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Type 2 diabetes mellitus (T2DM) affects an estimated 463 million people worldwide, equivalent to 1 in 11 adults. Moreover, the rapid growth of this disease has resulted in a high incidence of diabetic kidney disease (DKD), which, together with hypertension, is the main cause of chronic kidney disease (CKD). Hyperglycaemia, low-grade inflammation, altered lipid metabolism and hyperactivation of the renin-angiotensin-aldosterone system (RAAS) seem to be interrelated mechanisms contributing to both T2DM and microvascular complications. The introduction of drugs such as sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide 1 receptor agonists has improved the ability to slow the progression of DKD, and has also demonstrated benefits in cardiovascular disease. Beyond the effects of these novel antidiabetic drugs, a body of evidence suggests that the overactivation of the mineralocorticoid receptor also contributes to CKD progression. Moreover, new and ongoing trials have demonstrated that the selective nonsteroidal mineralocorticoid receptor antagonist (MRA) finerenone improves the risk of CKD progression and cardiovascular events in patients with CKD and T2DM and optimized RAAS blockade. We review the rationale for the development and use of MRA drugs to slow CKD progression in patients with DKD, as well as other pleiotropic effects, and highlight the warnings associated with these agents., Competing Interests: Disclosures: José Luis Gorriz has received speakers’ fees and funding for attending advisory boards from Bayer. Luis D’Marco, María Jesús Puchades, Lorena Gandía, Claudia Forquet, Elena Giménez-Civera, Nayara Panizo, Javier Reque, Isabel Juan-García and Valmore Bermúdez have no financial or nonfinancial relationships or activities to declare in relation to this article., (© Touch Medical Media 2021.)

Chronic kidney disease represents a true inflammatory state, and is related to multiple cardiovascular risk factors. Coronary artery disease is the major complication, and has usually been associated with non-classical or uraemic related factors that include the disturbance of calcium and phosphorus metabolism, among others. Recent clinical evidence shows that specific body fat deposition like epicardial adipose tissue is an additional factor to consider when evaluating cardiovascular risk in the general population and kidney patients. Direct interaction of this tissue and coronary vessels with consequent mediation of pro-atherogenic substances have a local process ending in endothelial damage. Although the population of renal patients has been poorly evaluated, future studies should determine precisely whether an increase in epicardial fat is truly associated with cardiovascular morbidity and mortality in this risk group., (Copyright © 2019 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.)

Pseudoxanthoma elasticum (PXE) is a rare genetic disorder characterized by calcification of elastic fibres, skin lesions, fundus lesions and systemic vascular complications. PXE affects approximately 1 in 160,000 people, typically appearing as a formation of yellow papules containing abnormally calcified elastic fibres. The renal involvement of PXE has been reported. Several factors are known to promote soft tissue and accelerated arterial calcification in chronic kidney disease, including systemic inflammation, altered calcium and phosphate homeostasis, hypertension and a deficiency of endogenous calcification inhibitors. Given the impact of this disease, nephrologists may seek additional supportive features to improve and avoid the risk of complications. Moreover, PXE per se represents an interesting model to evaluate vascular disease in the early stages of renal disease., Learning Points: Pseudoxanthoma elasticum represents a rare disease that can involve renal problems.Vascular compromise in patients affected by pseudoxanthoma elasticum shares some components observed in patients with chronic kidney disease.Disorders of mineral and bone metabolism may coexist or be hidden in patients with pseudoxanthoma elasticum., Competing Interests: Conflicts of Interests: The Authors declare that there are no competing interest, (© EFIM 2019.)

The development of end stage renal failure can be seen as a catastrophic health event and patients with this condition are considered at the highest risk of cardiovascular disease among any other patient groups and risk categories. Although kidney transplantation was hailed as an optimal solution to such devastating disease, many issues related to immune-suppressive drugs soon emerged and it became evident that cardiovascular disease would remain a vexing problem. Progression of chronic kidney disease is accompanied by profound alterations of mineral and bone metabolism that are believed to have an impact on the cardiovascular health of patients with advanced degrees of renal failure. Cardiovascular risk factors remain highly prevalent after kidney transplantation, some immune-suppression drugs worsen the risk profile of graft recipients and the alterations of mineral and bone metabolism seen in end stage renal failure are not completely resolved. Whether this complex situation promotes progression of vascular calcification, a hall-mark of advanced chronic kidney disease, and whether vascular calcifications contribute to the poor cardiovascular outcome of post-transplant patients is reviewed in this article.

The high incidence of cardiovascular events in chronic kidney disease (CKD) warrants an accurate evaluation of risk aimed at reducing the burden of disease and its consequences. The use of biomarkers to identify patients at high risk has been in use in the general population for several decades and has received mixed reactions in the medical community. Some practitioners have become staunch supporters and users while others doubt the utility of biomarkers and rarely measure them. In CKD patients numerous markers similar to those used in the general population and others more specific to the uremic population have emerged; however their utility for routine clinical application remains to be fully elucidated. The reproducibility and standardization of the serum assays are serious limitations to the broad implementation of these tests. The lack of focused research and validation in randomized trials rather than ad hoc measurement of multiple serum markers in observational studies is also cause for concern related to the clinical applicability of these markers. We review the current literature on biomarkers that may have a relevant role in field of nephrology.

Abstract. Epidemiological and clinical studies have shown that cardiovascular disease is associated with an increase in mortality in patients with chronic kidney disease (CKD). Vascular complications are mainly secondary to calcification and atherosclerosis. Interest in the association between uric acid levels and cardiovascular risk has been renewed in recent years. The objective of this research was to determine the relation between vascular calcification (VC) and atherosclerosis, through carotid ultrasound, with uric acid levels in patients with CKD in dialysis. VCs were observed in 56% of patients, 46% had ultrasound criteria for atherosclerosis with an overall average of 0.89 mm (SD +/- 0.28), being higher in patients with hypertension and diabetes; this group also showed increased susceptibility to VC (p = 0.01). The levels of urea (141.3 mg/dL) (p = 0.01) and uric acid (6.9 mg/dL) (p = 0.04) showed significant association with the presence of VC. Adverse cardiovascular events were observed mainly in patients with atherosclerosis and VC (p = 0.01). This investigation showed that an increase in uric acid levels above 6 mg/dL is associated with an increased risk of calcification and cardiovascular adverse events in CKD patients in dialysis.