Which of the following statement(s) is/are true concerning benign prostatic hypertrophy (BPH)?

a. Prostatic size has no consistent relationship to urethral obstruction

b. Renal failure secondary to obstructive uropathy occurs as bladder pressure rises and is eventually transmitted proximally to the renal pelvis

c. Hormonal treatment for BPH involves treatment with a 5 a-reductase inhibitor which blocks the conversion of testosterone to the dihydrotestosterone

The prototypic bladder outlet obstruction is prostatic hyperplasia, which urologists once visualized as a progressive encroachment on the urethral lumen related to prostatic growth. It is now clear that prostatic size has no consistent relationship to obstruction and the diagnosis of obstructive uropathy cannot be made by endoscopic inspection or by determination of prostatic size or appearance. Obstruction results in progressive increases in bladder pressure and decreased urine flow rates. If bladder pressures are high enough and sustained long enough, the ureteral pump mechanism is overcome, the ureter dilates, and by a hydraulic mechanism, intervesicular pressure is transmitted to the renal pelvis. At a pressure of 42–50 cm H2O, glomerular filtration ceases. These relatively simple sequential events lead to renal failure. Prostatic enlargement clearly has an endocrine basis since treatment with a 5 a-reductase inhibitor, which blocks conversion of testosterone to dihydrotestosterone (the active male hormone in the prostate) can induce a 30% to 50% regression in prostatic size. Although surgery or hormone therapy may be effective in initiating reversal of changes associated with obstructive uropathy, this does not occur invariably. Removal of the hyperplastic glandular tissue is the most effective treatment in terms of relief of symptoms. Patients who cannot be subjected to operation, however, show the same response to intermittent catheterization and periodic bladder emptying in terms of symptoms as well as bladder wall and pressure changes.