We evaluated the relationship between the acute phase and the development of end-stage renal disease (ESRD) and the outcome of renal transplant in patients with Shiga toxin-associated hemolytic uremic syndrome (Stx-HUS). A 20-year retrospective study was performed of 66 renal transplants in 62 patients with Stx-HUS compared with 189 renal allografts in 178 children with other diseases. Of 62 patients, 61 had >7 days of oliguria during the acute phase. Stx-HUS patient survival was not different from controls (92% vs. 83% 15 years after renal transplantation). In the cyclosporine (CsA) era, survival of grafts from living related (LRD) and cadaver (CD) donors in Stx-HUS and control patients was 83% versus 70% ( P<0.03) and 77% versus 49% ( P<0.05) at 10 years. Graft survival in Stx-HUS and dysplasia/obstructive uropathy patients was 79% versus 76% ( P=NS), but it was different from that of other diseases (79% vs. 58%, P<0.001). There was no clinical or histopathological evidence of Stx-HUS recurrence. In conclusion, in Stx-HUS patients the duration of the acute oliguric period was a good predictor for the progression to ESRD. Use of CsA and the absence of recurrence of the disease influenced the excellent prognosis in Stx-HUS patients after renal transplantation. The development of ESRD in Stx-HUS could be mediated by non-immunological factors.
MMF has been shown to decrease the incidence of acute rejection in children and adults at 1 and 3 yr. Other beneficial effects of MMF have been more difficult to demonstrate. Our open‐labeled study presents a 5‐yr data for patients and graft survival, allograft function, and growth in MMF‐treated patients. The trial included 29 patients who were treated with MMF in combination with cyclosporine and methylprednisone. Patients were compared with a preceding group of 29 patients treated with AZA instead of MMF. Patient and graft survival rate 5 yr after transplantation were 97 and 90% in the MMF group vs. 93 and 83% in the AZA group (p: NS). Acute rejection was 20.6% in the MMF group vs. 58.6% in the AZA group (p < 0.01). Chronic rejection was 10.3% in the MMF group and 25% in the AZA group (p: NS). The changes in the creatinine clearance from baseline to 5 yr (Δ) were different between groups (−6.0 ± 5.1 mL/min/1.73 m2 in the MMF group vs. −22.2 ± 7.6 mL/min/1.73 m2 in the AZA group, p < 0.05). Also, the slope of 1/Scr showed a significant lower incidence of worsening renal function after the second year of renal transplantation (p < 0.0001) in the MMF group compared with the AZA group. Δ Height SDS in prepubertal patients was 0.3 ± 0.4 SDS in the MMF group vs. −0.8 ± 0.2 SDS in the AZA group (p < 0.05). This study shows that long‐term MMF therapy has resulted in a decrease in acute rejection and was associated with a protection against renal function deterioration. The use of MMF enables a reduction in the dose of steroids and leads to a linear growth improvement of children after renal transplantation.
The rate of peritonitis, the absence of any documented ascending or descending infections and the lack of catheter dysfunction during the period of observation suggests that the presence of, or need for, a VPS should not preclude PD as a safe option for children requiring renal replacement therapy.
Proteinuria is the main indicator of renal disease progression in many chronic conditions. There is currently little information available on the efficacy, safety, and individual tolerance of patients with post-diarrheal hemolytic uremic syndrome (D+ HUS) nephropathy to therapies involving diet, enalapril, or losartan. A multicenter, double-blind, randomized controlled trail was conducted to evaluate the effect of a normosodic-normoproteic diet (Phase I) and the effect of normosodic-normoproteic diet plus enalapril (0.18-0.27 mg/kg/day) or losartan (0.89-1.34 mg/kg/day) (Phase II) on children with D+ HUS, normal renal function, and persistent, mild (5.1-49.9 mg/kg/day) proteinuria. Dietary intervention reduced the mean protein intake from 3.4 to 2.2 mg/kg/day. Of 137 children, proteinuria normalized in 91 (66.4 %) within 23-45 days; the remaining 46 patients were randomized to diet plus placebo (group 1, n = 16), plus losartan (group 2, n = 16), or enalapril (group 3, n = 14). In groups 1, 2, and 3, proteinuria was reduced by 30.0, 82.0, and 66.3%, respectively, and normalized in six (37.5%), three (81.3%), and 11 (78.6%) patients, respectively (χ(2)= 8.9, p = 0.015). These results suggest that: (1) a normosodic-normoproteic diet can normalize proteinuria in the majority of children with D+ HUS with mild sequelae, (2) the addition of enalapril or losartan to such dietary restrictions of protein further reduces proteinuria, and (3) these therapeutic interventions are safe and well tolerated. Whether these short-term effects can be extended to the long-term remains to be demonstrated.
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