skip to content »


Houston, Texas

As a premier academic medical center, BCM accepts the mantle of leadership in patient care, research, and education.
Department of Medicine - Section of Nephrology
not shown on screen

David Sheikh-Hamad, M.D., FAHA, FASN

Professor of MedicineDavid Shiekh-Hamad, M.D., FAHA, FASN, Molecular & Cellular Biology
Department of Medicine, Section of Nephrology
Chief, Renal Services, Ben Taub Hospital
One Baylor Plaza, M/S BCM395, Houston, TX 77030-3411

Physical Address: One Baylor Plaza, ABBR R706, Houston, TX 77030

Office: 713-798-1301, Fax: 713-798-5010, E-mail:


M.D. Hadassah Medical School, Jerusalem, Israel; Residency, Internal Medicine, UCLA-San Fernando Valley Program; Fellowship, Clinical Nephrology, University of California - Los Angeles, Calif.; Fellowship, Molecular mechanisms of the adaptive response of kidneycells to osmotic stress, Lab of Kidney and Electrolytes Mechanisms, National Institutes of Health

Clinical Interests

  • Inflammatory and acute kidney injury
  • Anti-GBM glomerulonephritis
  • Dysnatremias; volume regulation
  • Acid base homeostasis and RTAs
  • Toxic nephropathy
  • CKD and CVD

Research Interests

Overview: The overall goal of my NIH-funded research is to develop new strategies for the treatment of inflammatory and ischemic kidney injury. Our work has led to the identification of stanniocalcin-1 as a novel regulator of mitochondrial function; through upregulation of uncoupling proteins, stanniocalcin-1 decreases supeoxide generation and has profound impact on the function of several organ systems. In endothelial cells, stanniocalcin-1 inhibits cytokine-induced rise in permeability; while in macrophages, it blocks the effects of LPS and inhibits chemotaxis. Applying experimental anti-GBM glomerulonephritis to transgenic mice that display preferrential overexpression of stanniocalcin-1 in endothelial cells and macrophages we see renal protection. Moreover, in a new reasearch direction, we find that stanniocalcin-1 decreases superoxide generation in cardiomyocytes. Future research will examine the effect of stanniocalcin-1 on: 1) ischemia/reperfusion kidney injury; and 2) cardiac function in a number of pathological settings, including arrythmogenic potential.

Investigator: I am a tenured professor of Medicine in the Division of Nephrology (Baylor College of Medicine), and hold a joint appointment as tenured professor of Molecular and Cellular Biology, in the Department of Molecular and Cellular Biology. I am also chief of Renal Services at Ben Taub Hospital. My office and research laboratory are located in the new Alkek Biomedical Research Building.

Potential projects for fellows and graduate students:

  • Mechanism of anti-inflammatory action of staniocalcin-1
  • Cardioprotection by stanniocalcin-1
  • Effect of stanniocalcin-1 on sarcoplasmic reticulum calcium leak: relevance to arrythmogenic potential
  • Stanniocalcin-1 prevents ischemia/reperfusion kidney injury: mechanisms and consequences
  • Stanniocalcin-1-induced changes in [Ca2+]i: impact on mitochondrial function
  • Prevention of cisplatin-induced nephrotoxicity, using N-acetylcysteine
  • Lasix/Albumin mixture for diuresis in nephrotic patients.

E-mail this page to a friend