Post-transplant Granulomatous Tubulointerstitial Nephritis (GIN)

Introduction: GIN is identified in less than 1% of allograft biopsies. We describe a case of GIN contributing to graft failure. Case Description: A 69-year-old man with ESKD of unknown etiology & liver failure from concomitant hepatitis B/C infection received a Simultaneous Liver-Kidney Transplant in 2017. He previously underwent a Living Unrelated Kidney Transplant in 2007. Recently, Serum creatinine (sCr) increased from 2.9 mg/dl to 4.3 mg/d with nephrotic range proteinuria (UPCR 6.0 GR/GR) and urinalysis showing pyuria (WBC 49) with no hematuria. He required hemodialysis given declining allograft function. An allograft biopsy (Images) showed acute pyelonephritis with non-necrotizing granulomata and negative AFB stain. Occasional collapsing lesions are identified in the glomeruli. And recurrent diabetic nephrosclerosis was also identified. We were unable to prove active tuberculosis infection. Discussion: GIN is commonly associated infectious agents in up to 60% of cases. The etiology GIN in this patient is likely multifactorial. His second post-transplant course was complicated with recurrent urinary tract infections, antibody mediated rejection, and most recently, an episode of cellular mediated rejection treated with corticosteroids and thymoglobulin. However, granulomata in the interstitium rarely cause nephrotic range proteinuria. The observed proteinuria is attributed to collapsing lesions and concurrent diabetic kidney disease. De novo collapsing lesions, which can appear in 10-20% of kidney allografts, are linked to several risk factors including: high-risk ApoL1 genotype, viral infections such as HIV, SARS-CoV-2, CMV, EBV and BK virus, recent or active rejection, and acute vaso-occlusion.Allograft biopsy. H&E stain, 200x magnification.