1. Home
  2. About NIDDK
  3. Staff Directory
  4. Jeffrey B. Kopp, M.D

Jeffrey B. Kopp, M.D.

Photo of Jeffrey Kopp
Scientific Focus Areas: Cell Biology, Clinical Research, Genetics and Genomics, Health Disparities, Virology

Professional Experience

  • 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
  • Section Chief, Kidney Diseases, Section, Kidney Diseases Branch, NIDDK, 2013 - present
  • Senior Investigator, NIDDK, NIH, 1995-present
  • Medical Staff Fellow, NIH, 1987-1995
  • Completed Training in Internal Medicine and Nephrology, University of Washington, 1987
  • M.D., University of Pennsylvania Medical School, 1980
  • B.A., Harvard College, 1975
  • Fellow, American Society of Nephrology

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 glomerular cells
  • clarifying interactions between HIV-1 infection and APOL1 renal risk variants in inducing podocyte damage
  • examining whether cardiotrophin-like cytokine 1 is a permeability factor that contributes to recurrent FSGS following kidney transplant
  • participating in the ORD-funded NEPTUNE study and NIDDK-funded CureGN of nephrotic diseases

Information for Patients

We are not actively recruiting individuals for clinical studies at this time. 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 anti-mouse 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 will be available from ATTCC in Fall 2020

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

Select Publications

APOL1 renal risk variants exacerbate podocyte injury by increasing inflammatory stress.
Wakashin H, Heymann J, Roshanravan H, Daneshpajouhnejad P, Rosenberg A, Shin MK, Hoek M, Kopp JB.
BMC Nephrol (2020 Aug 27) 21:371. Abstract/Full Text
Podocytopathies.
Kopp JB, Anders HJ, Susztak K, Podestà MA, Remuzzi G, Hildebrandt F, Romagnani P.
Nat Rev Dis Primers (2020 Aug 13) 6:68. Abstract/Full Text
View More Publications

Research in Plain Language

Our lab wants to translate the results from research on kidney diseases into medical practices for people who have these diseases. We are studying causes and medical treatments for kidney diseases in which scarring occurs on parts of some of the glomeruli, the tissue structures in the kidney that filter unneeded and harmful substances out of the blood and into the urine. This disease condition is called focal segmental glomerulosclerosis (FSGS). Some highlights of what we have recently learned about FSGS include the following.

  • APOL1 is a gene that encodes a protein tha contributes to normal kidney function. A particular variant of this gene accounts for much of the increased risk that individuals of African descent have for both FSGS and for a similar disorder that is associated with HIV infection. Individuals with this risk gene variant are five times more likely to develop FSGS than individuals with other normally occurring variants of the gene. They are seven times more likely (if HIV infected) to develop glomerular disease. Podocytes are the cells on the outside of the glomerulus that regulate what substances in the blood are filtered out into the urine and what substances are retained in the bloodstream. We are testing the hypothesis that this risk gene variant makes the podocytes more fragile. We are also trying to determine whether the scarring of the glomerulus (glomerulosclerosis) leads to high blood pressure or whether an existing tendency to have high blood pressure (essential hypertension) makes the fragile podocytes more susceptible to damage.
  • We also offer other researchers some of the specialized tools we have developed for conducting our research. These tools include mice with specific alterations in their genes (transgenic mice), biomolecules produced by the immune system that bind very specifically to certain substances or cell parts (antibodies), and cultures of podocytes with specific inherited properties (podocyte cell lines).