Search

Abstract Background Arteriovenous fistula (AVF) due to renal allograft biopsy is mechanical trauma resulting from the penetration of small arteries and veins by a core needle. Most AVFs are reported to resolve asymptomatically and spontaneously. This report presents a patient with acute kidney injury (AKI) due to urinary tract obstruction caused by a bleeding AVF in a renal allograft. Case presentation A 22-year-old Japanese woman who underwent living-donor kidney transplantation (KT) at 3 years due to end-stage renal disease caused by focal segmental glomerulosclerosis (FSGS) presented with a renal transplant AVF (gourd-shaped; 42 × 19 × 20 mm). The AVF was unexpectedly discovered by ultrasound before a surveillance biopsy at 10 years after KT. The patient had a history of recurrent FSGS, had undergone several renal allograft biopsies after KT, and did not experience symptoms or growth of the AVF for years. Nineteen years after KT, the patient developed AKI with sudden, asymptomatic, gross hematuria and anuria. Plain computed tomography revealed a hematoma in the pelvis of the renal allograft and bladder tamponade. The AVF was successfully treated by coil embolization. Hemodialysis was performed for AKI, and graft function was gradually recovered. Conclusions Unexpected bleeding from a renal transplant AVF may lead to transplant dysfunction. Angiographic embolization against the ruptured renal transplant AVF may prevent rebleeding and rescue the renal allograft.

Background: Arteriovenous fistula (AVF) due to renal allograft biopsy is mechanical trauma resulting from the penetration of small arteries and veins by a core needle. Most AVFs are reported to resolve asymptomatically and spontaneously. This report presents a patient with acute kidney injury (AKI) due to urinary tract obstruction caused by a bleeding AVF in a renal allograft. Case presentation: A 22-year-old Japanese woman who underwent living-donor kidney transplantation (KT) at 3 years due to end-stage renal disease caused by focal segmental glomerulosclerosis (FSGS) presented with a renal transplant AVF (gourd-shaped; 42 × 19 × 20 mm). The AVF was unexpectedly discovered by ultrasound before a surveillance biopsy at 10 years after KT. The patient had a history of recurrent FSGS, had undergone several renal allograft biopsies after KT, and did not experience symptoms or growth of the AVF for years. Nineteen years after KT, the patient developed AKI with sudden, asymptomatic, gross hematuria and anuria. Plain computed tomography revealed a hematoma in the pelvis of the renal allograft and bladder tamponade. The AVF was successfully treated by coil embolization. Hemodialysis was performed for AKI, and graft function was gradually recovered. Conclusions: Unexpected bleeding from a renal transplant AVF may lead to transplant dysfunction. Angiographic embolization against the ruptured renal transplant AVF may prevent rebleeding and rescue the renal allograft. [ABSTRACT FROM AUTHOR]

Introduction: The kidney is exposed to a variety of crystalline substances which can cause tissue damage. There are limited studies on the frequency of crystal deposits in renal allograft biopsies especially from our part of the world. Objectives: The objective of this study was to find out the prevalence of crystal deposits among the allograft biopsies received at our centre over five years, and to identify its clinicopathological implications. Patients and Methods: We have retrospectively searched the records of renal biopsies reported during the period from 2014 to 2018, to identify allograft biopsies with crystal deposits. The histopathological findings including the density of deposits were noted and correlated with demographic and clinical profile in the light of available literature. Results: Of 1225 transplant biopsies received during the study period, 1.5% had crystal deposits reported on morphology. These biopsies were from 13 patients evaluated for graft dysfunction; 10 had oxalate crystals while three had the rare 2,8-dihydroxyadenine (DHA) crystals. Crystal density varied from 1 to 26/mm2 and all showed acute tubular injury. Around 39% of the biopsies with crystals, included in this study, were taken within a month of transplant and those cases with subsequent biopsies showed progressive interstitial fibrosis/tubular atrophy (IF/TA). All three cases of DHA nephropathy were first diagnosed only on allograft biopsies. Conclusion: In the process of graft dysfunction, interpretation of allograft biopsy should include a careful search for crystals including polarised microscopy as this might not only explain deterioration of renal function, but also clinch the diagnosis of native kidney disease. Though our study has limitations, it addresses a less discussed issue and further studies are required to reinforce the significance of crystal induced allograft injury.

