an intramuscular tract, which had been created by tapered dilators. Peritoneal dialysis was initiated immediately after catheter insertion without a break-in procedure. Catheter-related complications were surveyed during the 12 months after initiation of CAPD. Results Within the first month, only 1 pericatheter leakage (1.9%) was detected. There were no cases of visceral perforation or severe hemorrhage during catheter insertions. Catheter malfunction due to catheter tip migration, exit-site infection, and peritonitis developed in only 1.9%, 3.9%, and 3.9% of patients, respectively. After 1 month following catheter insertion, no further incidences of pericatheter leakage occurred during the follow-up period. All catheters, except one that was reinserted due to tip migration, survived throughout the study period. Conclusion The rates of pericatheter leakage and other catheter-related complications are relatively low in CAPD patients using our percutaneous catheter placement method without a break-in procedure. This procedure is comparatively simple and less invasive than other catheter placement methods, and allows for immediate start of PD after catheter insertion, without a break-in procedure.

Hypertension, a remediable risk factor for stroke, cardiovascular disease, and renal failure, affects 50 million individuals in the United States alone. African Americans (blacks) have a higher incidence and prevalence of hypertension and hypertension-associated target organ damage compared with Caucasian Americans (whites). Herein, we explored the hypotheses that transforming growth factor-beta(1) (TGF-beta(1)) is hyperexpressed in hypertensives compared with normotensives and that TGF-beta(1) overexpression is more frequent in blacks compared with whites. These hypotheses were stimulated by our recent demonstration that TGF-beta(1) is hyperexpressed in blacks with end-stage renal disease compared with white end-stage renal disease patients and by the biological attributes of TGF-beta(1), which include induction of endothelin-1 expression, stimulation of renin release, and promotion of vascular and renal disease when TGF-beta(1) is produced in excess. TGF-beta(1) profiles were determined in black and white hypertensive subjects and normotensive controls and included circulating protein concentrations, mRNA steady-state levels, and codon 10 genotype. Our investigation demonstrated that TGF-beta(1) protein levels are highest in black hypertensives, and TGF-beta(1) protein as well as TGF-beta(1) mRNA levels are higher in hypertensives compared with normotensives. The proline allele at codon 10 (Pro(10)) was more frequent in blacks compared with whites, and its presence was associated with higher levels of TGF-beta(1) mRNA and protein. Our findings support the idea that TGF-beta(1) hyperexpression is a risk factor for hypertension and hypertensive complications and provides a mechanism for the excess burden of hypertension in blacks.