Developmental loss, but not pharmacological suppression, of renal carbonic anhydrase 2 results in pyelonephritis susceptibility.

We examined the effect of pharmacological CA suppression using acetazolamide in an experimental murine UTI model. Car2-/- vs wild type mice were compared for differences in renal innate immunity. In our transplant scheme, mice only lacking CA-II in the kidney had increased pyelonephritis risk. Mice treated with acetazolamide had lower kidney bacterial burdens at 6-hours post-infection which appeared to be due to tubular flow from diuresis because comparable results were obtained when furosemide was substituted for acetazolamide. Isolated Car2-/-kidney cells enriched for intercalated cells demonstrate altered intercalated cell innate immune gene expression, notably increased Calgizzarin and Insulin receptor expression. Intercalated cell number and function along with renal tubular flow are determinants of pyelonephritis risk. PMID: 32390512 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Renal Physiology - Category: Physiology Authors: Tags: Am J Physiol Renal Physiol Source Type: research