Reply to Kelly et al.

Abstract

LETTERS TO THE EDITORReply to Kelly et al.Karl F. Hilgers, and Andrea HartnerKarl F. Hilgers, and Andrea HartnerPublished Online:01 May 2007https://doi.org/10.1152/ajprenal.00076.2007MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat reply: We thank Kelly and coworkers (3) for their comments. We agree that some of the Ren-2 animals in our study did develop malignant hypertension, as discussed in our report (see the penultimate paragraph of the discussion in Ref. 1). We included all animals which survived to the end of the study in the final analysis because we feel that the exclusion of animals with malignant hypertension would have confounded the results. First, exclusion before entry in the protocol is not possible because Ren-2 rats can develop malignant hypertension over several months (5). Second, early signs of malignant hypertension such as increased diuresis or weight loss are of little use in diabetic animals and could be used only in normoglycemic controls. A marked weight difference between diabetic and nondiabetic Ren-2 rats is obvious in our study as well as in the reports of Kelly and coworkers (2, 4). Third, exclusion of animals with malignant hypertension based on criteria like blood pressure or renal damage could obviously lead to a bias, especially if malignant hypertension occurs more frequently in one group.We observed some diabetes-induced glomerular matrix expansion superimposed on hypertension but no nodular glomerulosclerosis. The lower mortality in diabetic Ren-2 rats (Fig. 6C in Ref. 1) certainly does not point to more severe kidney damage either. Finally, we are surprised to read in the letter by Kelly and coworkers that they were “always careful to exclude” animals with malignant hypertension. No such statement can be found in their reports (2, 4). A procedure that bears such a high potential to affect the results should not be omitted from the description but needs to be clearly outlined.REFERENCES1 Hartner A, Cordasic N, Klanke B, Wittmann M, Veelken R, Hilgers KF. Renal injury in streptozotocin-diabetic Ren2-transgenic rats is mainly dependent on hypertension, not on diabetes. Am J Physiol Renal Physiol 292: F820–F827, 2007.PubMed | ISI | Google Scholar2 Kelly DJ, Wilkinson-Berka JL, Allen TJ, Cooper ME, Skinner SL. A new model of diabetic nephropathy with progressive renal impairment in the transgenic (mRen-2)27 rat (TGR). Kidney Int 54: 343–352, 1998.Crossref | PubMed | ISI | Google Scholar3 Kelly DJ, Wilkinson-Berka JL, Gilbert RE. Progressive diabetic nephropathy in the Ren-2 rat. Am J Physiol Renal Physiol 292: F1662, 2007.Link | ISI | Google Scholar4 Kelly DJ, Zhang Y, Hepper C, Gow RM, Jaworski K, Kemp BE, Wilkinson-Berka JL, Gilbert RE. Protein kinase C beta inhibition attenuates the progression of experimental diabetic nephropathy in the presence of continued hypertension. Diabetes 52: 512–518, 2003.Crossref | PubMed | ISI | Google Scholar5 Whitworth CE, Fleming S, Cumming AD, Morton JJ, Burns NJ, Williams BC, Mullins JJ. Spontaneous development of malignant phase hypertension in transgenic Ren-2 rats. Kidney Int 46: 1528–1532, 1994.Crossref | PubMed | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: K. F. Hilgers, Nephrologische Forschungslabors, Loschgestrasse 8, 91054 Erlangen, Germany (e-mail: [email protected]) Download PDF Previous Back to Top FiguresReferencesRelatedInformation More from this issue > Volume 292Issue 5May 2007Pages F1663-F1663 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/ajprenal.00076.2007History Published online 1 May 2007 Published in print 1 May 2007 Metrics