Deterioration of renal function with significant reduction in GFR following treatment with beta blockers have been outlined in clinical practice and experimental research (vide Wilkinson 1982). The beneficial role of dopamine have also been acknowledged, but clinical evidences about the effects of some specific beta blockers are conflicting, i.e., nadolol, propranolol etc. So what's the current guideline of beta blocker usage in patients who have moderate renal impairment?
Epstein M, Oster JR. Beta blockers and renal function: a reappraisal. J Clin Hypertens 1985; 1: 85-99.
Beta-blockers and renal function.
Wilkinson R.
Abstract
alpha-, beta 1- and beta 2-adrenergic receptors in the kidney mediate vasoconstriction, renin secretion and vasodilatation, respectively. Blockade of beta-receptors may therefore be expected to influence renal blood flow and possibly glomerular filtration rate by intrarenal effects as well as by reducing cardiac output and blood pressure. Since the various beta-adrenergic blocking drugs available differ in the degree to which they block beta 2-receptors (cardioselectivity) and also in their intrinsic sympathomimetic activity, they would be expected to have different effects on renal function. The acute administration of beta-blockers usually results in a reduction in effective renal plasma flow and glomerular filtration rate, whether or not the drug is cardioselective or has intrinsic sympathomimetic activity, with the exceptions of nadolol, which has actually increased effective renal plasma flow in some studies and of tolamolol. With chronic oral administration, the non-cardioselective beta-blockers reduced glomerular filtration rate and effective renal plasma flow. The cardioselective drugs do not usually produce significant reductions in glomerular filtration rate or effective renal plasma flow, although small increases in serum urea during treatment do occur. Interestingly, in contrast to findings with intravenous administration, orally administered nadolol produced a slight reduction in glomerular filtration rate in 1 study, so the effect of this agent on renal function under clinical conditions remains uncertain. It seems likely that beta-blockers reduce renal function predominantly by blocking beta 2-receptors in the kidney. To keep area of discussion in perspective, it is important to realise that although there have been isolated reports of serious deterioration in renal function coinciding with beta-blocker treatment, the great majority of reports are of reduction in glomerular filtration rate which are not of clinical significance, even in patients with pre-existing impairment of renal function. The beta-blockers with low lipid solubility-i.e. atenolol, nadolol and sotalol-are not metabolised, and their dose must be reduced in renal failure. Propranolol has active metabolites and its dose must also be reduced slightly in uraemia.
http://www.ncbi.nlm.nih.gov/pubmed/6122552
It may be that renin secreting kidneys, for example, in the course of renal artery stenosis, are more susceptible to GFR decrease by beta blockade. RJ Anderson, MS Taher, RE Cronin, KM McDonald, RW Schrier. Effect of beta-adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation. American Journal of Physiology--Legacy Content. 1975;229(3):731-6.
Much thanks for your answer Dr. Wesolowski.
Since Dr. Wesolowski raised the issue of renal artery stenosis, it may be relevant to mention that some drugs including ACEIs are contraindicated in bilateral renal artery stenosis, since that precipitates azotemia (and subsequently uraemia if untreated) due to efferent arteriolar dilation which causes increased BUN, and sodium retention. However, ACEIs can be used as a second line antihypertensives in patients with unilateral renal artery stenosis1. Beta blocker Carvedilol have been successfully used in patients with atherosclerotic bilateral renal artery stenosis2. Again, some experts question the rationality of using ACEIs in renal artery stenosis since they claim that indiscriminate use of ACEIs might increase the risk of cardiovascular death4. Renal artery stenosis stimulates renin release and may raise blood pressure, while beta blockers interfere with renal beta adrenergic receptors (by blocking it) and thus relieving the vasoconstriction (i.e. causing vasodilatation). This reduces GFR, and renal plasma flow, and may lead to sodium retention(??). However, nadolol is an exception which in fact increases effective renal plasma flow3. Is it possible to explain why this (contradictory phenomenon) occurs?
1http://www.ncbi.nlm.nih.gov/pubmed/11548082
2http://www.ncbi.nlm.nih.gov/pubmed/15222246
3http://www.ncbi.nlm.nih.gov/pubmed/6122552
4http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768825/
Best Regards, Sidharta