The increase in the prevalence of diabetes mellitus (DM) and the secondary kidney damage produces diabetic nephropathy (DN). Early nephropathy is defined as the presence of microalbuminuria (30–300 mg/day), including normal glomerular filtration rate (GFR) or a mildly decreased GFR (60–89 mL/min/1.73 m²), with or without overt nephropathy. The earliest change caused by DN is hyperfiltration with proteinuria. The acceptable excretion rate of albumin in urine is 300 mg/day. Chronic kidney disease (CKD) is characterized by abnormalities in renal function that persist for >3 months with health implications. Alterations in the redox state in DN are caused by the persistent state of hyperglycemia and the increase in advanced glycation end products (AGEs) with ability to affect the renin-angiotensin system and the transforming growth factor-beta (TGF-β), producing chronic inflammation and glomerular and tubular hypertrophy and favoring the appearance of oxidative stress. In DN imbalance between prooxidant/antioxidant processes exists with an increase in reactive oxygen species (ROS). The overproduction of ROS diminishes expression of the antioxidant enzymes (manganese superoxide dismutase, glutathione peroxidase, and catalase). The early detection of CKD secondary to DN and the timely identification of patients would permit decreasing its impact on health.

Early Chronic Kidney Disease (CKD) is a condition that tends to progress to End-Stage Kidney Disease (ESKD). Early diagnosis of kidney disease in the early stages can reduce complications. Alterations in renal function represent a complication of diabetes mellitus (DM). The mechanisms underlying the progression of CKD in diabetes could be associated with oxidative and inflammatory processes. This study aimed to evaluate the state of inflammation and oxidative stress (OS) on the progression of CKD in the early stages in patients with and without type 2 diabetes mellitus (T2DM). An analytical cross-sectional study was carried out in patients with CKD in early stages (1, 2, 3) with and without T2DM. The ELISA method determined the expression of pro-inflammatory cytokines IL-6 and TNF-α as well as lipoperoxides (LPO), nitric oxide (NO), and superoxide dismutase activity (SOD). Colorimetric methods determined glutathione peroxidase (GPx) and total antioxidant capacity (TAC). Patients with CKD and T2DM had significantly decreased antioxidant defenses for SOD (p < 0.01), GPx (p < 0.01), and TAC (p < 0.01) compared to patients without T2DM. Consequently, patients with T2DM had higher concentrations of oxidant markers, NO (p < 0.01), inflammation markers, IL-6 (p < 0.01), and TNF-α than patients without T2DM. CKD stages were not related to oxidative, antioxidant, and inflammatory marker outcomes in T2DM patients. Patients without T2DM presented an increase in SOD (p = 0.04) and a decrease in NO (p < 0.01) when the stage of CKD increased. In conclusion, patients with T2DM present higher levels of oxidative and inflammatory markers accompanied by a decrease in antioxidant defense. However, these oxidative status markers were associated with CKD stage progression in patients without T2DM. Thus, NO and SOD markers could help detect the early stages of CKD in patients who have not yet developed metabolic comorbidities such as T2DM.

Introduction. Nutritional risk is highly prevalent in patients with COVID-19. Relevant data on nutritional assessment in the critically ill population are scarce. This study was conducted to evaluate the modified Nutrition Risk in the Critically Ill (mNUTRIC)-Score as a mortality risk factor in mechanically ventilated patients with COVID-19. Methods. We conducted this retrospective observational study in critically ill patients with COVID-19. Patients’ characteristics and clinical information were obtained from electronic medical records. The nutritional risk for each patient was assessed at the time of mechanical ventilation using the mNUTRIC-Score. The major outcome was 28-day mortality. Results. Ninety-eight patients were analyzed (mean age, 57.22 ± 13.66 years, 68.4% male); 46.9% of critically ill COVID-19 patients were categorized as being at high nutrition risk (mNUTRIC-Score of ≥5). A multivariate logistic regression model indicated that high nutritional risk has higher 28-day hospital mortality (OR = 4.206, 95% CI: 1.147–15.425, ). A multivariate Cox regression analysis showed that high-risk mNUTRIC-Score had a significantly increased full-length mortality risk during hospitalization (OR = 1.991, 95% CI: 1.219–3.252, ). Conclusion. The mNUTRIC-Score is an independent mortality risk factor during hospitalization in critically ill COVID-19 patients.

Protein-energy wasting is common in critically ill patients with acute kidney injury. Renal replacement therapy (RRT) has negative effects on nutrient balance and can further deteriorate nutritional status. The prescribed dialysis modality is a determinant of micronutrient and amino acid losses, with continuous RRT (CRRT) leading to the greatest losses. It is essential to assess and monitor the nutritional status in any RRT modality, implementing conventional nutritional assessment tools (SGA) and technologies for monitoring hydration and body composition (BIA, US). Nutritional therapy should be initiated early via the enteral route, and if nutritional requirements cannot be achieved, parenteral nutrition can be implemented. Energy requirements range from 20-30 kcal/kg/day (quantifying nutritional/non-nutritional calories), and protein intake is 1.3-1.5 g/kg/day with conventional intermittent RRT, and 1.5-1.7 g/kg/day with prolonged intermittent and continuous RRT.