[Low cyclosporin levels induced by the brief use of rifampicin; immunosuppression may fail for several weeks].

Cyclosporin is an immunosuppressive agent with a wide range of therapeutic uses. In transplant patients, it is used for the prevention of rejection and graft-versus-host reactions. The metabolism and bioavailability of cyclosporin can be significantly and persistently influenced through induction of CYP3A4 caused by the concomitant use of rifampicin.

[DRESS syndrome as a result of sulfasalazine use].

A 24-year-old female developed DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms) as a result of sulfasalazine use. The DRESS syndrome is a severe and acute hypersensitivity reaction that can be caused by a variety of drugs. The clinical presentation is diverse; the most common symptoms are fever, exanthema and lymphadenopathy.

Differentiation between chronic rejection and chronic cyclosporine toxicity by analysis of renal cortical mRNA.

Background: In kidney transplantation, chronic allograft nephropathy (CAN) is the major cause of graft loss. Causes of CAN include chronic rejection and chronic cyclosporine A (CsA) nephrotoxicity. It is necessary to differentiate between these two entities in order to apply the appropriate therapeutic regimen for the individual patient, but this is hampered by the lack of discriminating functional and morphologic parameters.

Conversion from cyclosporine to azathioprine at three months reduces the incidence of chronic allograft nephropathy.

Background: Conversion from cyclosporine to azathioprine after renal transplantation has been shown to be beneficial in terms of allograft function, cardiovascular risk factor profile, and the incidence of gout. A higher incidence of acute rejection, however, has also been reported and uncertainty still exists about the long-term outcome after conversion. We report on the extended follow-up of an open-label, randomized trial that examined conversion to azathioprine as early as three months after transplantation.

Early interstitial accumulation of collagen type I discriminates chronic rejection from chronic cyclosporine nephrotoxicity.

Little is known regarding the composition of the interstitial extracellular matrix of kidney allografts with deteriorating function. Collagen I, III, and IV, the collagen IV alpha3 chain, and the laminin beta2 chain were investigated in biopsies of allografted kidneys with chronic cyclosporine A nephrotoxicity (CsAT) (n = 17), chronic rejection (CR) (n = 12), or chronic allograft nephropathy (CAN) (n = 19). alpha-Smooth muscle actin expression was also examined.

Renal tubular epithelial cell death and cyclosporin A.

Background: The pathogenesis of chronic cyclosporin A (CsA) nephrotoxicity is largely unknown. In this study we examined whether CsA produces cell death through necrosis or apoptosis of either cultured human proximal tubular epithelial cells (PTEC) or the porcine tubular cell line LLC-PK(1).

Methods: Primary isolates of human PTEC and LLC-PK(1) cells were treated for various time periods with CsA at concentrations of 0.