Type 1 Diabetes Mellitus (T1DM) can generate severe complications, such as Diabetic Kidney Disease (DKD) or Diabetic Nephropathy (DN), with it emerging as the leading cause of terminal (end-stage) renal disease all over the world. For T1DM, the clinical evaluation of DKD uses markers like the Glomerular Filtration Rate (GFR) and the Urinary Albumin Excretion (UAE). However, early diagnosis of DKD is still a challenge. For this reason, investigating molecular markers, such as microRNAs (miRNAs), offers a promising perspective to an early diagnosis, highlighting the stability and the ability to reflect incipient molecular manifestations. Thus, here we investigated four miRNAs (hsa-let-7i-5p, hsa-miR-143-3p, hsa-miR-501-3p, and hsa-miR-100-5p) regarding nephropathy in patients with T1DM, considering the albuminuria (micro and macro) as a standard to evaluate the groups. As a result, we found a reduced expression of miR-100-5p in patients with MIC, indicating a protective role in nephropathy. Beyond that, expression levels between the groups (Non vs. UAE) were not significant when comparing the miRNAs miR-501-3p and miR-143-3p. Finally, miR-143-3p and miR-100-5p were linked to some target genes such as AKT1, MMP13, and IGF1R, that are connected to signal pathways and cellular metabolism.

Background: Some authors evaluated the effect of VD on hyperglycemia in T1DM, but the results remain controversial. This study aims to analyze the effects of high-dose VD supplementation on T1DM patients’ glycemic levels, maintaining stable doses of insulin. Methods: Prospective, 12-week clinical trial including 67 T1DM patients, who were supplemented with high doses of cholecalciferol according to participants' VD value. Patients with VD levels below 30 ng/mL received 10,000 IU/day; those with levels between 30-60 ng/mL received 4,000 IU/day. Patients who had not achieved 25(OH)D levels > 30 ng/ml or presented insulin dose variation during the study were not analyzed. Results: Only 46 out of 67 patients accomplished the criteria at the end of the study. There was no general improvement in the glycemic control evaluated by HbA1c (9.4 ± 2.4 vs 9.4 ± 2.6, p=NS) after VD supplementation. However, a posthoc analysis, based on HbA1c variation, identified patients who had HbA1c reduced at least 0.6% (group 1, N = 13 (28%)). In addition, a correlation between 25(OH)D levels with HbA1c and total insulin dose at the end of the study was observed (r = -0.3, p<0.05; r=-0.4, p<0.05, respectively) and a regression model demonstrated that 25(OH)D was independent of BMI, duration of T1DM and final total insulin dose, being capable of determining 9.2% of HbA1c final levels (Unstandardized B coefficient = −0.033 (CI 95%: −0.064 to −0.002), r² = 0.1, p <0.05). Conclusion: Our data suggests that VD is not widely recommended for glycemic control. Nevertheless, specific patients might benefit from this approach.

Background/Objectives: Low vitamin D (VD) has been associated with diabetic kidney disease (DKD). Nevertheless, VD normality concentrations remain under discussion. Objectives: To evaluate VD concentrations in early and advanced DKD stages according to the Endocrine Society and Institute of Medicine standards in patients with type 2 diabetes mellitus (T2DM). Methods: A cross-sectional study included 80 patients with T2DM and DKD in early (urine albumin–creatinine ratio (UACR) between 30 and 299 mg/g), group 1 (n = 29), and advanced stage (UACR ≥ 300 mg/g), group 2 (n = 51). Results: Compared to group 1, patients in group 2 showed lower 25(OH)D concentrations (26.7 ± 10.1 vs. 30.2 ± 8.0 ng/mL; p ≤ 0.05). In group 2, when the serum VD concentrations were stratified according to the Endocrine Society, VD concentrations ≥ 30 ng/mL were associated with a considerably reduction in UACR compared with VD < 20 ng/mL (365.9 ± 268.3 vs. 937.6 ± 634 mg/g; p < 0.05), but not when compared to the range of 20–29.9 ng/mL (739.8 ± 1138 vs. 937.6 ± 634 mg/g; p = NS). Additionally, in this group, our regression model showed that each unit increase in VD was associated with a UACR reduction of 26.1 mg/g (R² = 0.103; p < 0.05). Conclusions: Higher vitamin D concentrations were associated with improved UACR only in clinical DKD, particularly when VD was at least 30 ng/mL.

Background/Objectives: Abnormal nocturnal dipping (ND) in diabetes mellitus is linked to adverse outcomes. Its association with vitamin D (VD), cardiovascular autonomic neuropathy (CAN), and diabetic kidney disease (DKD) remains unclear. We aim to evaluate the association of VD status with ND loss as well as CAN in type 2 diabetes mellitus (T2DM) across different DKD stages. Methods: 83 T2DM patients were included in this cross-sectional study: 36 with early-stage DKD (urine albumin-to-creatinine ratio [UACR] 30–299 mg/g; Group 1) as well as 47 with advanced-stage DKD (UACR ≥ 300 mg/g; Group 2). Results: Patients with advanced DKD exhibited higher CAN prevalence (72.70% vs. 52.80%; p < 0.05), lower 25(OH)D (26.90 ± 9.90 vs. 29.60 ± 8.00 ng/mL; p = 0.05), and lower systolic ND (0.82 ± 8.40 vs. 4.50 ± 7%; p < 0.05). Among patients with advanced DKD, lower 25(OH)D levels, classified according to the Institute of Medicine (IOM) criteria (normal ≥ 20 ng/mL), were associated with reduced systolic ND (1.90 ± 7.80 vs. −5.60 ± 9.30%; p < 0.05), while the Endocrine Society criteria showed a progressive reduction in systolic ND across VD classification (insufficiency 20–29.9, deficiency <20, and sufficiency ≥30 ng/mL), (−5.60 ± 9.30 vs. −0.20 ± 7.30 vs. 3.30 ± 8%, respectively; p < 0.05). Patients with definite/severe CAN exhibited lower systolic ND (−4.38 ± 7.41 vs. 3.34 ± 8.00%; p < 0.01) than those with absent/early CAN. In addition, lower VD levels were associated with greater CAN severity according to both the Endocrine Society criteria (p < 0.01, r = 0.40), and the IOM criteria (p < 0.05, r = 0.30). In the regression model, VD remained an independent predictor of absence of diastolic ND (Rsqr = 0.393; p < 0.05). Conclusions: These findings suggest a potential link between vitamin D status, autonomic dysfunction, and ND in patients with T2DM and advanced DKD.