The Banff 97 working classification of renal allograft pathology

Endothelial Cells in Physiology and in the Pathophysiology of Vascular Disorders

Consensus statement on the pathology of IgG4-related disease

methods We evaluated the natural history of chronic allograft nephropathy in a prospective study of 120 recipients with type 1 diabetes, all but 1 of whom had received kidney–pancreas transplants. We obtained 961 kidney-transplant–biopsy specimens taken regularly from the time of transplantation to 10 years thereafter. results Two distinctive phases of injury were evident as chronic allograft nephropathy evolved. An initial phase of early tubulointerstitial damage from ischemic injury (P<0.05), prior severe rejection (P<0.01), and subclinical rejection (P<0.01) predicted mild disease by one year, which was present in 94.2 percent of patients. Early subclinical rejection was common (affecting 45.7 percent of biopsy specimens at three months), and the risk was increased by the occurrence of a prior episode of severe rejection and reduced by tacrolimus and mycophenolate therapy (both P<0.05) and gradually abated after one year. Both subclinical rejection and chronic rejection were associated with increased tubulointerstitial damage (P<0.01). Beyond one year, a later phase of chronic allograft nephropathy was characterized by microvascular and glomerular injury. Chronic rejection (defined as persistent subclinical rejection for two years or longer) was uncommon (5.8 percent). Progressive high-grade arteriolar hyalinosis with luminal narrowing, increasing glomerulosclerosis, and additional tubulointerstitial damage was accompanied by the use of calcineurin inhibitors. Nephrotoxicity, implicated in late ongoing injury, was almost universal at 10 years, even in grafts with excellent early histologic findings. By 10 years, severe chronic allograft nephropathy was present in 58.4 percent of patients, with sclerosis in 37.3 percent of glomeruli. Tubulointerstitial and glomerular damage, once established, was irreversible, resulting in declining renal function and graft failure. conclusions Chronic allograft nephropathy represents cumulative and incremental damage to nephrons from time-dependent immunologic and nonimmunologic causes.

The natural history of chronic allograft nephropathy.

https://www.cybernephrology.ualberta.ca/banff/2009/publications/publication_banff2007_1.pdf

Banff 07 Classification of Renal Allograft Pathology: Updates and Future Directions

A 45-yr-old Japanese male underwent living-related kidney transplantation in August 2005, and immunosuppression consisted of tacrolimus, mycophenolate mofetil, methylprednisolone, basiliximab, and rituximab 200 mg. Allograft function was good, and the protocol biopsy post-transplant day 11 showed no evidence of rejection. The serum creatinine (s-Cr) level was maintained at the 1.2 mg/dL for 18 months. On February 2007, the patient's s-Cr level had increased to 2.03 mg/dL, and an episode biopsy was performed. The biopsy specimen demonstrated moderate to severe tubulitis and moderate interstitial infiltration of plasma cells and lymphocytes. The inflammatory cell infiltrate consisted of > 30% plasma cells. The histopathological findings were consistent with plasma cell-rich acute rejection (PCAR). The PCAR was treated by steroid pulse therapy, and his s-Cr level decreased to 1.58 mg/dL. A biopsy three months after the steroid pulse therapy showed no evidence of rejection. The patient's allograft function is currently stable, and s-Cr level is 1.7 mg/dL. This is a case of PACR, that was successfully treated with steroid pulse therapy alone.

A case of plasma cell‐rich acute rejection 18 months after kidney transplantation successfully treated with steroid pulse therapy

We describe a middle-aged woman in whom granulomatous interstitial nephritis (GIN) developed in a renal allograft. She had undergone bowel resection due to an uncertain diagnosis of active granulomatous bowel disease 30 years earlier. Thereafter, frequent hyperoxaluria as well as calcium oxalate stone and recurrent urinary tract infections had resulted in a progressive deterioration in kidney function over a period of 20 years. She underwent living donor kidney transplantation; however, her kidney function progressively deteriorated, despite transplantation. A biopsy of the renal allograft revealed GIN with granulomatous vasculitis accompanied by calcium oxalate crystals. These as well as the laboratory findings indicated a diagnosis of sarcoidosis. We considered that the aggravated granulomatous inflammation on the allograft was caused by recurrent sarcoidosis accompanied by hyperoxaluria.

/pdf/granulomatous-interstitial-nephritis-in-a-renal-allograft-100hawz1kq.pdf

Granulomatous interstitial nephritis in a renal allograft.

Endothelial chimerism in association with vascular rejection in patients after kidney transplantation.

Injury of peritubular capillaries correlates with graft function in chronic renal allograft nephropathy.

Henoch-Schonlein purpura nephritis (HSPN) frequently recurs in patients following kidney transplantation, and pregnancy has been reported to be an exacerbating factor However, little is known about the recurrence of HSPN during pregnancy in patients with superimposed pre-eclampsia having excellent graft function who had experienced kidney transplantation Here, we report a case of recurrent HSPN complicating severe pre-eclampsia six yr after transplantation A 31-yr-old woman who had received a living-related kidney transplant at age 25 became pregnant The cause of her end-stage renal disease was biopsy-proven HSPN She had an excellent clinical course after transplantation, with good allograft function (serum creatinine < 09 mg/dL, no proteinuria or hematuria, no episode of rejection), and normal blood pressure We discontinued the angiotensin II receptor blocker that had been prescribed to prevent glomerular hyperfiltration After week 17 of pregnancy, proteinuria and blood pressure increased markedly, and then her kidney function deteriorated progressively with intermittent mild microhematuria At week 28 of pregnancy, umbilical blood flow and fetal growth were impaired, prompting preterm cesarean delivery Subsequently, her blood pressure and serum creatinine normalized immediately, although the urinary protein excretion decreased insufficiently from 60 to 10 g/d at six months postpartum In general, hematuria has a predictive value for the recurrence of HSPN Clinically, we considered this case to be superimposed pre-eclampsia, not recurrent HSPN However, a biopsy conducted seven months postpartum suggested recurrent HSPN on her renal allograft In addition, focal segmental membranous nephropathy with Clq deposition was observed It was difficult to determine when the HSPN and membranous lesions occurred This case suggests that a pathological evaluation is important in HSPN patients after transplantation to reduce adverse risks during and after pregnancy

Yutaka Yamaguchi

Papers

A case of plasma cell‐rich acute rejection 18 months after kidney transplantation successfully treated with steroid pulse therapy

Granulomatous interstitial nephritis in a renal allograft.

Endothelial chimerism in association with vascular rejection in patients after kidney transplantation.

Injury of peritubular capillaries correlates with graft function in chronic renal allograft nephropathy.

Recurrence of Henoch–Schönlein purpura nephritis superimposed on severe pre‐eclampsia in a kidney transplant patient