Introduction: The kidney is exposed to a variety of crystalline substances which can cause tissue damage. There are limited studies on the frequency of crystal deposits in renal allograft biopsies especially from our part of the world. Objectives: The objective of this study was to find out the prevalence of crystal deposits among the allograft biopsies received at our centre over five years, and to identify its clinicopathological implications. Patients and Methods: We have retrospectively searched the records of renal biopsies reported during the period from 2014 to 2018, to identify allograft biopsies with crystal deposits. The histopathological findings including the density of deposits were noted and correlated with demographic and clinical profile in the light of available literature. Results: Of 1225 transplant biopsies received during the study period, 1.5% had crystal deposits reported on morphology. These biopsies were from 13 patients evaluated for graft dysfunction; 10 had oxalate crystals while three had the rare 2,8-dihydroxyadenine (DHA) crystals. Crystal density varied from 1 to 26/mm2 and all showed acute tubular injury. Around 39% of the biopsies with crystals, included in this study, were taken within a month of transplant and those cases with subsequent biopsies showed progressive interstitial fibrosis/tubular atrophy (IF/TA). All three cases of DHA nephropathy were first diagnosed only on allograft biopsies. Conclusion: In the process of graft dysfunction, interpretation of allograft biopsy should include a careful search for crystals including polarised microscopy as this might not only explain deterioration of renal function, but also clinch the diagnosis of native kidney disease. Though our study has limitations, it addresses a less discussed issue and further studies are required to reinforce the significance of crystal induced allograft injury. [ABSTRACT FROM AUTHOR]

Objective Gene expression profiling by microarrays or RT PCR has been studied in certain western centers to enhance the diagnostic accuracy of allograft biopsy, however, such sophisticated tests are difficult to apply in developing countries. This study was conducted to evaluate the expression of von Willebrand factor (VWF) and Interferon-gamma (IFNγ) as an end PCR product in renal allograft biopsy with different pathological categories. Methods Forty-nine (49) indicated renal allograft biopsies were analyzed histologically by the Banff 2017 classification, inflammatory cell infiltration was analyzed by immunohistochemistry study for CD4, CD8, CD16, and CD68 markers, and a fresh tissue used for molecular study. Results The biopsy findings were acute T-cell mediated rejection (A-TCMR) 30.6%, interstitial fibrosis and tubular atrophy 22.4%, C4d- Transplant glomerulopathy 12.2%, calcineurin inhibitor toxicity 10.2%, C4d+antibody mediated rejection 10.2% and normal histology 14.3%. The only significant difference in VWF expression was between acute TCMR and normal, P=0.01, Spearman's correlation also showed a significant relationship between VWF and acute TCMR (r=0.53, P=0.01), and VWF was found to correlate with the numbers of interstitial CD4+ (r=0.29, P=0.03) and CD68+ (r=0.37, P=0.007) cells. IFNγ expression was significant in acute TCMR versus normal, P=0.009. Spearman's pair-wise testing showed that INFγ correlated with CD8 in both the glomerular (r=0.38, P=0.006) and interstitial (r=0.30, P=0.04) compartments and with CD16+ interstitial cells (r=0.36, P=0.01). Conclusions Molecular and immunohistochemistry data of this study distinguish acute TCMR from other forms of transplant pathology and mildly dysfunctional kidneys with normal histology. [ABSTRACT FROM AUTHOR]

