Hemodynamic responses to verapamil monotherapy in patients with renal disease.

We have explored the effect of verapamil on renal hemodynamics and the renin-aldosterone system in ten patients with chronic renal disease and hypertension before and after 3 months of therapy. The mean +/- SEM glomerular filtration rates were 55 +/- 7 mL/min pre- and 55 +/- 8 mL/min posttherapy; the renal plasma flow was 231 +/- 29 mL/min pre and 244 +/- 35 mL/min posttherapy. The filtration fraction (0.24 pre; 0.23 post) and the renal vascular resistance (492 +/- 144 pre; 422 +/- 101 post) also remained stable with verapamil therapy. Blood pressure was lower after treatment (P less than .02) in 7 of 10 patients. Urinary albumin excretion was reduced only when blood pressure was lowered. Verapamil had a modest effect on the renin-aldosterone axis. While the mean increase in plasma renin activity from a pretreatment value of 1.8 +/- 0.42 ng/mL/h to 2.1 +/- 0.56 ng/mL/h failed to reach statistical significance, the increases in urinary aldosterone excretion from 8.2 +/- 2.2 mg/24 h to 11.1 +/- 2.3 mg/24 h did (P less than .001). Our results demonstrate that verapamil lowered blood pressure without renal hemodynamic compromise in hypertensive patients with chronic renal disease. The antihypertensive response was associated with a rise in urinary aldosterone excretion, with unchanged serum electrolytes. We conclude that verapamil is effective, safe, and well-tolerated in patients with renal impairment and hypertension, and may be suitable for clinical trials evaluating long-term progression of renal disease.

Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation.

11 patients with atheromatous renovascular hypertension had a history of multiple episodes of pulmonary oedema. 7 had stenosis of both renal arteries, 2 had stenosis of the artery to a solitary kidney, and 2 had unilateral stenosis with an intact contralateral kidney. Successful revascularisation (by angioplasty in 8, and surgery in 3) improved blood pressure and renal function, and virtually eliminated pulmonary oedema. In a second series of 55 consecutive patients with azotaemia and renovascular hypertension, pulmonary oedema occurred in 13 (23%). Blood pressure and renal function were not significant predictors of pulmonary oedema, but coronary heart disease and bilateral (vs unilateral) renal artery stenosis were. Bilateral renal artery stenosis may be a specific and treatable predisposing factor to pulmonary oedema in azotaemic hypertensive patients.