# Acute Rejection With DSA‐Negative Severe Microvascular Inflammation in a Kidney Transplant Recipient With an Isolated DPB1*04‐Mismatch Successfully Stabilised With Daratumumab

## TL;DR

A kidney transplant patient with severe inflammation but no detectable antibodies was successfully treated with daratumumab, suggesting new mechanisms of rejection.

## Contribution

Demonstrates successful treatment of DSA-negative microvascular inflammation with daratumumab in a kidney transplant case.

## Key findings

- Severe microvascular inflammation was reversed with daratumumab in a DSA-negative kidney transplant recipient.
- The patient had an HLA-DPB1*04 mismatch but no detectable donor-specific anti-HLA antibodies.
- The case suggests NK cell alloreactivity as an alternative mechanism of rejection in the absence of B cell alloreactivity.

## Abstract

Microvascular inflammation (MVI) in kidney allografts in the absence of detectable donor‐specific anti‐HLA antibodies (DSA) is increasingly recognised as a cause of premature graft failure following kidney transplantation. Potential mechanisms include NK cell alloreactivity mediated by recognition of mismatched HLA class I molecules (missing‐self) via killer‐immunoglobulin‐like receptors. Here, we report the case of an early kidney allograft rejection with severe MVI on biopsy in a patient that was fully HLA‐matched except for a HLA‐DPB1*04 mismatch in the donor. There were no detectable DSA at any time. MVI was successfully reversed and clinically stabilised with a 9‐month course of daratumumab (anti‐CD38 mAb). This case suggests alternative mechanisms of alloreactivity, such as NK cell‐mediated effects, and highlights the existence of MVI in the absence of detectable B cell alloreactivity. Moreover, this case exemplifies the potential of anti‐CD38 treatment in these patients.