Introduction: Herein, we discuss clinicopathological analyses of cases of chronic renal allograft arteriopathy (CRA) after renal transplantation and clarify the mechanisms underlying the development and prognostic significance of CRA., Methods: CRA was diagnosed in 34 renal allograft biopsy specimens (BSs) obtained from 27 renal transplant patients who were followed up at the Department of Urology and Transplant Surgery, Toda Chuo General Hospital, between January 2010 and December 2020., Results: CRA was diagnosed at a median of 33.4 months post-transplantation. Of the 27 patients, 16 had a history of rejection. Among the 34 BSs showing evidence of CRA, CRA was mild (cv1 in Banff's classification) in 22, moderate (cv2) in 7, and severe (cv3) in 5 patients. We then classified the 34 BSs showing evidence of CRA based on their overall histopathological features as follows: cv alone seen in 11 (32%) BSs, cv + antibody-mediated rejection (AMR) in 12 (35%), and cv + T-cell-mediated rejection (TCMR) in 8 (24%). Loss of the renal allograft occurred during the observation period in 3 patients (11%). Of the remaining patients with functioning grafts, deterioration of renal allograft function after biopsies occurred in 7 cases (26%)., Conclusions: Our study results suggest that AMR contributes to CRA in 30-40% of cases, TCMR in 20-30% of cases, isolated v lesions in 15% of cases, and cv lesions alone in 30%. The intimal arteritis was a prognostic factor in CRA., (© 2023 S. Karger AG, Basel.)

Focal segmental glomerulosclerosis commonly recurs following kidney transplantation. A 33-year-old man underwent living donor kidney transplantation. Proteinuria appeared two months after transplantation, and an episode biopsy on postoperative day 66 revealed recurrent focal segmental glomerulosclerosis lesions of the cellular variant by Columbia classification. We reviewed the native kidney biopsy and confirmed collapsing variant focal segmental glomerulosclerosis. Plasma exchange therapy was performed, and his proteinuria temporarily resolved. A second allograft biopsy performed on postoperative day 200 showed no evidence of focal segmental glomerurosclerosis. He experienced incomplete remission with a proteinuria of 0.5 g/day during the subsequent three years until his urinary protein level rose to 1.3 g/day. A third biopsy performed on postoperative day 1248 showed focal segmental glomerulosclerosis cellular variant lesions. Plasma exchange was resumed in combination with additional rituximab, but his proteinuria persisted. Intermittent plasma exchange was performed 42 times in total. However, his proteinuria continued, and his renal function gradually worsened. A fourth biopsy performed on postoperative day 2540 showed focal segmental glomerulosclerosis collapsing variant lesions with severe interstitial fibrosis and tubular atrophy. He ultimately required hemodialysis seven years after transplantation. Intensive therapy with long-term intermittent plasma exchange and rituximab suppressed proteinuria and preserved graft function for seven years, at which time graft failure occurred. We here present the clinical course and histological findings from consecutive allograft biopsies. [ABSTRACT FROM AUTHOR]

Till the early 1990s there was no standardized international classification of renal allograft biopsies resulting in considerable heterogeneity in reporting among the various centers. A group of dedicated renal pathologists, nephrologists, and transplant surgeons developed a schema in Banff, Canada in 1991. Subsequently there have been updates at regular intervals. The following review presents the evolution of the Banff classification and its utility for clinicians. [ABSTRACT FROM AUTHOR]

