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Kidney allograft torsion (KAT) is a rare but critical complication of kidney transplantation that can lead to graft loss due to acute ischemia. This report presents a case of KAT resulting in graft loss 9 months following intraperitoneal simultaneous pancreas and kidney (SPK) transplant and reviews previous reports to identify potential high-risk features. A 38-year-old female with end-stage renal disease secondary to Type 1 diabetes mellitus underwent an intraperitoneal enteric drained SPK transplant.

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The impact of pancreas transplantation on diabetic complications: A systematic review.

Transplant Rev (Orlando)

January 2025

Faculty of Biology, Medicine & Health, University of Manchester, UK; Manchester Centre for Transplantation, Manchester Royal Infirmary, Manchester University NHS Foundation Trust, UK.

Background: Pancreas Transplantation (PT) provides optimal treatment for patients with severe complicated Type 1 Diabetes Mellitus (T1DM). Restoration of beta-cell mass allows return to euglycaemia and insulin independence. We aimed to examine its impact on the secondary complications associated with severe T1DM including diabetic eye disease, neuropathy and cardiovascular disease.

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Type 1 diabetes (T1D) is related to the autoimmune destruction of β-cells, leading to their almost complete absence in patients with longstanding T1D. However, endogenous insulin secretion persists in such patients as evidenced by the measurement of plasma C-peptide. Recently, a low level of insulin has been found in non-β islet cells of patients with longstanding T1D, indicating that other islet cell types may contribute to persistent insulin secretion.

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20% acute pancreatitis (AP) develops into severe AP (SAP), a global health crisis, with an increased mortality rate to 30%-50%. Mitochondrial damage and immune disorders are direct factors, which exacerbate the occurrence and progression of AP. So far, mitochondrial and immunity injury in SAP remains largely elusive, with no established treatment options available.

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The impact of islet neuronal nitric oxide synthase (nNOS) on glucose-stimulated insulin secretion (GSIS) is less understood. We investigated this issue by performing simultaneous measurements of the activity of nNOS versus inducible NOS (iNOS) in GSIS using isolated murine islets. Additionally, the significance of extracellular NO on GSIS was studied.

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