Despite the importance of hemodialysis vascular access, the cost of vascular access care has not been studied in detail. A prospective cost analysis was performed among incident hemodialysis patients to determine the cost of vascular access care overall and on the basis of access type. Detailed clinical and demographic information, as well as data on access type, was collected for all local incident hemodialysis patients between July 1, 1999, and November 1, 2001. A comprehensive measure of total vascular access costs, including surgery, radiology, hospitalization for access complications, physician costs, costs for management of outpatient bacteremia, and vascular access monitoring costs, was obtained. Costs are reported in 2002 Canadian dollars (1 CAN dollar = 0.69 US dollar). A total of 239 consecutive incident hemodialysis patients were identified, 49, 157, and 33 of whom were dialyzed exclusively with a catheter or had a native arteriovenous fistula or synthetic graft attempted, respectively. In year 1, 18.4% of all hospital admissions were for vascular access-related complications. The mean cost of all vascular access care in year 1 was 6890 CAN dollars(median 4020 dollars; interquartile range [IQR] 2440 dollars to 7540 dollars). The mean cost of access care per patient-year at risk for maintaining a catheter exclusively, attempting an arteriovenous fistula, or attempting a graft was 9180 dollars (median 3812 dollars; IQR 2250 dollars to 7762 dollars), 7989 dollars (median 4641 dollars ; IQR 3035 dollars to 8832 dollars), and 11,685 dollars (median 8152 dollars; IQR 3395 dollars to 12,908 dollars), respectively (P = 0.01). Vascular access care is responsible for a significant proportion of health care costs in the first year of hemodialysis. These results support clinical practice guidelines that recommend preferential placement of a native fistula.

We conducted a randomized, multicenter study to determine whether treatment of subclinical rejection with increased corticosteroids resulted in beneficial outcomes in renal transplant patients receiving tacrolimus (TAC), mycophenolate mofetil (MMF) and prednisone. One hundred and twenty-one patients were randomized to biopsies at 0,1,2,3 and 6 months (Biopsy arm), and 119 to biopsies at 0 and 6 months only (Control arm). The primary endpoint of the study was the prevalence of the sum of the interstitial and tubular scores (ci + ct) > 2 (Banff) at 6 months. Secondary endpoints included clinical and subclinical rejection and renal function. At 6 months, 34.8% of the Biopsy and 20.5% of the Control arm patients had a ci + ct score ≥ 2 (p = 0.07). Between months 0 and 6, clinical rejection episodes were 12 in 10 Biopsy arm patients and 8 in 8 Control arm patients (p = 0.44). Overall prevalence of subclinical rejection in the Biopsy arm was 4.6%. Creatinine clearance at 6 months was 72.9 ± 21.7 in the Biopsy and 68.90 mL/min ± 18.35 mL/min in the Control arm patients (p = 0.18). In conclusion, we found no benefit to the procurement of early protocol biopsies in renal transplant patients receiving TAC, MMF and prednisone, at least in the short term. This is likely due to their low prevalence of subclinical rejection.

Abstract. This study is an investigation of whether a protocol biopsy may be used as surrogate to late graft survival in multicenter renal transplantation trials. During two mycophenolate mofetil trials, 621 representative protocol biopsies were obtained at baseline, 1 yr, and 3 yr. The samples were coded and evaluated blindly by two pathologists, and Chronic Allograft Damage Index (CADI) score was constructed. At 1 yr, only 20% of patients had elevated (Ͼl.5 mg/100 ml) serum creatinine, whereas 60% of the biopsies demonstrated an elevated (Ͼ2.0) CADI score. The mean CADI score at baseline, 1.3 Ϯ 1

Chronic rejection has several histological appearances, depending on the type of organ graft Common to all of them is transplant arteriosclerosis associated with an ongoing inflammatory response in the transplanted graft. To the contrary of classical atherosclerosis, in which the manifestations are mostly focal, proximal, and asymmetric, transplant arteriosclerosis is generalized, and the intimal thickening is concentric In this article, we describe an experimental animal model whereby transplant arteriosclerosis may be investigated in the inbred rat Aortic allografts were transplanted from DA (RTF) to major histocompatibility complex-incompatible WF (RTF) rats or, for control, to rats of the DA strain. Transplantation was followed by an acute inflammation episode in the aortic adventitia of the allograft, largely lacking in the syngeneic graft, with a prominence of lymphoid activation markers (Cd25) in the cells of the inflammatory infiltrate. The inflammation episode peaked at 2 months after transplantation, became attenuated, and was followed by a proliferative response of myocytes in the allograft media. An increase in the migration of myocytes to the subendothelial space (presumably through small breaks generated in the internal elastic lamina) was observed thereafter, and myocyte proliferation continued in the intima with some intermingled macrophages. Finally, necrosis and disappearance of myocytes and their replacement by fibrous tissue were observed in the media. These alterations are virtually identical with the vascular lesion of chronically rejecting parenchymal organ transplants in human subjects. We suggest that aortic allografts exchanged between histoincompatible rat strains may be used as an experimental model for transplant arteriosclerosis. (Arteriosclerosis and Thrombosis 1991;ll:671-680)

To determine the contribution of independent variables to the dependant variable of loss of primary functional patency, a multivariable analysis using logistic regression was performed.Results: The incidence of primary failure was 10% (81 of 831). Multivariable analysis found that older age (>65 years, odds ratio [OR] 3.6, P < 0.001), history of diabetes (OR 2.3, P ‫؍‬ 0.007), history of smoking (OR 4.3, P < 0.001), presence of forearm fistulas (OR 4.0, P < 0.001), and low initial IABF (<500 ml/min, OR 29, P < 0.001) were independently associated with loss of primary patency.Conclusions: The set of patient risk factors identified in this study, particularly initial IABF, can be used to identify patients who are most at risk for developing vascular access failure and to guide a more directed approach for a vascular access screening protocol.

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Background and objectives: IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide. Accurately identifying patients who are at risk for progressive disease is challenging. The extent to which histopathologic features improves prognostication is uncertain.Design, setting, participants, & measurements: We studied a retrospective cohort with biopsy-proven IgAN in Calgary, Canada. Renal biopsies were reviewed by a nephropathologist with histopathologic data abstracted using a standardized form. The primary outcome was the composite of doubling of serum creatinine, ESRD, or death. Spline models defined significant levels of interstitial fibrosis, glomerulosclerosis, hypertension, proteinuria, and creatinine. The prognostic significances of clinical and histopathologic parameters were determined using Cox proportional hazards models.Results: Data from 146 cases were available for analysis with a median follow-up of 5.8 years. Greater than 25% interstitial fibrosis, >40% glomerular sclerosis, and a systolic BP >150 mmHg were risk thresholds. In univariable analyses, baseline creatinine, proteinuria, systolic BP, glomerular sclerosis, interstitial fibrosis, and crescentic disease were predictors of the primary outcome. In multivariable models adjusted for clinical characteristics, interstitial fibrosis (hazard ratio [HR]2.7; 95% confidence interval [CI] 1.2 to 6.0), glomerular sclerosis (HR 2.6; 95% CI 1.2 to 4.5), and crescents (HR 2.4; 95% CI 1.2 to 5.1) remained independent predictors of the primary outcome and significantly improved model fit compared with clinical characteristics alone.Conclusions: Baseline histopathologic parameters are independent predictors of adverse outcomes in IgAN even after taking into consideration clinical characteristics. Relatively small degrees of interstitial fibrosis confer an increased risk for progressive IgAN.