Background: In the early post-transplant period, renal allograft rejection with diffuse peritubular capillary (PTC) C4d deposition predicts poor graft survival. In the late post-transplant setting, that is, one or more yr after transplantation, the implication of diffuse PTC C4d deposition is still a topic of debate. The purpose of our study was to see if diffuse PTC C4d deposition, in late acute rejection (LAR), occurring more than one yr post-transplant, has any impact on graft survival and function. Methods: We selected cases, both cadaveric as well as living donor renal transplant recipients, in whom acute rejection with PTC C4d deposition was first detected after the first year post-transplant. Recipients with multiple acute rejection episodes during the first year post-transplant were excluded from the study. The first biopsy diagnosed with LAR was considered the index biopsy (n = 40). We formed two groups: group 1, C4d-positive LAR (n = 20), and group 2, C4d-negative LAR (n = 20). Groups were matched for maintenance and post-rejection immunosuppressive therapy, baseline serum creatinine levels before the time of the index biopsy, time from transplant to index biopsy, as well as chronic allograft damage index (CADI) score in the index biopsies. We compared the rate of graft loss, and the graft function of the surviving grafts at the end of the study period, as well as histologic parameters in the index biopsy specimens between the two groups. The mean follow-up period was 20 months. Results: No significant differences in the rate of graft loss or graft function were found between groups 1 and 2 at the end of the follow-up period. Histologically, PTC margination and transplant glomerulopathy were more common in the C4d-positive group, and this difference was statistically significant. There was no statistically significant difference in the degree of plasma cell infiltrates. Conclusions: Unlike in the acute setting, the presence or absence of PTC C4d staining in renal allografts with LAR may not have a predictive value regarding graft outcome. [ABSTRACT FROM AUTHOR]

Antibody-mediated rejection is an important cause of chronic allograft dysfunction. We report a case of chronic antibody-mediated rejection 13 yr after transplantation. This patient is a 19-yr-old man who had renal insufficiency since infancy because of bilateral polycystic kidneys. Peritoneal dialysis was started when he was four yr old and he received a renal allograft from his mother at the age of six yr. Donor and recipient were ABO compatible and immunosuppressive treatment was started with cyclosporine, mizoribine, and methylprednisolone. No acute rejection was experienced and histological acute rejection was not proven on any subsequent protocol biopsies. Ten yr after transplantation, a protocol biopsy revealed moderate chronic allograft nephropathy and severe cyclosporine-associated arteriolopathy. His allograft function was preserved at this time and the cyclosporine dose was tapered to 125 mg/d. His renal function gradually deteriorated starting 12 yr after transplantation. Although mizoribine was changed to mycophenolate mofetil, he required dialysis one yr later. A diagnosis of antibody-mediated rejection was made based upon the renal biopsy findings (including C4d staining) and circulating anti-human leukocyte antigen (HLA) antibody levels (12 yr after transplantation). We conclude that it is necessary to pay attention to antibody-mediated rejection, even in allograft cases with good function for over 10 yr and no risk factors for the development of de novo anti-HLA antibodies. [ABSTRACT FROM AUTHOR]

Introduction: Subcapsular cortical damage (SCCD) is a characteristic pathological change, which is seen in renal allograft biopsy specimen obtained immediately after laparoscopic donor nephrectomy (LDN). In this study we evaluated the early and late histopathological effect of SCCD examining renal allograft biopsy specimens obtained after kidney transplantation. Materials and methods: Laparoscopic donor nephrectomy was performed on 250 donors between July 2000 and September 2004 in our institution. Allograft biopsy of all 250 kidneys was performed immediately after LDN (zero hour biopsy). Of 250 biopsy specimens, 105 were diagnosed as SCCD and the allograft biopsy specimens obtained from 105 recipients after transplantation were enrolled in this study. All specimens were routinely examined by using light microscopy and immunofluorescence. Results: In 87 patients 256 allograft biopsy specimens did not show post-pathological changes of SCCD. Twenty biopsy specimens obtained from 18 recipients showed tubular necrosis and a partly tubular regeneration and patchy interstitial hemorrhage, which seemed to be caused by SCCD. Ten allograft biopsy specimens from nine recipients demonstrated residual pathologic changes in SCCD early after transplantation. The other 10 specimens from nine recipients had abnormal histopathologic changes including interstitial edema and fibrosis, tubular atrophy and glomerular sclerosis in the subcapsular cortex late after transplantation. Conclusion: The early change of SCCD after transplantation remained intact and partial regeneration and the late showed subcapsular fibrosis with glomerular sclerosis. The incidence of the subcapsular lesions due to SCCD after transplantation was 17% in 105 allografts. [ABSTRACT FROM AUTHOR]

