Updated Canadian Expert Consensus on Assessing Risk of Disease Progression and Pharmacological Management of Autosomal Dominant Polycystic Kidney Disease.

Purpose: The purpose of this article is to update the previously published consensus recommendations from March 2017 discussing the optimal management of adult patients with autosomal dominant polycystic kidney disease (ADPKD). This document focuses on recent developments in genetic testing, renal imaging, assessment of risk regarding disease progression, and pharmacological treatment options for ADPKD.

Sources Of Information: Published literature was searched in PubMed, the Cochrane Library, and Google Scholar to identify the latest evidence related to the treatment and management of ADPKD.

Assessing Risk of Disease Progression and Pharmacological Management of Autosomal Dominant Polycystic Kidney Disease: A Canadian Expert Consensus.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited renal disorder worldwide. The disease is characterized by renal cysts and progressive renal failure due to progressive enlargement of cysts and renal fibrosis. An estimated 45% to 70% of patients with ADPKD progress to end-stage renal disease by age 65 years.

Malignancy after renal transplantation: incidence and role of type of immunosuppression.

Background: Cancer, particularly skin cancer and lymphoma, is a complication of posttransplantation immunosuppression. We investigated the characteristics of cancers in our renal transplant population, the role of type of immunosuppression on cancer incidence, and whether newer, more potent immunosuppressive agents produce cancers sooner after transplantation.

Methods: The charts of patients who developed cancer after renal transplantation between 1958 and 2000 were reviewed.

The role of glycosyl phosphatidyl inositol (GPI)-anchored cell surface proteins in T-cell activation.

Glycosylphosphatidylinositol (GPI)-anchored cell surface proteins are widely expressed in tissues, including cells of immunohematopoietic origin. Cross-linking of GPI-linked proteins on T lymphocytes, such as Thy-1 (CD90), Ly-6 A/E, CD48, CD59 and others, induces T-cell mitogenesis. Similar to cross-linking with T-cell receptor (TcR)-specific antibodies, ligation of GPI-anchored proteins induces an intracellular flux of calcium, an up-regulation of activation-associated cell surface proteins and the elaboration of growth-promoting lymphokines.