EXPANDING ROLE OF ALPHA ADRENOCEPTOR BLOCKADE IN THE TREATMENT OF BENIGN PROSTATIC HYPERPLASIA

SUMMARY This review analyses the expanding role of alpha adrenoceptor blockers in the treatment of BPH and examines the rationale for their use. The safety and efficacy of currently available alpha adrenoceptor blockers is reviewed, with emphasis on the most extensively studied agent, doxazosin. Like other alpha adrenoceptor blockers, doxazosin improves both symptoms of BPH and urinary flow rates by a statistically significant effect compared with placebo. Doxazosin also significantly reduces blood pressure in the 30% of BPH sufferers who also have hypertension; furthermore, there is a beneficial effect on lipid metabolism, which may translate into a reduced risk of coronary heart disease. It is concluded that existing alpha adrenoceptor blockers constitute a valuable adjunct to other BPH therapies, and further refinement of alpha adrenoceptor selectivity based on the alpha-1A subtype in the near future promises even better targeted alpha blockade.     

Transforming growth factor-β (TGF-β) activity in urine of patients with glomerulonephritis is related to their renal functional and structural changes

Transforming growth factor-β (TGF-β) has been considered the principal cytokine involved in the pathogenesis of renal fibrosis. In the present study, we evaluated TGF-β activity in occasional samples from 22 normal individuals and 29 patients (11 with focal glomerulosclerosis, 11 with membranous nephropathy, five with Berger disease, one with type I membranoproliferative glomerulonephritis and one with postinfectious glomerulonephritis) using a CCL-64 mink lung cell growth inhibition assay.
A significantly increased urinary TGF-β activity (reported in relation to urine creatinine, Ucreat. and median) was observed in patients with glomerulonephritis compared with normal individuals ( P <0.01). The patients with Berger disease [median (Md)=9.96/10 μg Ucreat.], membranous glomerulonephritis (Md=7.23/10 μg Ucreat.) and focal glomerulosclerosis (Md=16.6/10 μg Ucreat.) showed higher urinary TGF-β than normal individuals (Md=1.09/10 μg Ucreat.) ( P <0.01). We found a positive correlation between the TGF-β activity in the urine of these patients and the incidence of segmental glomerulosclerosis ( r =0.45, P <0.05) and their plasma creatinine levels ( r =0.87, P <0.01). A negative correlation was observed between the TGF-β activity in the urine of these patients and their creatinine clearance ( r =−0.75, P <0.01).
Our data suggest that measurement of urinary TGF-β activity could be a useful non-invasive procedure for the evaluation of renal TGF-β production, permitting the assessment of prognosis and the evaluation of therapeutic efficacy in patients with renal disease.