Rapid Resolution of Proteinuria of Native Kidney Origin
To assess the contribution of the protein content of urine from the native kidneys to post-transplant proteinuria, we prospectively studied 14 live donor transplant recipients with a pre-transplant random urine protein to creatinine ratio (UPr:Cr) >0.5. Seven patients received preemptive transplants, and seven patients were on dialysis pre-transplant (with residual urine output). Resolution of proteinuria was defined as UPr:Cr < 0.2. Immunosuppression consisted of tacrolimus, mycophenolate mofetil and corticosteroids. Anti-hypertensive drugs that might reduce proteinuria were avoided during the study. The serum creatinine was 8.7 ± 0.7 mg/dL pre-transplant, and the nadir post-transplant serum creatinine was 1.4 ± 0.1 mg/dL. The pre-transplant UPr:Cr ranged between 0.5 and 9.2 (mean = 2.9 ± 0.6). The UPr:Cr decreased to <0.2 in all 14 patients at a mean of 4.5 weeks post-transplant (range 1-10 weeks). In conclusion, in live donor renal transplant recipients with immediate graft function, proteinuria of native kidney origin resolves in the early post-transplant period. After the immediate post-transplant period, proteinuria cannot be attributed to the native kidneys, and work up for proteinuria should focus on the allograft.

Recent studies have shown the advantage of preemptive renal transplantation over transplantation after dialysis for both patient and allograft survival. In addition, the duration of dialysis preceding renal transplantation has been shown to be an independent risk factor for inferior post-transplant outcomes. As a result, an increasing proportion of patients with end-stage renal disease are now receiving preemptive transplants, and transplant programs are also attempting to minimize the period of dialysis pre-transplant.

Preemptively transplanted patients and patients receiving transplants after being on dialysis only for a short time usually have significant residual native renal function and urine output. The mean glomerular filtration rate (GFR) has been reported to be 9.9 mL/min at the time of preemptive transplantation. At this level of GFR, the urine output from the native kidneys is well maintained and contains increased amounts of protein as a result of the native renal disease. The source of proteinuria following renal transplantation could, therefore, be the diseased native kidneys with residual urine output or the transplanted kidney affected by a variety of disorders such as delayed graft function, various forms of rejection, calcineurin-inhibitor nephrotoxicity and recurrent or de novo renal diseases. Delineation of the source of proteinuria (native kidneys versus allograft) is important for appropriate management.

The aims of our study were to determine the course of proteinuria of native kidney origin following transplantation and to identify the post-transplant period beyond which proteinuria cannot be attributed to the native kidneys.