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 ◽  
...  

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.

2003 ◽  
Vol 60 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Zeljka Tatomirovic ◽  
Radojka Bokun ◽  
Jovan Dimitrijevic ◽  
Ljiljana Ignjatovic ◽  
Anastasija Aleksic ◽  
...  

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.


2004 ◽  
Vol 36 (10) ◽  
pp. 2997-3001 ◽  
Author(s):  
S.A. Lopes de Souza ◽  
L.M. Barbosa da Fonseca ◽  
R. Torres Gonçalves ◽  
D. Salomão Pontes ◽  
T.J. Holzer ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Siddhesh Prabhavalkar ◽  
Agnes Masengu ◽  
Declan O'Rourke ◽  
Joanne Shields ◽  
Aisling Courtney

Acute kidney injury (AKI) is a recognised complication of intravenous pentamidine therapy. A direct nephrotoxic effect leading to acute tubular necrosis has been postulated. We report a case of severe renal allograft dysfunction due to nebulised pentamidine. The patient presented with repeated episodes of AKI without obvious cause and acute tubular necrosis only on renal histology. Nebulised pentamidine was used monthly as prophylaxis forPneumocystis jiroveciipneumonia, and administration preceded the creatinine rise on each occasion. Graft function stabilised following discontinuation of the drug. This is the first report of nebulized pentamidine-induced reversible nephrotoxicity in a kidney allograft. This diagnosis should be considered in a case of unexplained acute renal allograft dysfunction.


1999 ◽  
Vol 10 (8) ◽  
pp. 1806-1814
Author(s):  
SHANE M. MEEHAN ◽  
CHRISTOPHER T. SIEGEL ◽  
ANDREW J. ARONSON ◽  
SHARON M. BARTOSH ◽  
J. RICHARD THISTLETHWAITE ◽  
...  

Abstract. The relationship of borderline infiltrates to acute rejection by Banff criteria in renal allografts of patients receiving only maintenance immunosuppression is not clear. Renal allograft biopsies with borderline lesions that were not treated with additional anti-rejection therapy were retrospectively studied. Sixty-five such biopsies were identified from 50 patients, and their outcome was determined by serum creatinine and/or histologic findings in subsequent biopsies, up to 40 d after the initial biopsy. In addition to the borderline infiltrates, there was evidence of acute cyclosporine or tacrolimus toxicity (58%), acute tubular necrosis (12%), and urinary obstruction (12%). Forty-day follow-up after 30 (46%) biopsies revealed serum creatinine <110% of baseline, and repeat biopsies were not indicated. In 17 (26%), the serum creatinine initially decreased, then increased, and follow-up biopsies showed acute rejection in nine. In 18 (28%), the creatinine remained elevated and follow-up biopsies revealed acute rejection in nine. The untreated borderline infiltrates were thus nonprogressive after 47 biopsies (72%) and progressed to histologic acute rejection after 18 (28%). When there was increasing or persistently elevated creatinine after the initial biopsy, 51% of cases (18 of 35) progressed to acute rejection. Infiltrates that progressed to rejection had more frequent glomerulitis (7 of 18 versus 3 of 47, P = 0.003) and Banff acute score indices (i+t+v+g) >2 (16 of 18 versus 29 of 47, P = 0.03). A majority (72%) of borderline infiltrates not given additional anti-rejection therapy did not progress to acute rejection over 40 d of follow-up, suggesting that conservative management of these lesions, at least in the short term, may be more appropriate than routine treatment as acute rejection.


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