Menstrual Hormones May Give Women Some Resistance To Kidney Damage Interview with:

A.Univ.-Prof. Dr. Judith Lechner Div. Physiology Medical University of Innsbruck Innsbruck Austria

Dr. Judith Lechner

A.Univ.-Prof. Dr. Judith Lechner
Div. Physiology
Medical University of Innsbruck
Innsbruck Austria What is the background for this study? What are the main findings?

Dr. Lechner: Women are not just small men. Sex differences affect most, if not all the organ systems in the body. Over the past decades biomedical researchers have been mainly using male models. Therefore, there is a significant gap in knowledge of female physiology except for organ functions involved in reproduction. While the necessity to fill in these gaps has been advocated, our understanding of sex and gender differences in human physiology and pathophysiology is still limited. This holds especially true for the kidneys, e.g. while international registries show that fewer women than men are in need of renal replacement therapy due to end stage renal disease, the potentially underlying causes are still not known.

The aim of our study was to find out, if hormone changes due to the female menstrual cycle would affect normal renal cells. For this purpose, urinary samples of healthy women of reproductive age were collected daily and analyzed for menstrual cycle-associated changes of marker proteins. Specifically, two enzymes (Fructose-1,6-bisphosphatase, Glutathione-S-transferase alpha) were measured, which are intracellular components of proximal tubular cells, a key population of renal cells. Upon cell damage, these enzymes are released into the urine, qualifying them as clinical markers for early detection of tubular injury. Since even in healthy persons low amounts of these enzymes can be detected in the urine, we used these marker proteins to analyze potential effects of the female hormone cycle on normal functioning of this cell population. As a result, we could detect transient increases of Fructose-1,6-bisphosphatase and Glutathione-S-transferase alpha correlating with specific phases of the female hormone cycle, namely ovulation and menses.

This finding suggests that cyclical changes of female hormones might affect renal cell homeostasis, potentially providing women with an increased resistance against kidney damages. Thus, recurring changes of sex hormone levels, as during the natural menstrual cycle, might be involved in periodic tissue re-modeling not only in reproductive organs, but to a certain extent in the kidneys as well. What should clinicians and patients take away from your report?

Dr. Lechner: Our study aimed at increasing knowledge on the mechanisms that might be responsible for the lower susceptibility of women to renal failure as compared to men. The hormone changes brought about by the natural menstrual cycle might be key components to enhance kidney cell health and provide women with increased resistance against kidney damage. What recommendations do you have for future research as a result of this study?

Dr. Lechner: We hope that our findings will encourage other researchers and clinicians to more closely monitor the potential effects the female hormone cycle might have on their systems under study.

With regard to our own research, we plan to further investigate the mechanisms involved in the effects of female hormones on proximal tubular epithelial cell layers in vivo and in vitro. In vitro experiments using cells in culture will offer the possibility to directly study on a molecular level how hormone treatment might influence the outcome of nephrotoxic challenges. Is there anything else you would like to add?

Dr. Lechner: Basic research aimed at understanding the mechanisms involved in kidney function and disease development might provide important cues for improved patient care in the future. In this respect, we hope that our research will contribute to develop new strategies for the benefit of men and women alike. Thank you for your contribution to the community.


Sex Differences in Renal Proximal Tubular Cell Homeostasis

Thomas Seppi, Sinikka Prajczer, Maria-Magdalena Dörler, Oliver Eiter,Daniel Hekl, Meinhard Nevinny-Stickel, Iraida Skvortsova,Gerhard Gstraunthaler, Peter Lukas, and Judith Lechner

JASN ASN.2015080886; published ahead of print April 28, 2016,doi:10.1681/ASN.2015080886

Note: Content is Not intended as medical advice. Please consult your health care provider regarding your specific medical condition and questions.

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