Shimizu T, Tanabe K, Ishida H, Toma H and Yamaguchi Y. Histopathological evaluation of 0-h biopsy specimens of donor kidney procured by laparoscopic donor nephrectomy Clin Transplant 2004: 18 (Suppl. 11): 24–28. © Blackwell Munksgaard, 2004 We evaluated the histopathology of donor kidneys procured by laparoscopic donor nephrectomy (LDN), by examining allograft biopsy specimens obtained immediately after donor nephrectomy (0-h biopsies). LDN was performed on 65 donors between December 1999 and November 2002, in our institution. Their mean age was 56 years, and there were 19 males and 46 females. Hand-assisted LDN (HALDN) was used in 10 cases and retroperitoneal LDN (RPLDN) in 55 cases. Allograft biopsy of all 65 kidneys was performed immediately after LDN (0-h biopsy), and the biopsy specimens were used in this study. All specimens were routinely examined by light and immunofluorescence microscopy. The 43 donors who underwent traditional open donor nephrectomy (ODN) between January 2001 and June 2001 served as controls. There was no significant difference in the rate of glomerular sclerosis and moderate interstitial fibrosis with tubular atrophy, the severity of arteriosclerosis, and the severity of arteriolar hyalinosis among the specimens from kidneys removed by the three different methods: HALDN, RPLDN, and ODN. Prominent and characteristic histopathological changes which are not usually seen in 0-h biopsy specimens of kidneys obtained by traditional ODN were ‘subcapsular cortical damage (SCCD) with capsular lesions (CL)’. The SCCD with CL changes included a subcapsular degeneration and necrosis of tubular cells and a congestion of glomerular and peritubular capillaries (SCCD) associated with haemorrhage and fibrin deposits in the renal capsule (CL). In this study, such characteristic ‘SCCD with CL’ findings were observed in 35 specimens (54%). The damage was much milder in donor kidneys procured by RPLDN than by HALDN. SCCD with CL occurred in donor kidneys procured by LDN, which may be due to a compression of the renal parenchyma and veins. RPLDN may be better method for donor nephrectomy. [ABSTRACT FROM AUTHOR]

Abstract: We examined histological features of allograft biopsies in ABO minor-mismatched kidney transplantation. Forty-five patients who underwent ABO minor-mismatched kidney transplantation between September 1999 and December 2001 at our institute. The mean age was 32.6 years, with 28 males and 17 females. We divided them into five groups based on the donor and recipient ABO blood groups. Group 1, O renal allografts given to A patients (13 patients); Group 2, O to B (9), Group 3, O to AB (2); Group 4, A to AB (9); and Group 5, B to AB (12). From September 1999 to April 2002, we performed 127 allograft biopsies in these 45 ABO minor-mismatched kidney transplant recipients. Among a total of 127 biopsy specimens, 47 specimens were taken as 0- or 1-h biopsies and 6 were protocol biopsies. Pathological analysis of 74 episode biopsy specimens showed: acute humoral rejection (AHR) in 13 (18%); acute cellular rejection (ACR) in 17 (23%); combined AHR and ACR in eight (11%); borderline change in six (8%); chronic rejection in 10 (12%); cyclosporin or tacrolimus nephrotoxicity in seven (10%) and chronic allograft nephropathy in three (4%). In total, some form of acute rejection (AR) was seen histologically in 38 biopsy specimens (48%) from 19 patients (42%). When we investigated AR in two separate categories, i.e. AHR and ACR, AHR was diagnosed in 21 biopsy specimens (26%) from 15 patients (33%) and ACR was seen in 25 biopsy specimens (31%) from 13 patients (29%). We compared the incidence rate of acute rejection in the cases of ABO minor-mismatched renal transplantation with ABO-incompatible and ABO-compatible cases between January 1989 and December 1999. The incidence rate of AR in ABO minor-mismatched cases (42%) was statistically lower than that in ABO-incompatible cases (63%). There was no statistical difference in the incidence rate of AR between ABO minor-mismatched cases and ABO-compatible cases (49%). There was statistical difference in the incidence of AR... [ABSTRACT FROM AUTHOR]

Background. Chronic allograft nephropathy (CAN) is a composite term for various types of damage to a kidney transplant. We wanted to analyse its components in relation to baseline biopsy findings, transplant function, and outcome. [ABSTRACT FROM PUBLISHER]

Competing Interests: The authors have nothing to disclose.

