Update October 4, 2018

 

 

Section 1

Content 1

Pathology

Acute renal allograft rejection is defined as an acute deterioration in allograft function associated with specific pathologic changes in the graft. There are two principal histologic forms of acute rejection:

Acute T cell-mediated (cellular) rejection (TCMR), which is characterized by lymphocytic infiltration of the tubules, interstitium, and, in some cases, the arterial intima.

Acute antibody-mediated rejection (ABMR), the diagnosis of which requires morphologic evidence of acute tissue injury, circulating donor-specific alloantibodies, and immunologic evidence of an antibody-mediated process (such as C4d deposition in the allograft).

ABMR and acute TCMR may coexist at the same time in the allograft.

Subclinical rejection is defined as the presence of histologic evidence of acute rejection on biopsy without an elevation in the serum creatinine concentration [1-10]. Subclinical rejection is primarily detected by a protocol, or surveillance, biopsy, which is obtained at a protocol-driven, prespecified time after transplantation rather than for a clinical indication such as allograft dysfunction. Most of the reports of subclinical rejection involve TCMR [1-8]. However, there are reports of allografts with histologic manifestations of ABMR in the absence of functional deterioration of kidney function [11]. (See 'Subclinical rejection' below.)

 

Pathophysiology

Acute renal allograft rejection is a major cause of allograft dysfunction. Some kidneys do not regain function even with maximal antirejection therapy.

Even among patients who recover, acute rejection episodes can have a negative impact on long-term graft survival. Acute rejection is a major predictor of interstitial fibrosis/tubular atrophy (IF/TA), formerly called chronic allograft nephropathy, which is responsible for most death-censored graft loss after the first year posttransplant.

There has been a dramatic reduction in the incidence of acute rejection due to the introduction of potent immunosuppressive drugs in the past three decades.

However, optimizing immunosuppression to both prevent allograft rejection and minimize drug toxicity, new-onset diabetes, dyslipidemia, infection, and malignancy remains challenging.

 

 

When neurofibromatosis causes large tumors or tumors that press on a nerve, surgery can help ease symptoms. Some people may benefit from other therapies, such as stereotactic radiosurgery or medications to control pain.