Jeffrey Burnett Kopp, M.D.

Senior Investigator

Kidney Diseases Branch

NIDDK

Building 10, Room 3N114
10 Center Dr
Bethesda, MD 20814

+1 301 594 3403

jeffrey.kopp@nih.gov

Research Topics

Current Research

Dr. Kopp leads a translational research group within the Kidney Disease Section, Kidney Diseases Branch, studying focal segmental glomerulosclerosis (FSGS) and related podocyte diseases.

Recent Highlights

  • Chromosome 22 harbors a major risk locus for kidney disease in African Americans, including FSGS, HIV-associated nephropathy, and arterionephrosclerosis (hypertension-attributed kidney disease). APOL1 coding variants, which protect against trypanosomal infection, are strongly associated with kidney disease (odds ratios 7-29). The mechanism of glomerular injury is unknown.
  • The HIV-1 protein Vpr, expressed in the glomerular podocytes, is sufficient to reproduce the chief features of HIV-associated collapsing glomerulopathy in transgenic mice.

Current Research Efforts

  • determining the mechanisms by which Apol1 variants damage the glomerulus
  • examining whether cardiotrophin-like cytokine 1 is a permeability factor that contributes to recurrent FSGS following kidney transplant
  • an open label phase II trial examining the efficacy of rituximab combined with cyclosporine (for 48 weeks) for treatment of refractory podocyte disease
  • participating in the ORD-funded NEPTUNE study of nephrotic diseases

Information for Patients

  • We are actively recruiting individuals with focal segmental glomerulosclerosis and those with undiagnosed nephrotic syndrome or proteinuria.
  • All NIH trials are listed at clinicaltrials.gov.
  • Information about glomerular diseases is available on the Glomerular Disease Primer page.

Reagents Available to the Research Community

Transgenic Mice

  • Podocin promoter/rTTA (reverse tetracycline transactivator)—also available from JAX and as herozygotes or homozygotes
  • TRE (tet responsive element)/Vpr
  • Alb/TGF-beta mice (request permission from Dr. Snorri Thorgeirsson, NCI)

Antibodies

  • rabbit polyclonal antibody to Vpr1-50 peptide—also available from AIDS Research and Reference Reagent Program
  • rabbit antiserum to human podocin (cross-reactive with mouse podocin)
  • rabbit antiserum to human nephrin (no cross-reactivity with mouse nephrin)
  • goat antimouse mesangial cell serum, for induction of glomerulonephritis in mice

Podocyte Cell Lines

  • mouse podocytes, immortalized with thermosensitive SV40 T Ag and bearing podocin/rtTA, for expression of genes of interest in cultured mouse podocytes
  • same, plus TRE silencer to reduce background expression
  • human urine derived podocyte-like epithelial cells (HUPECs), immortalized with hTERT and thermosensitive SV40 T Ag

Please contact us for further details. NIDDK MTAs are available through Technology Advancement and Transfer.

Biography

  • Consulting Nephrologist, Mark Hatfield Clinical Research Center, NIH, Present
  • Commissioned Officer (Captain), U.S. Public Health Service, Retired
  • Adjunct Professor of Medicine, Uniformed Services University of the Health Sciences, Present
  • Branch Chief, Kidney Diseases Branch, NIDDK, 2013 - present
  • Senior Investigator, NIDDK, NIH, 1995-present
  • Medical Staff Fellow, NIH, 1987-1995
  • Complete Training in Internal Medicine and Nephrology, University of Washington, 1987
  • M.D., University of Pennsylvania Medical School, 1980
  • B.A., Harvard College, 1975

Selected Publications

  1. Lertdumrongluk P, Streja E, Rhee CM, Moradi H, Chang Y, Reddy U, Tantisattamo E, Kalantar-Zadeh K, Kopp JB. Survival Advantage of African American Dialysis Patients with End-Stage Renal Disease Causes Related to APOL1. Cardiorenal Med. 2019;9(4):212-221.

  2. Kopp JB, Rosenberg AZ. One Actor, Many Roles: Histopathologies Associated With APOL1 Genetic Variants. Adv Anat Pathol. 2019;26(3):215-219.

  3. Ryu JH, Ge M, Merscher S, Rosenberg AZ, Desante M, Roshanravan H, Okamoto K, Shin MK, Hoek M, Fornoni A, Kopp JB. APOL1 renal risk variants promote cholesterol accumulation in tissues and cultured macrophages from APOL1 transgenic mice. PLoS One. 2019;14(4):e0211559.

  4. Okamoto K, Rausch JW, Wakashin H, Fu Y, Chung JY, Dummer PD, Shin MK, Chandra P, Suzuki K, Shrivastav S, Rosenberg AZ, Hewitt SM, Ray PE, Noiri E, Le Grice SFJ, Hoek M, Han Z, Winkler CA, Kopp JB. APOL1 risk allele RNA contributes to renal toxicity by activating protein kinase R. Commun Biol. 2018;1:188.

  5. Doshi MD, Ortigosa-Goggins M, Garg AX, Li L, Poggio ED, Winkler CA, Kopp JB. <i>APOL1</i> Genotype and Renal Function of Black Living Donors. J Am Soc Nephrol. 2018;29(4):1309-1316.


This page was last updated on August 28th, 2019