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Central nervous system ( CNS) involvement with diffuse large B-cell lymphoma ( DLBCL) is a relatively uncommon manifestation; with most cases of CNS involvement occuring during relapse after primary therapy. CNS dissemination typically occurs early in the disease course and is most likely present subclinically at the time of diagnosis in many patients who later relapse in the CNS. CNS relapse in these patients is associated with poor outcomes. Based on a CNS relapse rate of 5% in DLBCL and weighing the benefits against the toxicities, universal application of CNS prophylaxis is not justified. The introduction of rituximab has significantly reduced the incidence of CNS relapse in DLBCL. Different studies have employed other agents for CNS prophylaxis, such as intrathecal chemotherapy and high-dose systemic agents with sufficient CNS penetration. If CNS prophylaxis is to be given, it should be preferably administered during primary chemotherapy. However, there is no strong evidence that supports any single approach for CNS prophylaxis. In this review, we outline different strategies of administering CNS prophylaxis in DLBCL patients reported in literature and discuss their advantages and drawbacks. [ABSTRACT FROM AUTHOR]

Diabetic kidney disease continues to be the leading cause of end-stage renal disease despite therapies targeted towards glycemic and blood pressure control, and drugs that block the renin-angiotensin-aldosterone system. New therapeutic agents are being studied to retard the progression of kidney damage due to diabetes. Glycosaminoglycans (e.g., sulodexide) target the glomerular basement membrane and have been shown to reduce albuminuria in multiple Phase II clinical trials. Inhibitors of advanced glycation end-product formation (e.g., pyridoxamine) reduce the renal accumulation of these pathogenic substrates with mixed clinical efficacy results. Protein kinase C inhibitors (e.g., ruboxistaurin) reduce renal damage from overexpression of this kinase, and have shown encouraging results in Phase II studies. Iron chelators, as antioxidant agents, work in reducing cellular damage by reactive oxygen species that are part of common final pathways in diabetic kidney disease. Other agents discussed in this review target multiple molecular pathways in diabetic kidney disease. If successfully developed, future clinical trials will evaluate the efficacy of these new drugs in slowing the progression of diabetic kidney disease. [ABSTRACT FROM AUTHOR]