Biomedical subjects

Lukas Haragsim

Publications and source records attributed to Lukas Haragsim.

4 recordsLinked to original sources

PubMed2006

Calcineurin nephrotoxicity.

Calcineurin inhibitors, cyclosporine and tacrolimus, have improved allograft survival in solid organ transplantation. Indeed, they have reduced the incidence of acute rejection episodes of cadaveric allograft recipients. Although marked progression has been made in initial survival rates, long-term kidney graft survival has yet to show such encouraging results. Chronic allograft dysfunction is the major hindrance to long-term graft survival and many components contribute to this entity, both immunologic and nonimmunologic. Chronic calcineurin nephrotoxicity is a major factor in chronic allograft dysfunction. This review will highlight the current understanding and management of calcineurin nephrotoxicity in kidney transplantation.

Animals↗

PubMed2006

Chronic allograft nephropathy.

With the advent of calcineurin inhibitors, the success of kidney and other solid-organ transplants has improved significantly from the standpoint of reducing the incidence of acute rejection. Over the past 2 decades, both short-term allograft survival and acute rejection rates have dramatically improved with improved diagnostic and therapeutic techniques such as standardized pathology scoring; potent antirejection drugs such as anti-thymocyte globulin, interleukin-2 receptor antibodies, cyclosporine, tacrolimus, sirolimus, and mycophenolate mofetil; and improved infection control such as valganciclovir and antifungal therapy. However, long-term graft loss has remained at nearly constant levels over the same period of time, with the average half-life of a deceased-donor kidney transplant in the United States remaining approximately 1 decade. In addition to death with a functioning allograft and calcineurin toxicity, a chronic fibrotic process-known at various times as chronic rejection, chronic allograft dysfunction, and chronic allograft nephropathy (CAN)-account for the leading causes of transplant failure.

Graft Survival↗

PubMed2006

Nephrotoxicity as a complication of antiretroviral therapy.

Since 1984, human immunodeficiency virus-associated nephropathy has been established as a clinical entity that presents with nephrotic syndrome and progressive kidney failure. The pathological description is usually consistent with a collapsing form of focal segmental glomerulosclerosis. Podocytes and renal tubular cells have been proposed as a reservoir for the human immunodeficiency virus. This nephropathy is the third leading cause of end-stage renal disease in the population of African descent. It is documented that highly active antiretroviral therapy (HAART) successfully reverses or at least controls nephropathy in HIV-positive patients. The success of the treatment of HIV nephropathy now poses 2 problems to nephrologists: (1) an increased population of HIV-positive patients with chronic kidney disease not yet on dialysis and (2) potential nephrotoxicity of antiretroviral medications as well as medications used to treat opportunistic infections. HAART is defined by the combination of 2 reverse transcriptase inhibitors with a protease inhibitor or 3 reverse-transcriptase inhibitors. Many of these antiretrovirals have well-defined nephrotoxic effects. The objective of this text is to review data pertaining to some of the most common antiretrovirals (ARTs) and include information regarding nephrotoxicity of the medications frequently used to combat opportunistic infections. ARTs included in the review are (1) nucleoside reverse-transcriptase inhibitors (zidovudine and didanosine), (2) nucleotide reverse transcriptase inhibitors (adefovir and tenofovir), (3) the protease inhibitors (indinavir and saquinavir), and (4) the HIV fusion inhibitors.

Anti-Retroviral Agents↗

PubMed2006

HIV-associated nephropathy.

Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is one of the most important causes of progressive kidney failure in HIV-1-seropositive patients. Since the 1980s, much has been published regarding the epidemiology, pathogenesis, and treatment of HIVAN. Our knowledge of the clinical features, pathologic manifestations, course, and potential outcome of HIVAN has increased considerably. The use of highly active antiretroviral therapy has shown significant improvement in the outcome of human immunodeficiency virus infection and is found to be effective in preventing end-stage renal disease. The purpose of this review is to summarize the data about the clinical manifestations, pathogenesis and pathophysiologic mechanisms of HIVAN with particular attention on treatment including pharmaceutical and renal replacement options.

AIDS-Associated Nephropathy↗