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Am J Physiol Renal Physiol 292: F1662, 2007; doi:10.1152/ajprenal.00464.2006
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LETTER TO THE EDITOR

Progressive diabetic nephropathy in the Ren-2 rat

To the Editor: We thank Hartner and colleagues (1) for their interest in the studies by our group and their efforts to replicate our findings. As detailed in their discussion, there are several aspects regarding their experimental design that may have contributed to the observed differences between their findings and ours. In addition and not mentioned by the authors is the possibility that their animals developed malignant hypertension, thereby confounding the interpretability of their study findings. We note both the substantial decline in mean arterial pressure (MAP) between weeks 5 and 20 that suggest the development of heart failure and histopathological findings in Fig. 5 that are reminiscent of myointimal proliferation.

While malignant hypertension has been reported to occur on average in 18% of male and 4% of female Hannover/Ren-2 heterozygotes, there is considerable variability (3). For these reasons we have mostly used female heterozygotes in our longer term studies and are always careful to exclude any animal that develops evidence of malignant hypertension. Given the likely development of a malignant phenotype in their male Hannover/Ren-2 heterozygotes, we are not surprised that Hartner and colleagues were unable to detect an effect of superimposed diabetes. In contrast, we have published extensively that in the absence of malignant hypertension the diabetic Ren-2 rat develops diffuse and nodular glomerulosclerosis not seen in their equally hypertensive nondiabetic counterparts (2).

There are many instances where technical issues precluded the ability of laboratories to replicate the finds of others. We are happy to share our experience with the diabetic Ren-2 rat and invite Hartner and colleagues to contact us.

FOOTNOTES


Address for reprint requests and other correspondence: D. J. Kelly, Dept. of Medicine, St. Vincent's Hospital, Univ. of Melbourne, Fitzroy, Victoria, Australia (e-mail: dkelly{at}medstv.unimelb.edu.au)

REFERENCES

  1. Hartner A, Corasic N, Klanke B, Wittmann M, Veelken R, Hilgers KF. Renal injury in streptozotocin-diabetic Ren-2-transgenic rats in mainly dependent on hypertension, not on diabetes. Am J Physiol Renal Physiol 292: F820–F827, 2007.[Abstract/Free Full Text]
  2. Kelly DJ, Zhang Y, Hepper C, Gow RM, Jaworski K, Kemp BE, Wilkinson-Berka JL, Gilbert RE. Protein kinase C beat inhibition attenuates the progression of experimental diabetic nephropathy in the presence of continued hypertension. Diabetes 52: 512–518, 2003.[Abstract/Free Full Text]
  3. Whitworth CE, Fleming S, Kotelevtsev Y, Manson L, Brooker GA, Cumming AD, Mullins JJ. A genetic model of malignant phase hypertension in rats. Kidney Int 47: 529–535, 1995.[Web of Science][Medline]

Darren J. Kelly1,2
Jennifer L. Wilkinson-Berka3
Richard E. Gilbert1,2
 1Department of Medicine
St. Vincent's Hospital
University of Melbourne
Fitzroy
Victoria; 2Department of Medicine
St. Michael's Hospital
University of Toronto
Toronto
Ontario
Canada; and 3Department of Immunology
Monash University
Prahran
Victoria
Australia




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K. F. Hilgers and A. Hartner
Reply to Kelly et al.
Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1663 - F1663.
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