The Chronology of Renal Allograft Dysfunction: The Pathological Perspectives.

BACKGROUND

Antibody-mediated rejection (ABMR), T-cell-mediated rejection (TCMR), BK polyomavirus nephropathy, and calcineurin inhibitor (CNI) toxicity are all common causes of kidney allograft dysfunction that can affect long-term allograft function.

SUMMARY

The prevalence of various pathological diagnoses changes over time for both indication and protocol biopsies. Active ABMR and CNI toxic tubulopathy are the leading causes of kidney allograft dysfunction in the early posttransplant period. Active ABMR can also manifest as thrombotic microangiopathy. Acute TCMR, borderline for acute TCMR, and BK polyomavirus nephropathy will occur, then comes a causal peak of renal allograft dysfunction, followed by chronic active ABMR. Active ABMR in the late posttransplant period would progress to chronic active ABMR, indicating sequential evolution from the incipient to advanced phase of chronic active ABMR. CNI toxicity also manifests as chronic lesions of arteriolar hyalinosis. Interstitial fibrosis and tubular atrophy are the result of multiple insults and are linked to underlying diseases, particularly in the late posttransplant period. Even with established pathological criteria of the Banff scheme, it can be still challenging to clearly delineate the causes of the allograft dysfunction, especially in the complicated cases. Understanding the chronological causes of renal allograft dysfunctions improves comprehension of renal allograft pathology.

KEY MESSAGES

Identifying the time-dependent prevalence of renal allograft dysfunction can be a critical and effective approach to pathological diagnosis.