Dr. Stewart H Lecker M.D.
Nephrologist (Kidney Specialist) | Nephrology
330 Brookline Avenue Bi Renal Unit Dana 5 Boston MA, 02215About
Dr. Stewart Lecker is a nephrologist practicing in Boston, MA. Dr. Lecker specializes in the care and treatment of the kidneys. As a nephrologist, Dr. Lecker most typically treats conditions like kidney stones, chronic kidney disease, acute renal failure, polycystuc kidney disease, high blood pressure and more. Nephrologists are also experts on kidney transplantation and dialysis. They are usually referred to by primary care physicians for problems related to the kidneys, and while they can perform tests to diagnose kidney disorders, they do not perform surgeries.
Education and Training
Univ of Ca, Los Angeles, Ucla Sch of Med, Los Angeles Ca 1992
University of California 1992
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Nephrology
Internal MedicineAmerican Board of Internal MedicineABIM
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Construction and analysis of mouse strains lacking the ubiquitin ligase UBR1 (E3alpha) of the N-end rule pathway.
- Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy.
- Patterns of gene expression in atrophying skeletal muscles: response to food deprivation.
- Slowing muscle atrophy: putting the brakes on protein breakdown.
- Ubiquitin-protein ligases in muscle wasting: multiple parallel pathways?
- TNF-alpha increases ubiquitin-conjugating activity in skeletal muscle by up-regulating UbcH2/E220k.
- Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy.
- Ubiquitin-protein ligases in muscle wasting.
- Atrophy-related ubiquitin ligases atrogin-1 and MuRF-1 are associated with uterine smooth muscle involution in the postpartum period.
- PGC-1alpha protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription.
- Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases.
- The muscle-specific ubiquitin ligase atrogin-1/MAFbx mediates statin-induced muscle toxicity.
- FoxO3 coordinately activates protein degradation by the autophagic/lysosomal and proteasomal pathways in atrophying muscle cells.
- Electrolyte-free water clearance: a key to the diagnosis of hypernatremia in resolving acute renal failure.
- Calpain activity and muscle wasting in sepsis.
Treatments
- Chronic Kidney Disease, Glomerular Diseases
Fellowships
- Beth Israel Deaconess Medical Center in Nephrology, Boston, MA 2000
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