Back
Vascular injury associated with rejection events impacts graft survival and should be considered when sudden deterioration in renal function occurs. Quantifying the extent and vascular involvement is important in the treatment of transplant rejection. In normal kidney biopsies, only limited portions of the renal artery or arterioles can be visualized. The case of a male patient who presented due to worsening renal function after discontinuation of immunosuppressive therapy. In this case, various vascular lesions could be observed.
A 48-year-old patient with CKD since 2004. Transplantation from a deceased donor in 2007, without rejection events, baseline CrS 1.2 mg/dl, immunosuppressive treatment with prednisone, cyclosporine and mycophenolic acid. In 2020 with irregular adherence to immunosuppressive treatment, last creatinine in July 2022 at 1.8 mg/dl. In October 2022, with asthenia, nausea and sudden decrease in urine output; worsening in renal function (SCr 14.80 mg/dl) due to uremic syndrome start of renal replacement therapy. A kidney biopsy was performed showing active interstitial tubular rejection (I3, T3) with vascular component (V2) suggesting humoral component (G3, PTC3, V2), superimposed on chronic changes (CG2, I-IFTA2, CI2, CT2). C4D3+ in peritubular capillaries. Interstitial fibrosis grade II (30%). Although fibrosis is not greater than 50%, the degree of edema, inflammation and interstitial hemorrhage causes practically total loss of the renal parenchyma.
Based on renal biopsy findings, methylprednisolone treatment was initiated without restoring renal function; the patient continued renal replacement therapy. In January 2023, he had intermittent macroscopic hematuria and urinary tract infection, so a nephrectomy of the graft was performed with a pathology report similar to the data reported in the previous biopsy, active glomerular thrombotic microangiopathy was added, as well as fibrosis increased by 50%. Off note, diffuse interstitial hemorrhage occurs with coagulative necrosis with endotheliitis and endarteritis occluding the capillary lumens; in the hilum and renal sinus with inflammatory infiltrate affecting the entire thickness of the hilar vessels. Macroscopically, the graft was described as an irregular dark red specimen with a hemorrhagic appearance. immunosuppression.
When endarteritis occurs, whether antibody-mediated rejection or tubulointerstitial rejection, graft survival is worse. The spectrum of vascular involvement can range from luminal narrowing to hyalinosis, endotheliitis, endarteritis, and thrombotic microangiopathy (TMA). Clinically, the disease is manifested by rapid deterioration of renal function, difficult control of blood pressure, decreased urine output, and macroscopic hematuria, all of which appeared as signs of vascular involvement. Vascular pathological manifestations in active/chronic humoral rejection include a broad repertoire with significant clinical implications. Vascular involvement helps predict kidney graft survival. Therefore, the degree and extent of these vascular lesions should be clarified to treat allograft rejection and predict graft survival prognosis. We need to recognize the pathological features of severe vascular lesions and even consider the possibility that vascular lesions may reach the larger renal artery and explain the acute deterioration of renal graft function.