Testosterone Deficiency at the Crossroads of Cardiometabolic Complications in CKD  Juan Jesús Carrero, PhD  American Journal of Kidney Diseases  Volume 64, Issue 3, Pages 322-325 (September 2014) DOI: 10.1053/j.ajkd.2014.06.002 Copyright © 2014 National Kidney Foundation, Inc. Terms and Conditions

Figure 1 The genesis of testosterone deficiency in the setting of chronic kidney disease (CKD) is multifactorial. While originating in the loss of kidney function per se, important risk factors for CKD and common medications to treat CKD-related complications further suppress testosterone production. Its potential clinical consequences mostly are derived, to date, from observational evidence and may convey a negative impact on quality of life, catabolism, anemia, bone loss, cardiovascular complications, transplant survival, and death risk. Abbreviations: ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; ESA, erythropoiesis-stimunlating agent; LH, luteinizing hormone. American Journal of Kidney Diseases 2014 64, 322-325DOI: (10.1053/j.ajkd.2014.06.002) Copyright © 2014 National Kidney Foundation, Inc. Terms and Conditions