Dustri Online Services

Search Results

Books: 0	Journals: 1	Articles: 2

Originals

Early progressive interstitial fibrosis in human renal allografts

H. Abo-Zenah, S. Katsoudas, D. de Takats, J. Shortland, G. Wild, C.B. Brown and A.M. El Nahas

Price
42.00 $

Add to Cart

Price

42.00 $

Volume 57 (2002) p. 9 - 18

Abstract

H. Abo-Zenah, S. Katsoudas, D. de Takats, J. Shortland, G. Wild, C.B. Brown and A.M. El Nahas

¹Sheffield Kidney Institute, ²Histopathology,

and ³Immunology Departments, Northern General Hospital Trust, Sheffield, UK
Background: Early fibrosis has been described in renal allografts and implicated in the progression of chronic allograft nephropathy (CAN). The precise factors implicated in the initiation and progression of early allograft fibrosis remain uncertain. Patients and methods: We studied retrospectively 23 cadaveric renal allograft recipients over a 3-year period, who had paired renal biopsies (Bx) (at implantation and as clinically indicated) within 3 months of transplantation (Tx). Eight of them have progressed over an average period of 3.16 ± 0.83 years to CAN. Histological evaluation of interstitial fibrosis (IF) relied on point count analysis of Masson’s trichrome (MT) staining as well as immunostainable collagens III (iCol III) and IV (iCol IV). The severity of the IF scores was correlated with the clinical, biochemical and histological parameters. The nature and severity of the interstitial inflammatory infiltrate were also evaluated by immunofluorescence. In addition, patients were subdivided into those whose fibrosis progressed (> 50% increase in IF/iCol III; Group 1) and non-progressors (< 50% increase in fibrosis score; Group 2) in an attempt to determine discriminatory features. Results: In the whole group, there was a significant increase in the IF score, as estimated by MT staining and iCol III, from implantation to follow-up Bx (p = 0.0027 and p = 0.0088, respectively). The changes in iCol IV were not significant. Further, the increase in interstitial inflammatory infiltrate of total T lymphocytes, and not of macrophages, from implantation (modal category = 2) to follow-up (modal category = 0) was significant (p = 0.0121). The predictive value of such increase was significant (R2 = 0.617, p = 0.03). The donor’s age (R2 = 0.892, p = < 0.0001), death from cerebrovascular accident (CVA) (R2 = 0.822, p = 0.047), as well as recipient’s body weight (R2 = 0.892, p = 0.001), male gender (R2 = 0.687, p = 0.041) and elevated mean arterial pressure (MAP) (R2 = 0.892, p = < 0.0001) were all significant risk factors for early IF. Delayed graft function (DGF) proved to be a significant predictor of early IF (R2 = 0.822, p = 0.003) and became more significant in the presence of superimposed acute rejection (AR) (p = 0.0001). Proteinuria > 1 g/day (R2 = 0.882, p = 0.004) and hypertriglyceridemia > 2.25 mmol/l (R2 = 0.808, p = < 0.0001) were also associated with early IF. Of the implantation histological parameters, iCol III proved to be a highly significant predictor of early IF (R2 = 0.892, p = < 0.0001). Interestingly, the predictive value of iCol III for graft survival in terms of CAN was significant (Cox p = 0.088). Group 1 progressor patients (n = 10) were all males (p = 0.038) and received their kidneys from donors who died from CVAs in 90% of cases (p = 0.011). They had, compared to non-progressors, a lower cyclosporin A level (p = 0.047), a higher incidence of AR episodes (80% versus 54%), a higher serum creatinine at 10 days post-Tx (p = 0.005), a higher proteinuria (2.07 ± 3.89 g/l vs 0.96 ± 0.97 g/l, p = 0.041) and a higher serum triglyceride (2.48 ± 1.37 mmol/l vs 1.69 ± 0.81 mmol/l, p = 0.039) level. 8% of Group 1 patients had DGF compared to 30% in Group 2 (p = 0.023). Of note, the modal category of cytotoxic: helper T lymphocytes ratio was greater than 1 in Group 1 (2 : 1) patients and not in Group 2 (1 : 1). Conclusion: Implantation histology, and in particular iCol III, is a predictor of early IF in a subgroup of patients with DGF and AR. Additional risk factors include hypertension, proteinuria and hypertriglyceridemia especially in patients receiving kidneys from older donors who died of CVAs.

Case Report

T-cell large granular lymphocyte leukemia presenting as end-stage renal disease: the diagnostic role of flow-cytometric and clonality analysis of the urine sediment T-cell large granular lymphocyte leukemia presenting as end-stage renal disease: the diag

P.D. Christopoulos, S. Katsoudas, A. Androulaki, L. Nakopoulou, T. Economopoulos and D.V. Vlahakos

Price
42.00 $

Add to Cart

Price

42.00 $

Volume 71 (2009) p. 198 - 202

Abstract

P.D. Christopoulos¹, S. Katsoudas², A. Androulaki³, L. Nakopoulou⁴, T. Economopoulos¹ and D.V. Vlahakos²

¹Department of Medicine II, ²Division of Nephrology, Attikon University Hospital, ³Department of Pathology, Elpis General Hospital, and ⁴First Department of Pathology, Medical School of the University of Athens, Athens, Greece
A 65-year-old white female patient with normal baseline renal function was referred to our hospital with nonoliguric renal failure requiring hemodialysis after progressive deterioration over the previous 6 months. Her past medical history was remarkable for easy fatigability, weight loss, low-grade fever, hypogammaglobulinemia and mild hepatosplenomegaly manifested over the past 6 years. Several liver and bone marrow biopsies during that period had shown a nonspecific polyclonal T-cell infiltration, and she was administered low-dose steroids for symptomatic relief. Physical examination, laboratory workup and imaging studies at presentation showed pancytopenia, hepatosplenomegaly, large symmetric kidneys with normal cortices and no evidence of obstructive uropathy, aseptic pyuria with neutrophils and lymphocytes and mild proteinuria. On biopsy the renal interstitium was infiltrated by large, granular CD3⁺CD8⁺CD56^–CD57⁺ lymphocytes, clonal by molecular analysis, which established the diagnosis of T-cell large granular lymphocyte leukemia. Most urinary and peripheral blood lymphocytes bore the same T-LGL surface markers and were also clonal, as shown by flow-cytometry and PCR amplification of the T-cell receptor g-chain genes. A subsequent bone marrow biopsy revealed infiltration by lymphoma cells and excluded a myelodysplastic or hemophagocytic syndrome. After exclusion of an underlying EBV, CMV, HBV, HCV or HIV infection with negative serology and blood PCR the patient received one cycle of chemotherapy with cyclophosphamide, vincristine and prednisone. No improvement of renal function was achieved, while complication with a prolonged pulmonary infection and severe sepsis precluded further treatment. Our report indicates that the T-LGL leukemia should be considered in the differential diagnosis of renal failure with large-sized kidneys, especially when hepatosplenomegaly, pancytopenia and aseptic pyuria are also present. In the latter case, flow-cytometric and clonality analysis of the urine sediment can aid in establishing a diagnosis. Since renal function may deteriorate rapidly, chemotherapy should not be delayed.Correspondence to:
P.D. Christopoulos, MD; Sundgauallee 51, 79114 Freiburg, Germany
Email: [email protected]

Shopping Overview

Shopping Overview
Type	Qtty	Discount	VAT	Price
Your basket is empty

View Cart

Search Results

Shopping Overview

Send us an E-Mail