Ravi Parasuraman

Rapid Resolution of Proteinuria of Native Kidney Origin Following Live Donor Renal Transplantation

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.

Recurrence of Scedosporium Apiospermum Infection Following Renal Re-Transplantation

Immunosuppression for organ transplantation results in increased susceptibility to opportunistic infections including fungal, such as Scedosporium apiospermum. Even though many reported cases of this infection had both local and systemic manifestations, majority of the systemic infections had a fatal outcome. We report a case of a 50‐year‐old Caucasian male with lymphocutaneous and presumed pulmonary Scedosporium infection 4 years after renal transplantation that was successfully treated with voriconazole and discontinuation of immunosuppression. He received a second transplant 3 years later in the absence of clinical evidence of S. apiospermum infection. Unfortunately, 4 months after transplantation he developed recurrence of the same infection localizing to the soft tissues. Presently this infection is under control with surgical excision and voriconazole therapy. To our knowledge this is the first reported case of recurrent S.apiospermum infection in a renal transplant recipient. We suggest prophylactic antifungal therapy in all re‐transplants with this infection.

The Role of Microscopic Hematuria in the Evaluation of Urologic Malignancy in Renal Transplant Recipients

Urologic malignancy is a relatively uncommon but serious complication following kidney transplantation. The reported prevalence of renal cell carcinoma (RCC) of the native kidneys is 4.4% and of bladder malignancy is 2.6%. However, presently there are no universal guidelines for prospective screening of urologic malignancies after kidney transplantation. We routinely monitored all renal transplant recipients for microscopic hematuria and persistent hematuria (>3 separate occasions) results in imaging studies (ultrasound or computed tomography scan) of both native kidneys and the allograft. Cystoscopy is performed if imaging studies are negative. This retrospective study identified a total of 18 urologic malignancies among the study cohort, which consisted of 539 patients with an incidence of 3.3% (12 cases of RCC of native kidneys [10/12 had hematuria], and six cases of bladder and ureteral malignancies [6/6 had hematuria]). There were no significant differences between cyclosporine- and tacrolimus-based immunosuppression (IS). Among RCC recipients, two lost the allograft from chronic allograft nephropathy and one patient died unrelated to malignancy. Among patients with bladder and ureteral malignancies, two lost the graft possibly from IS reduction and one had BK virus nephropathy prior to diagnosis of bladder carcinoma. In conclusion, screening transplant recipients routinely for persistent microscopic hematuria may identify urologic malignancies in renal transplant recipients.

Rapid Progression of Native Renal Artery Fibromuscular Dysplasia Following Kidney Donation

Fibromuscular dysplasia is the second commonest anatomical abnormality apart from multiple renal arteries in the potential live donors. Pretransplant evaluation of the donors may include an angiography to evaluate the renal arteries, and failure to recognize renal arterial stenosis, particularly fibromuscular dysplasia, by noninvasive methods may eventually lead to hypertension and ischemic renal failure. We report a case of fibromuscular dysplasia that was undetected by computed tomographic angiography prior to donation. One year after kidney donation, it rapidly progressed to severe symptomatic stenosis with hypertension and acute renal failure. Following renal artery angioplasty, her blood pressure normalized over a period of 2 weeks without any need for antihypertensive medications and the serum creatinine returned to her baseline. The acceptability of renal donors with fibromuscular dysplasia depends on the age, race and the availability of the other suitable donors. Mild fibromuscular dysplasia in a normotensive potential renal donor cannot be considered a benign condition. Such donors need regular follow‐up postdonation for timely detection and treatment.

Proposed Relationship Between Intravenous Immunoglobulin and Thrombosis in Renal Transplant Recipients

Objective: To report 2 cases of intravenous human immunoglobulin (IVIG)–associated thrombosis in kidney transplant patients. Case Summary: Both cases involved female patients presenting to Henry Ford Hospital in Detroit for renal transplantation. Patient 1 presented with systemic lupus erythematosus, positive for both anticardiolipin and anti-DNA antibody. Patient 2, post nephrectomy, was found to have moderate hyperhomocysteinemia, with a total plasma homocysteine level of 3.9 mg/L. Both patients were considered highly sensitized and at high risk for rejection due to the presence of either high panel reactive antibody or a positive B cell flow cytometry crossmatch, in addition to other risk factors. Therefore, IVIG was considered a viable treatment option to be included in induction therapy. IVIG was administered both peri- and postoperatively, and both patients experienced immediate graft function with good urine output. Within 24 hours following transplantation, elevations in serum creatinine and decreases in urine output were seen. Subsequently, kidney exploration was performed and palpable thrombi in renal arteries and veins were detected. Immediate nephrectomy was performed in both cases. Discussion: Currently, evidence derived from case reports highlights numerous risk factors for IVIG-associated thrombosis, one of which appears to be a hypercoagulable state. It has also been reported that some IVIG products contain amounts of anticardiolipin antibodies; these antibodies may potentiate thrombosis in the presence of hypercoagulable states, such as hyperhomocysteinemia or antiphospholipid syndrome, in these 2 patients, the Naranjo probability scale indicated that there was a possible association between the thrombotic events and the use of IVIG. Conclusions: Prospective trials evaluating the safety of IVIG in highly sensitized transplant patients are scarce. Therefore, it is imperative that the benefits and risks be weighed when considering the use of IVIG in highly sensitized transplant patients.