Post-transplant lymphoproliferative disorder ( PTLD) is a neoplastic complication with a potentially fatal outcome that develops as a consequence of immunosuppression, and is mainly associated with Epstein- Barr virus ( EBV) infection. A 70-year-old woman underwent a live unrelated, ABO-incompatible renal transplant for end-stage renal disease. One year after transplantation, protocol biopsy revealed pathological changes indicative of the histological subtype of 'early lesions of PTLD' according to the World Health Organization classification, while the patient showed no clinical signs or symptoms. The patient was finally diagnosed with EBV-positive PTLD by in situ hybridization for EBER ( EBV-encoded RNA), and was successfully treated based on the reduction of immunosuppression. Protocol biopsy within the first post-transplant year is the only diagnostic measure to detect asymptomatic early PTLD, which allows for early intervention and leads to better outcomes. [ABSTRACT FROM AUTHOR]

Aim: We aimed to perform a clinicopathological analysis of cases presenting with borderline changes (BC) after renal transplantation and discuss whether BC might be clinically or pathologically important., Materials and Methods: BC was diagnosed in 22 renal allograft biopsy specimens obtained from 20 renal transplant recipients between April 2010 and March 2019 after follow-up at the Department of Transplant Surgery, Kidney Center, Toda Chuo General Hospital., Results: BC was diagnosed at a median of 500 days following transplantation. Among the 22 renal allograft biopsy specimens showing evidence of BC, tubulitis was observed in all specimens. Interstitial inflammation was present in 18 specimens (82%), peritubular capillaritis in 14 (64%), interstitial fibrosis (ci) and tubular atrophy (ct) in 4 (18%), and C4d deposition in the peritubular capillary was present in 6 specimens (27%). Glomerulitis and intimal arteritis were not observed. There was no renal graft loss during the observation period, but deterioration of renal allograft function after biopsy occurred in 9 patients (45%)., Conclusions: In BC, tubulitis and interstitial inflammation were the main constituents. Because glomerulitis was not observed in our study, we suspect that BC contributes to acute T-cell-mediated rejection. Although BC did not lead to renal graft loss, renal graft function deterioration was seen in nearly half of the patients after the renal graft biopsy. We conclude that BC is important clinically and pathologically and needs to be monitored and treated appropriately., (© 2020 S. Karger AG, Basel.)

Evolving BK polyomavirus–associated nephropathy (BKPyVAN) is characterized by tubulointerstitial inflammation that closely resembles acute T‐cell–mediated allograft rejection if tubulitis is significant. The cellular composition of the inflammation varies during the course of BKPyVAN, and clusters of plasma cells may herald resolution of the infection. Less commonly, BKPyVAN can present with a predominance of histiocytes and granuloma formation. Granulomatous interstitial nephritis is uncommon in biopsies of either native or transplant kidneys. In both settings, this distinctive type of inflammatory response requires a systematic approach with careful clinicopathological assessment to determine its etiology. We present three patients with granulomatous BKPyVAN in the first year post‐transplantation. These allograft biopsies at 4, 6, and 12 months post‐transplant exemplify spontaneously resolving BKPyVAN, resolving infection after immunosuppression reduction, and early BKPyVAN, respectively. In immunosuppressed patients, BKPyVAN should be added to the relatively broad differential diagnosis of granulomatous tubulointerstitial nephritis. [ABSTRACT FROM AUTHOR]