Copper is a fundamental element for the homeostasis of the body. It is the third most abundant essential transition metal in humans. Changes in the concentration of copper in the blood are responsible for numerous diseases affecting various organs, including the heart, brain, kidneys, and liver. Even small copper deficiencies can lead to the development and progression of several pathologies. On the other hand, excessive exposure to copper can cause toxicity in many human organs, leading to various systemic alterations. In the kidney, increased copper concentration in the blood can cause deposition of this element in the kidneys, leading to nephrotoxicity. One of the most interesting aspects of copper balance is its influence on diabetes and the progression of its complications, such as Diabetic Kidney Disease (DKD). Several studies have shown a close relationship between copper serum levels and altered glycemic control. An imbalance of copper can lead to the progression of diabetes-related complications and impaired antioxidant homeostasis. A high Zinc/Copper (Zn/Cu) ratio is associated with improved renal function and reduced risk of poor glycemic control in patients with type two diabetes mellitus (T2DM). Furthermore, the progression of DKD appears to be related to the extent of urinary copper excretion, while regulation of adequate serum copper concentration appears to prevent and treat DKD. The aim of this review is to evaluate the possible role of copper in DKD patients.

Chronic kidney disease (CKD) is a progressive disease that affects > 10% of the total population worldwide or >800 million people. CKD poses a particularly heavy burden in low- and middle-income countries, which are least able to cope with its consequences. It has become one of the leading causes of death worldwide and is one of the few non-communicable diseases where the number of related deaths has increased over the last two decades. The high number of people affected, and the significant negative impact of CKD should be a reason to increase efforts to improve prevention and treatment. The interaction of lung and kidney leads to highly complex and difficult clinical scenarios. CKD significantly affects the physiology of the lung by altering fluid homeostasis, acid-base balance and vascular tone. In the lung, haemodynamic disturbances lead to the development of alterations in ventilatory control, pulmonary congestion, capillary stress failure and pulmonary vascular disease. In the kidney, haemodynamic disturbances lead to sodium and water retention and the deterioration of renal function. In this article, we would like to draw attention to the importance of harmonising the definitions of clinical events in pneumology and renal medicine. We would also like to highlight the need for pulmonary function tests in routine clinical practise for the management of patients with CKD, in order to find new concepts for pathophysiological based disease-specific management strategies.

Copper is an essential element in the diet of mammals, including humans. It plays an important role in the physiological regulation of various enzymes and is consequently involved in several biological processes such as angiogenesis, oxidative stress regulation, neuromodulation, and erythropoiesis. Copper is essential for facilitating the transfer of iron from cells to the bloodstream, which is necessary for proper absorption of dietary iron and the distribution of iron throughout the body. In particular, patients with end-stage renal failure who require renal replacement therapy are at increased risk for disorders of copper metabolism. Many studies on hemodialysis, peritoneal dialysis, and kidney transplant patients have focused on serum copper levels. Some reported mild deficiency, while others reported elevated levels or even toxicity. In some cases, it has been reported that alterations in copper metabolism lead to an increased risk of cardiovascular disease, malnutrition, anemia, or mielopathy. The aim of this review is to evaluate the role of copper in patients undergoing hemodialysis and its potential clinical implications.

Magnesium is a cofactor in cellular energy metabolism and insulin signaling, with recognized effects on vascular tone and cardiac electrophysiology. Hypomagnesemia affects roughly one-third of people with type 2 diabetes mellitus (T2DM) in pooled observational data and becomes more frequent in diabetic kidney disease (DKD). Reduced dietary intake accounts for part of the deficit; renal magnesium wasting linked to attenuated insulin signaling and reduced TRPM6 activity at the distal convoluted tubule is a plausible mechanism for the remainder, characterized mainly in cellular and experimental systems. In observational cohorts, lower serum magnesium accompanies poorer glycemic control and an excess of cardiovascular and microvascular events, and in DKD it independently predicts progression to kidney failure. Prescribed oral repletion has been associated with fewer cardiovascular events in hypomagnesemic patients, with no corresponding association in normomagnesemic ones, in propensity-matched data that cannot substitute for randomized confirmation. Mendelian randomization offers suggestive evidence for coronary artery disease and none for incident T2DM, a dissociation compatible with insulin resistance acting upstream of renal magnesium wasting, although instrument limitations leave other readings open. Hypomagnesemia is substantially less frequent in adult type 1 diabetes, where the association with glycemic control concentrates among patients with the highest insulin requirements. SGLT2 inhibitors raise serum magnesium modestly, whereas thiazide and loop diuretics and proton-pump inhibitors lower it. Randomized trials have shown modest effects on glycemic intermediates, larger in patients with documented deficiency, and no trial has yet tested renal progression. Magnesium status is a reproducible prognostic marker in T2DM and DKD; its value as a therapeutic target awaits randomized trials with clinical endpoints.