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      Renal Growth Factors: Past, Present and Future

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          It is known that a series of mediators, so-called growth factors, are able to induce hypertrophy of the kidney in a patient after uninephrectomy. The first investigator who demonstrated this phenomenon was C. Sacerdotti, an Italian pathologist of Bizzozero’s School in Turin, who published an important report in 1896. He attempted to explain how compensatory renal hypertrophy occurred and how this hypertrophy might be induced in a normal dog. Interestingly, he demonstrated that when the kidneys of a normal dog received a blood transfusion from uni- or binephrectomized dogs several mitoses appeared in the renal epithelium. These mitoses, expression of renal hypertrophy, were more evident in dogs receiving several blood transfusions for 6–7 days. He concluded that hypertrophy was induced by specific substances circulating in the blood of uni- or binephrectomized dogs. This hypothesis was in the next 100 years confirmed by the discovery of renal growth factors such as epidermal growth factor, insulin-like growth factor-1, hepatocyte growth factor, platelet-derived growth factor and others. The pathogenic role of these mediators is evident in the recovery of tubules after acute tubular necrosis and in the remnant glomeruli after glomerular damage. Today, attempts to use these growth factors for improving renal function in patients with acute tubular necrosis and to block their action in the progression of renal damage in chronic glomerulonephritides are under investigation. Future trends in these growth factors will be set by drug companies designing specific therapies such as gene therapy. In conclusion, the outstanding observation by Sacerdotti, over a century ago, remains an important step in nephrologic history for prognosis and therapy of renal diseases.

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          Natural inhibitor of transforming growth factor-beta protects against scarring in experimental kidney disease.

          The central pathological feature of human kidney disease that leads to kidney failure is the accumulation of extracellular matrix in glomeruli. Overexpression of transforming growth factor-beta (TGF-beta) underlies the accumulation of pathological matrix in experimental glomerulonephritis. Administration of an antibody raised against TGF-beta to glomerulonephritic rats suppresses glomerular matrix production and prevents matrix accumulation in the injured glomeruli. One of the matrix components induced by TGF-beta, the proteoglycan decorin, can bind TGF-beta and neutralize its biological activity, so decorin may be a natural regulator of TGF-beta (refs 3, 4). We tested whether decorin could antagonize the action of TGF-beta in vivo using the experimental glomerulonephritis model. We report here that administration of decorin inhibits the increased production of extracellular matrix and attenuates manifestations of disease, confirming our hypothesis. On the basis of our results, decorin may eventually prove to be clinically useful in diseases associated with overproduction of TGF-beta.
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            Suppression of experimental glomerulonephritis by antiserum against transforming growth factor beta 1.

            Glomerulonephritis is an inflammation of the kidney characterized by the accumulation of extracellular matrix within the damaged glomeruli, impaired filtration and proteinuria. In its progressive form, the disease destroys kidney function leading to uraemia and death, unless dialysis therapy or kidney transplantation is available. The pathogenesis of glomerulonephritis is incompletely understood, but the eliciting factor is thought often to be an immunological injury to mesangial and/or other resident cells in the glomeruli. We have used an animal model of acute mesangial proliferative glomerulonephritis to show that this disease is associated with increased production and activity of transforming growth factor beta 1 (TGF-beta 1), an inducer of extracellular matrix production. Here we report that administration of anti-TGF-beta 1 at the time of induction of the glomerular disease suppresses the increased production of extracellular matrix and dramatically attenuates histological manifestations of the disease. These results provide direct evidence for a causal role of TGF-beta 1 in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.

              Author and article information

              Am J Nephrol
              American Journal of Nephrology
              S. Karger AG
              April 1999
              23 April 1999
              : 19
              : 2
              : 308-312
              Department of Intensive Care and Transplantation, Division of Nephrology, University of Bari, Polyclinic, Bari, Italy
              13466 Am J Nephrol 1999;19:308–312
              © 1999 S. Karger AG, Basel

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              Page count
              Tables: 3, References: 34, Pages: 5
              Self URI (application/pdf):
              Origins of Nephrology – The Modern Era


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