Inflammation is a key player in the development of an increasing amount of diseases. The soluble urokinase plasminogen activator receptor (suPAR) is a highly flexible molecule with intrinsic chemotactic properties. This glycoprotein has been evaluated as a biomarker of inflammation, immune activation, organ damage and clinical outcome in several pathologies, including cardiovascular disease, hepatitis, renal disorders and rheumatic pathologies. The use of this early warning inflammatory biomarker could potentially improve the prediction of the severity of these diseases and mortality. In the present paper, we describe the general characteristics of suPAR and its intriguing role as a biomarker in different inflammatory diseases.

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Background: Galectin-3 is a member of a closely related lectin family, which is detected in several vertebrate epithelial and myeloid cell types. This beta-galactoside-binding soluble protein plays an important role in multiple biological processes. Depending on its location, type of injury or site of damage, the effects by galectin-3 can be various and sometimes contrasting. Summary: In this review, we discuss the general characteristics and functions of galectin-3. More specifically, we focus on the role of galectin-3 in the onset and development of diabetic and non-diabetic nephropathies. Finally, the therapeutic potential of anti-galectin-3 inhibitors is discussed. Key Messages: Due to its multifunctional character, galectin-3 plays a pivotal role in interstitial fibrosis and progression of chronic kidney disease. Inhibition of galectin-3 may be a promising therapeutic strategy to prevent end-stage renal disease.

Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies.