Diabetic kidney disease (DKD) is one of the most serious complications of both type 1 (T1DM) and type 2 diabetes mellitus (T2DM). Current guidelines recommend a personalized approach in order to reduce the burden of DM and its complications. Recognizing sex and gender- differences in medicine is considered one of the first steps toward personalized medicine, but the gender issue in DM has been scarcely explored so far. Gender differences have been reported in the incidence and the prevalence of DKD, in its phenotypes and clinical manifestations, as well as in several risk factors, with a different impact in the two genders. Hormonal factors, especially estrogen loss, play a significant role in explaining these differences. Additionally, the impact of sex chromosomes as well as the influence of gene–sex interactions with several susceptibility genes for DKD have been investigated. In spite of the increasing evidence that sex and gender should be included in the evaluation of DKD, several open issues remain uncovered, including the potentially different effects of newly recommended drugs, such as SGLT2i and GLP1Ras. This narrative review explored current evidence on sex/gender differences in DKD, taking into account hormonal, genetic and clinical factors.

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.

Diabetic Kidney Disease (DKD) represents the most common cause of Chronic Kidney Disease (CKD) in developed countries. Approximately 30% to 40% of diabetes mellitus (DM) subjects develop DKD, and its presence significantly increases the risk for morbidity and mortality. In this context, Zinc seems to have a potential role in kidney and body homeostasis in diabetic individuals as well as in patients at a high risk of developing this condition. This essential element has functions that may counteract diabetes-related risk factors and complications, which include stabilization of insulin hexamers and pancreatic insulin storage and improved glycemic control. In our review, we analyzed the current knowledge on the role of zinc in the management of renal impairment in course of DM. Several studies underline the critical role of zinc in reducing oxidative stress levels, which is considered the common denominator of the mechanisms responsible for the progression of kidney disease. Reaching and maintaining a proper serum zinc level could represent a valuable target to reduce symptoms related to DM complications and contrast the progression of kidney impairment in patients with the high risk of developing end-stage renal disease. In conclusion, analyzing the beneficial role of zinc in this review would advance our knowledge on the possible strategies of DM and DKD treatment.

Youth-onset Type 2 Diabetes Mellitus (T2DM) represents a major burden worldwide. In the last decades, the prevalence of T2DM became higher than that of Type 1 Diabetes Mellitus (T1DM), helped by the increasing rate of childhood obesity. The highest prevalence rates of youth-onset T2DM are recorded in China (520 cases/100,000) and in the United States (212 cases/100,000), and the numbers are still increasing. T2DM young people present a strong hereditary component, often unmasked by social and environmental risk factors. These patients are affected by multiple coexisting risk factors, including obesity, hyperglycemia, dyslipidemia, insulin resistance, hypertension, and inflammation. Juvenile T2DM nephropathy occurs earlier in life compared to T1DM-related nephropathy in children or T2DM-related nephropathy in adult. Diabetic kidney disease (DKD) is T2DM major long term microvascular complication. This review summarizes the main mechanisms involved in the pathogenesis of the DKD in young population and the recent evolution of treatment, in order to reduce the risk of DKD progression.

Pregnancy is still a challenge in women with autoimmune diseases or kidney transplantation. In this context, management of the immunosuppressive therapy is critical, but, in spite of more than 60 years of experience, many issues remain open, also because of the difficulty in disentangling, in complex patients, the effect of the disease and of the frequent multiple treatments. For this purpose, we have tried to synthesize the existing knowledge and the unresolved issues, to support counseling and promote patient empowerment.

Background/Objectives: Hemodialysis (HD) patients with advanced chronic kidney disease (CKD) are highly vulnerable to complications from SARS-CoV-2 infection. Anemia management in this population is complex, particularly due to erythropoietin resistance, which may be exacerbated by COVID-19-related inflammation. To this aim, in this small-scale retrospective study, we investigated trends in the erythropoietin resistance index (ERI) over time in patients with and without SARS-CoV-2 infection. Methods: This single-center retrospective study included 25 HD patients, divided into two groups: 15 with a history of SARS-CoV-2 infection (CoV2 group) and 10 without (nonCoV2 group). The ERI was assessed over four visits, with 70–100-day intervals between them. Linear mixed models were used to evaluate factors associated with ERI changes. Results: Patients in the CoV2 group exhibited significantly higher ERI increases between T1 (baseline) and T2 (post-infection) compared to the nonCoV2 group (median ΔERI: +4.65 vs. −0.27, p < 0.001). During the T2–T4 recovery period, CoV2 patients demonstrated a delayed but substantial decline in the ERI, converging to baseline levels by T4. Male sex and hemoglobin levels were negatively associated with the ERI. Conclusions: SARS-CoV-2 infection induces transient but significant erythropoietin resistance in HD patients, likely due to inflammation and disrupted erythropoiesis. Tailored anemia management strategies, including the potential use of hypoxia-inducible factor stabilizers, are warranted. Larger, multicenter studies are needed to validate these findings and improve treatment protocols.