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This profile was last updated on 9/29/14  and contains information from public web pages and contributions from the ZoomInfo community.

Dr. William G. Goodman

Wrong Dr. William G. Goodman?

Clinical Research Medical Directo...

Local Address: THOUSAND OAKS, California, United States
Amgen Inc.
One Amgen Center Drive
Thousand Oaks , California 91320
United States

Company Description: Amgen Inc. is a biotechnology company that discovers, develops, manufactures and markets human therapeutics-based on advances in cellular and molecular biology. The...   more

Employment History

  • Professor of Medicine
  • Researcher
  • Professor of Medicine, Division of Nephrology
  • Professor of Medicine
    David Geffen School of Medicine at the University of California , Los Angeles
  • Director of the Bone Histology Laboratory
    David Geffen School of Medicine at the University of California , Los Angeles
  • Kidney Specialist
    David Geffen School of Medicine at UCLA
  • Professor of Medicine and Kidney Specialist
    David Geffen School of Medicine at UCLA


  • MD
  • medical degree
    The Ohio State University College of Medicine
38 Total References
Web References
BioDiscussion, 5 Oct 2014 [cached]
William Goodman, MD BioDiscussion
William Goodman, MD Professor of Medicine Director, Bone, Histology and Molecular Bone Labs of the CRC UCLA School of Medicine
William Goodman, MD has documented that he/she has nothing to disclose.
ARANESP and Calcimimetics Clinical Data Presented At American Society Of Nephrology Meeting, 15 Oct 2000 [cached]
"ESRD patients suffer many complications from high levels of parathyroid hormone including vascular and soft tissue calcification," said William Goodman, M.D., professor of medicine, UCLA . "These encouraging results suggest that therapy with calcimimetics may provide great benefit to patients by suppressing the secretion of PTH and helping to normalize serum calcium and phosphorus."
Vital news for Kidney (renal), Heart, and Diabetes Patient, 5 Mar 2006 [cached]
William Goodman, MD, the UCLA researcher who is the lead author of the study, says that he puts his patients on a mixed regimen of Renagel and calcium in an effort to moderate calcium intake while containing costs.
William Goodman, ..., 2 June 2014 [cached]
William Goodman, MD
William Goodman, MD Professor of Medicine, Division of Nephrology, UCLA School of Medicine, UCLA Medical Center, Los Angeles, CA.
Dr. Goodman discloses no apparent conflicts of pertaining to the material discussed in this talk.
Mednet - CME, CHE | Management of Bone and Mineral Abnormalities in Chronic Kidney Disease, 16 Aug 2012 [cached]
“This decline occurs before there is any elevation in serum phosphorus,†Dr. William Goodman, Professor of Medicine, David Geffen School of Medicine, noted. Abnormalities in vitamin D metabolism in turn adversely affect intestinal calcium transport. Thus, in Dr. Goodman’s view, elevations in PTH in early-stage CKD is an appropriate physiological response that helps maintain serum calcium levels. In both healthy individuals as well as in patients with mild to moderate CKD, phosphorus loading impairs the kidney’s production of 1,25-dihydroxyvitamin D3, while restricting phosphorus will increase its production.
The literature suggests that even if phosphorus level is normal, restricting phosphorus in the diet or through the use of phosphate binders will drive up 1,25-dihydroxy-vitamin D3 production and help prevent bone disease. Increases in 1,25-dihydroxyvitamin D3 levels correspond with subsequent reductions in plasma PTH levels, “so it is the change in circulating 1,25-dihydroxyvitamin D3 levels that mediates the reduction in PTH, not phosphorus per se,†Dr. Goodman indicated.
He also argued that patients with earlier-stage CKD are fundamentally different than those on dialysis, largely because they still have residual kidney function and they can excrete phosphorus. In patients who have mild to moderate CKD, serum phosphorus levels are usually normal, while serum calcium levels are typically in the lower range of normal, he added; and the fact that patients with mild CKD excrete relatively little calcium is a sign that the kidney is trying to conserve calcium. “I’m not arguing with the fact that phosphate restriction and phosphate binders are appropriate when serum phosphate levels are elevated,†Dr. Goodman stated.
Data supporting a non-calcium-based phosphate binder strategy are limited but one prospective studyâ€"the “treat-to-goal†trialâ€"showed that vascular calcification did not worsen over one year of follow-up in dialysis patients treated with sevelamer, whereas it did progress in patients treated with a calcium phosphate binder. “Theoretically, the use of lanthanum carbonate might have a similar beneficial effect because it is also calcium-free,†Dr. Goodman indicated, although this has not yet been demonstrated in a prospective trial.
However, he stated that the choice of a phosphate binding agent could influence progression of calcification once it is present, even though it is not clear how vascular calcification develops in the first place.
“Your choice of phosphate binder is going to be influenced very significantly by other biochemical abnormalities,†Dr. Goodman cautioned.
In an interview, Dr. Goodman also suggested that this agent might be equivalent in potency to the old aluminum-containing binders and more potent than calcium carbonate nor calcium acetate.
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