Magnetic resonance-defined perinephric edema after clinical islet transplantation: a benign finding associated with mild renal impairment.

Immunosuppression with sirolimus and low-dose tacrolimus has facilitated successful clinical islet transplantation (CIT). Because the long-term effects on the kidney are unknown and immunosuppressant drugs can be nephrotoxic, CIT is currently restricted to patients with preserved renal function or a functioning renal transplant. The impact of CIT on the native kidney of islet-alone recipients was assessed with magnetic resonance imaging (MRI). After successful CIT, MRI revealed perinephric edema (PNE) in 10 of 30 recipients. PNE was associated with a mild degree of renal impairment but was not associated with preexisting diabetic nephropathy, albuminuria, microscopic hematuria, graft function, or other clinical and metabolic parameters. The presence of PNE on MRI after CIT seems to be a common but benign finding, most likely an adverse effect of sirolimus. Although this novel observation does not seem to be of concern, further studies are required to examine the long-term impact of CIT and immunosuppression on renal function.

Prevalence of hepatic steatosis after islet transplantation and its relation to graft function.

Islet allotransplantation can provide insulin independence in selected individuals with type 1 diabetes. The long-term effects of these transplants on the liver are unknown. Recently, two cases of periportal steatosis after islet transplantation have been described. In this study, we performed ultrasound and magnetic resonance imaging (MRI) in 30 C-peptide-positive islet transplant recipients to detect steatosis and to explore the association of the radiological findings with clinical and metabolic factors. Steatosis was observed on MRI in six (20%) subjects. Histological findings of hepatic steatosis concurred with the imaging findings. Steatosis completely resolved in one subject whose graft failed. More subjects with steatosis required supplementary exogenous insulin than not (67 vs. 21%; P < 0.05). The clinical features of subjects with and without steatosis were otherwise similar, although C-peptide levels were higher in insulin-independent subjects with steatosis (0.98 +/- 0.12 vs. 0.70 +/- 0.18 nmol/l; P = 0.05), despite similar blood glucose levels. Serum triglycerides and the use of exogenous insulin were associated with increased odds of steatosis in a logistic regression model (chi(2) [degrees freedom] = 13.6 [2]); P = 0.001). MRI-detected steatosis is a common finding; the steatosis appears to be due to a paracrine action of insulin secreted from intrahepatic islets. Hepatic steatosis may be associated with insulin resistance or graft dysfunction.