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I am an Active Emeritus Professor Medicine/ Nephrology at Stanford University. I began my long career in investigative medicine over 40 years ago. My first major contribution was one of the earliest randomized clinical trials evaluating beta-blockade for angina (Rabkin R et al. The prophylactic value of propranolol in angina pectoris. Am J Cardiol. 1966;18:370-83.). Moving from clinical investigation, (e.g. The effect of renal disease on the renal uptake and excretion of insulin in man. Rabkin R et al, NEJM, 1970, 282:182-187), my research became more basic orientated and focused on the renal metabolism of peptide hormones (Factors influencing the handling of insulin by the isolated rat kidney. Rabkin, R. and A.E. Kitabchi. J. Clin. Invest. 1978, 161:169-175. The handling of immunoreactive vasopressin by the isolated perfused rat kidney. Rabkin, R et al. J. Clin. Invest. 1979. 63:6-13). More recently I have focused on the mechanisms accounting for the resistance to growth hormone, insulin-like growth factor-1 and amino acids in uremia to explain their role in the impaired body growth and muscle wasting that is common in chronic kidney disease (CKD) (Schaefer F, Chen Y, Tsao T, Nouri P, and Rabkin R. (2001). Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia. J Clin Invest 108: 467-475) Chen Y, Sood S, McIntire K, Roth R, Rabkin R. Leucine stimulated mTOR signaling is partly attenuated in skeletal muscle of chronically uremic rats especially when work overloaded. American Journal of Physiology. Endocrinology and metabolism. (2011) 301, E873-871. Intrigued by my findings in rats with CKD, that exercise can correct some of the skeletal muscle abnormalities in signal transduction and IGF-1 and myostatin gene expression, I have been motivated to go from the bench to the bedside, and have brought together an outstanding group of clinical investigators with expertise in exercise rehabilitation as well as clinical trials in CKD patients and together we are embarking on a 4 year VA Merit Review Funded study “Exercise to Prevent Muscle Mass and Functional Loss in Elderly Dialysis Patients”.
Testosterone Replacement Therapy in Advanced Chronic Kidney Disease
Muscle wasting is common in advanced chronic kidney disease (CKD) and adversely affects
morbidity and mortality. In 2/3 of males with advanced CKD serum testosterone (TT) levels are
reduced, and likely contributes to the wasting. As TT in relatively safe physiologic
replacement doses, increases muscle mass in otherwise normal TT deficient subjects, we
hypothesize that physiologic TT replacement will be effective in preventing and treating the
loss of muscle mass and function in CKD patients, will improve quality of life and may reduce
some cardiovascular disease (CVD) risk factors.
Stanford is currently not accepting patients for this trial.
For more information, please contact SPECTRUM, .
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Exercise to Prevent Muscle Mass and Functional Loss in Elderly Dialysis Patients
The majority of individuals with advanced ESRD have reduced exercise capacity in part due to
decreased muscle mass. This leads to a reduced ability to perform daily activities, a greater
incidence of falls, and a reduced quality of life. The mechanisms responsible for the loss of
muscle mass in ESRD are not understood very well. This study is designed to determine the
effectiveness of an exercise program on improving muscle mass, exercise capacity and quality
of life in persons with ESRD. In addition, the study will attempt to better understand why
muscle loss occurs in people with ESRD, the influence exercise has on these mechanisms, and
whether the response to exercise can be enhanced with nutrient supplementation.