NSAIDs in the Treatment of Postoperative Pain.

PURPOSE OF REVIEW: Postoperative pain results in multiple undesirable physiologic and psychological outcomes, and it should be managed in a multimodal approach. This article reviews the latest scientific literature of NSAIDs in the treatment of postoperative pain. The goal is to answer the following questions: (1) Are NSAIDs effective in the postoperative period? (2) Are NSAIDs safe in all surgical patients? and (3) Are adverse effects of NSAIDs increased or diminished in the acute postoperative period? RECENT FINDINGS: NSAIDs are safe and effective in the treatment of postoperative pain, and they should be administered to all postoperative surgical patients unless contraindicated. Based on literature, NSAIDs have been shown to increase patient satisfaction and decrease opioid requirements, minimizing opiate-induced adverse events. They have no increased incidence of adverse effects during the acute postoperative period. NSAIDs and COX-2 inhibitors, however, should be used with caution in colorectal surgery as they are proven to increase the risk of anastomotic leak.

Murine membranous nephropathy: immunization with α3(IV) collagen fragment induces subepithelial immune complexes and FcγR-independent nephrotic syndrome.

Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults and a significant cause of end-stage renal disease, yet current therapies are nonspecific, toxic, and often ineffective. The development of novel targeted therapies requires a detailed understanding of the pathogenic mechanisms, but progress is hampered by the lack of a robust mouse model of disease. We report that DBA/1 mice as well as congenic FcγRIII(-/-) and FcRγ(-/-) mice immunized with a fragment of α3(IV) collagen developed massive albuminuria and nephrotic syndrome, because of subepithelial deposits of mouse IgG and C3 with corresponding basement membrane reaction and podocyte foot process effacement. The clinical presentation and histopathologic findings were characteristic of MN. Although immunized mice produced genuine anti-α3NC1 autoantibodies that bound to kidney and lung basement membranes, neither crescentic glomerulonephritis nor alveolitis ensued, likely because of the predominance of mouse IgG1 over IgG2a and IgG2b autoantibodies. The ablation of activating IgG Fc receptors did not ameliorate injury, implicating subepithelial deposition of immune complexes and consequent complement activation as a major effector pathway. We have thus established an active model of murine MN. This model, leveraged by the availability of genetically engineered mice and mouse-specific reagents, will be instrumental in studying the pathogenesis of MN and evaluating the efficacy of novel experimental therapies.