Likely Recurrence of C3 Glomerulonephritis in Kidney Transplantation: An Entity to Bear in Mind: Case Report.

BACKGROUND: C3 glomerulonephritis (C3GN) is an unusual entity that is caused by dysregulation and hyperactivity of the alternative complement pathway. Renal biopsy immunofluorescence study shows C3 deposits with absence of immunoglobulins and markers of the classical complement pathway. More than 50% of cases develop end-stage renal disease. Less well-known is the course of C3GN after kidney transplantation. CASE REPORT: We present the case of a 60-year-old woman with chronic kidney disease secondary to chronic glomerulonephritis of unknown origin who received a kidney transplant. Two years later, she presented worsening renal function with non-nephrotic proteinuria and microhematuria. Complement testing revealed low serum levels of C3. Kidney biopsy showed alterations compatible with C3GN that we interpreted as a relapse of the underlying disease.

Islet Amyloid in Whole Pancreas Transplants for Type 1 Diabetes Mellitus (DM): Possible Role of Type 2 DM for Graft Failure.

Long-term results with whole pancreas (WPTx) and islet transplantation (IT) continue to be suboptimal. Graft failure with undetectable C-peptide level is attributed to graft sclerosis (chronic rejection), recurrence of Type 1 diabetes mellitus (DM), or insufficient islet mass. In contrast, graft failure with measurable C-peptide has overlapping clinical features with Type 2 DM (suggesting persistent but insufficient ß cell function), but is poorly understood. In general, the morphological substrate for islet failure is unclear because grafted islets are not routinely evaluated. We present two patients with graft failure at 5 and 8 years after successful WPTx for Type 1 DM, presenting with preserved C-peptide levels. On histopathology, the islets had preserved both α and ß cell populations but also prominent accumulation of islet amyloid (IA), the morphological hallmark of Type 2 DM. IA previously reported in IT, represents fibrillary aggregates of islet amyloid polypeptide, a hormone normally cosecreted with insulin. Accumulation of IA correlates quantitatively with the development of hyperglycemia and is known to cause ß cell dysfunction and loss. Accumulation of IA and development of Type 2 DM should be considered and studied as a potential cause of long-term islet failure in IT and WPTx.