Peritubular Capillaritis in Early Renal Allograft Dysfunction Is an Indicator of Acute Rejection

2013 ◽  
Vol 45 (1) ◽  
pp. 163-171 ◽  
Author(s):  
J. Jin ◽  
Y. Xu ◽  
H. Wang ◽  
H. Huang ◽  
Q. He ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Renal Allograft ◽  
Allograft Dysfunction ◽  
Peritubular Capillaritis

scholarly journals The value of urine cytologic examination findings in the diagnosis of the acute renal allograft rejection

2003 ◽  
Vol 60 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Zeljka Tatomirovic ◽  
Radojka Bokun ◽  
Jovan Dimitrijevic ◽  
Ljiljana Ignjatovic ◽  
Anastasija Aleksic ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Allograft Rejection ◽  
Renal Allograft ◽  
Urine Cytology ◽  
Acute Allograft Rejection ◽  
Histological Findings ◽  
Renal Allograft Rejection ◽  
Renal Tubular Cells ◽  
Allograft Dysfunction ◽  
Acute Renal Allograft Rejection

Background. Acute rejection of allograft is one of the most serious complications of renal transplantation that requires fast and precise diagnostic approach. In this paper our experience in cytologic urinalysis as a diagnostic method of the acute renal allograft rejection was reviewed. Methods. The study group included 20 of 56 patients with transplanted kidneys who were assumed for the acute allograft rejection according to allograft dysfunction and/or urine cytology findings. Histological findings confirmed allograft rejection in 4 patients. Urine sediment obtained in cytocentrifuge was air-dried and stained with May-Grunwald-Giemsa. Acute allograft rejection was suspected if in 10 fields under high magnification 15 or more lymphocytes with renal tubular cells were found. Results. Acute transplant rejection occured in 32.1% patients. In 15 patients clinical findings of the acute renal allograft rejection corresponded with cytological and histological findings (in the cases in which it was performed). Three patients with clinical signs of the acute allograft rejection were without cytological confirmation, and in 2 patients cytological findings pointed to the acute rejection, but allograft dysfunction was of different etiology (acute tubular necrosis, cyclosporine nephrotoxicity). In patients with clinical, cytological and histological findings of the acute allograft rejection urine finding consisted of 58% lymphocytes, 34% neutrophilic leucocytes and 8% monocytes/macrophages on the average. The accuracy of cytologic urinalysis related to clinical and histological finding was 75%. Conclusion. Urine cytology as the reliable noninvasive, fast and simple method is appropriate as the a first diagnostic line of renal allograft dysfunction, as well as for monitoring of the graft function.

scholarly journals Differentiation of cytomegalovirus infection from acute rejection using renal allograft fine needle aspirates.

1991 ◽  
Vol 1 (11) ◽  
pp. 1204-1211
Author(s):  
C C Nast ◽  
A Wilkinson ◽  
J T Rosenthal ◽  
L Barba ◽  
P N Bretan ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Renal Allograft ◽  
Transplant Rejection ◽  
Positive Staining ◽  
Cmv Infection ◽  
Fine Needle ◽  
Tubular Cells ◽  
Fine Needle Aspirates ◽  
Allograft Dysfunction ◽  
Clinical Diagnoses

Cytomegalovirus (CMV) infection is an important cause of renal allograft dysfunction and may be difficult to distinguish from acute transplant rejection both clinically and histologically. To establish the early diagnosis of CMV infection, we used immunohistochemical staining with antibodies against CMV early nuclear protein (CMV-A) and histocompatibility leukocyte class II antigen (DR) in renal transplant fine needle aspirates. Fifty-eight aspirates from 27 patients were assessed, 53 for CMV-A and 53 for DR. Positive staining was defined as greater than or equal to 35% stained tubular cells for CMV-A and greater than or equal to 30% stained tubular cells for DR. Clinical diagnoses were made retrospectively without using the information obtained from aspirate diagnoses. CMV-A staining was negative in 44 aspirates, none at the time of CMV infection. CMV-A was positive in nine aspirates, seven during CMV infection (78%, P less than 0.00001 versus CMV-A negative). DR staining was never present in the absence of acute rejection. All aspirates performed during acute rejection had positive DR staining (P less than 0.00001 versus DR negative). Aspirates with acute rejection comprised 80% of all DR-positive aspirates, whereas those with CMV infection included only 13%. The percent CMV-A staining increased with CMV disease progression; DR staining decreased after successful treatment of acute rejection. These data demonstrate that CMV-A staining is associated with CMV infection whereas DR staining is not. DR staining is specifically related to acute rejection. CMV-A and DR staining of fine needle aspirates is a potentially valuable diagnostic tool to distinguish rapidly between CMV infection and acute transplant rejection as the etiology of renal allograft dysfunction.

scholarly journals The significance of cytologic examination of urine in the diagnosis of renal allograft dysfunction

2003 ◽  
Vol 60 (3) ◽  
pp. 299-304
Author(s):  
Zeljka Tatomirovic ◽  
Radojka Bokun ◽  
Ljljana Ignjatovic ◽  
Anastasija Aleksic ◽  
Vesna Skuletic ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Acute Tubular Necrosis ◽  
Allograft Rejection ◽  
Renal Allograft ◽  
Acute Allograft Rejection ◽  
Urine Sediment ◽  
Cytologic Examination ◽  
Allograft Dysfunction ◽  
Tubular Necrosis ◽  
Cyclosporine Nephrotoxicity

