Angiotensin II receptors mediate increased distal nephron acidification caused by acid retention
Kidney International, 08/08/2012
Exclusive author commentary
Wesson DE et al. – Nephron reduction that moderately reduced glomerular filtration rate with no metabolic acidosis is characterized by increased angiotensin II activity. This mediates increased distal nephron acidification and is induced by acid retention.
Donald E Wesson (07/27/2012) comments:
Subjects with chronic kidney disease (CKD) and reduced GFR must excrete more acid per nephron to maintain acid balance if they continue to eat the acid-inducing diets typical of industrialized societies. We modeled such subjects with reduced GFR but no metabolic acidosis using rats with 2/3 nephrectomy. These animals eating standard, acid-inducing rat chow had increased distal nephron acidification that was mediated through angiotensin II (AII)receptors and was associated with increased kidney AII levels. Acid retention that accompanied the reduced GFR induced the high kidney AII levels. Consequently, reduced GFR in rats is a state of increased kidney AII activity. Because AII mediates nephropathy progression in rat CKD models and dietary alkali that reduces this acid retention slows nephropathy progression in these experimental models, dietary alkali might be an effective kidney-protective strategy in patients with reduced GFR.