Joseph Bonventre, M.D., Ph.D.

One in nine adults worldwide has some kind of kidney disease, and kidney failure is becoming more common everywhere. Growing functional kidney tissue in a lab could accelerate kidney disease treatments and restore kidney function. In humans, the kidney forms naturally as a consequence of two building blocks: metanephric mesenchyme and ureteric bud.

Seven years ago, researchers in Dr. Joseph Bonventre’s laboratory discovered how to create the first building block, known as metanephric mesenchyme, from human stem cells. Dr. Bonventre is the Chief of the Renal Unit and Founding Chief of the Engineering in Medicine Division at the Brigham and Women’s Hospital… Continue reading.

Kidney disease affects one in nine adults globally and the incidence of kidney failure is steadily rising around the world. Being able to grow working kidney tissue in a laboratory could help accelerate medical treatments for kidney disease and restore kidney function. The kidney forms normally in humans as a result of two building blocks—metanephric mesenchyme and ureteric bud. The laboratory of Joseph Bonventre, MD, Ph.D., Chief of the Renal Unit and Founding Chief of the Engineering in Medicine Division at the Brigham, figured out how to generate the first building block—metanephric mesenchyme—resulting in many components of the kidney from human stem cells seven years ago.

The same laboratory has now developed a highly efficient method to generate the second building block (ureteric bud), which matures into the adult kidney collecting system. Furthermore, they demonstrated features of interaction between the cells of these two building blocks, reproducing aspects of interaction which normally occur when the kidney develops. In addition, for the first time ever, the Bonventre laboratory has developed human cell lines of principal and intercalated cell lines, the two cell lines that make up the last urine processing component of the kidney… Continue reading.

Chronic kidney disease is a global health concern, affecting about 10 percent of the world’s population–and increasing in prevalence. A final, common pathway in chronic kidney disease is fibrosis. Just as fibrosis–or the formation of fibrous connective tissue–can cause devastating effects in the lung, liver, heart and elsewhere, fibrosis of the kidneys can ultimately lead to end-stage kidney failure. In recent years, investigators have found that after acute kidney injury, the kidneys often fail to completely repair themselves, and kidney cells may get stuck during the cell cycle in a state in which they release profibrotic factors. A new study, published in Science Translational Medicine, builds upon these findings, identifying key factors involved in this cell cycle arrest and illuminating their consequences. Based on these discoveries, the research team, led by investigators at Brigham and Women’s Hospital, also identifies a novel intracellular structure and new therapeutic targets for kidney fibrosis.

“As a disease mechanism, fibrosis may account for more deaths than any other,” said corresponding author Joseph Bonventre, MD, PhD, chief of the Division of Renal Medicine at the Brigham and a faculty member of the Harvard Stem Cell Institute. “Our lab has been studying acute and chronic kidney injury and fibrosis for many years. We’re now focused on the transition from acute to chronic kidney disease and what leads to fibrosis in the kidneys.”

Bonventre and colleagues studied the transition from acute to chronic kidney disease in mice, using extracted epithelial cells and conducting unbiased gene expression analyses… Continue reading.