Background. This paper presents our experience with cytologic examination of urine in diagnosing renal allograft dysfunction. Methods. The study group included 23 patients with renal allograft dysfunction, selected from 56 patients who underwent renal transplantation. Etiologic diagnosis was made according to the clinical picture, histological findings during allograft biopsy, and cytologic examination of urine. Urine sediment was obtained in cytocentrifuge and was air dried and stained with May Grunwald Giemsa. Results. Out of 23 patients with allograft dysfunction in 18 (78.3%) patient it was caused by acute rejection, and in 5 (8.9%) patients by allograft infarction, cyclosporine nephrotoxicity, acute tubular necrosis and chronic nephropathy. In eighteen patients (78.3%) cytologic examination of urine was pathologic, while in 16 (70%) clinical and histology findings coincided with urine cytology findings. Out of 18 patients with acute allograft rejection in 15 patients cytologic examination of urine coincided with acute rejection. Out of 7 patients with expressed cyclosporine nephrotoxicity, in 5 cytologic examination of urine confirmed the cause of allograft dysfunction, as well as in one of 2 patients with acute tubular necrosis. Cytologic examination of urine indicated parenchymal damage in 2 patients with reccurent disease (membranoproliferative and focal sclerosing glomerulonephritis). In 4 of 5 patients suffering from chronic rejection in a year?s monitoring period, urine sediment periodically consisted of lymphocytes, neutrophilic leucocytes, monocyte/macrophages, tubular cells and cilindres, without the predominance of any cell type. In 3 patients allograft dysfunction was caused by infective agents (bacteria, fungus cytomegalovirus). Conclusion. Cytologic examination of urine might be an alternative to histological in diagnosing acute allograft rejection and acute tubular necrosis or nephtotoxicity. Also it might indicate parenchymal disease while the importance of urine cytology in chronic allograft nephropathy needs to be investigated further.

scholarly journals Plasma cell-rich acute rejection of renal allograft: an unusual case of acute allograft dysfunction

2016 ◽  
Vol 26 (3) ◽  
pp. 200-202
Author(s):  
Kian-Guan Lee ◽  
Sobhana Thangaraju ◽  
Syed Salahuddin Ahmed ◽  
Hwai Liang Loh ◽  
Alvin Ren Kwang Tng ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Disease Progression ◽  
Plasma Cell ◽  
Poor Prognosis ◽  
Unusual Case ◽  
Renal Allograft ◽  
Treatment Approach ◽  
Current Management ◽  
Allograft Dysfunction ◽  
Wide Range

We report a case of renal allograft dysfunction due to plasma cell-rich acute rejection (PCAR), which is an uncommon clinical entity with a wide range of differential diagnoses. Extensive diagnostic workup, treatment approach and outcome are discussed and we provide a brief summary of the current management dilemma. Nevertheless, the diagnosis of PCAR portends a poor prognosis and therefore timely diagnosis and intensification of treatment is crucial to prevent disease progression.

scholarly journals Preservation of epoxyeicosatrienoic acid bioavailability prevents renal allograft dysfunction and cardiovascular alterations in kidney transplant recipients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thomas Duflot ◽  
Charlotte Laurent ◽  
Anne Soudey ◽  
Xavier Fonrose ◽  
Mouad Hamzaoui ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Kidney Transplant ◽  
Plasma Levels ◽  
Renal Allograft ◽  
Transplant Recipients ◽  
Loss Of Function ◽  
Kidney Transplant Recipients ◽  
Allograft Dysfunction ◽  
Allograft Function ◽  
The Impact

AbstractThis study addressed the hypothesis that epoxyeicosatrienoic acids (EETs) synthesized by CYP450 and catabolized by soluble epoxide hydrolase (sEH) are involved in the maintenance of renal allograft function, either directly or through modulation of cardiovascular function. The impact of single nucleotide polymorphisms (SNPs) in the sEH gene EPHX2 and CYP450 on renal and vascular function, plasma levels of EETs and peripheral blood monuclear cell sEH activity was assessed in 79 kidney transplant recipients explored at least one year after transplantation. Additional experiments in a mouse model mimicking the ischemia–reperfusion (I/R) injury suffered by the transplanted kidney evaluated the cardiovascular and renal effects of the sEH inhibitor t-AUCB administered in drinking water (10 mg/l) during 28 days after surgery. There was a long-term protective effect of the sEH SNP rs6558004, which increased EET plasma levels, on renal allograft function and a deleterious effect of K55R, which increased sEH activity. Surprisingly, the loss-of-function CYP2C9*3 was associated with a better renal function without affecting EET levels. R287Q SNP, which decreased sEH activity, was protective against vascular dysfunction while CYP2C8*3 and 2C9*2 loss-of-function SNP, altered endothelial function by reducing flow-induced EET release. In I/R mice, sEH inhibition reduced kidney lesions, prevented cardiac fibrosis and dysfunction as well as preserved endothelial function. The preservation of EET bioavailability may prevent allograft dysfunction and improve cardiovascular disease in kidney transplant recipients. Inhibition of sEH appears thus as a novel therapeutic option but its impact on other epoxyfatty acids should be carefully evaluated.

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