Search Results (81)

This study aimed to determine the prevalence of type 1 diabetes mellitus (T1DM) in French Guiana and describe the social profiles of the patients. We conducted a multicenter cross-sectional study of children under 18 years who were diagnosed with type 1 diabetes and followed up from 2002 to 2021. Over a 20-year period, 48 children under 18 years with type 1 diabetes living in French Guiana were included in the study, out of a total of 59 cases. There were 26 girls and 22 boys. The median age at diagnosis was 8.52 years [IQR 6–12]. The incidence rate was 5.9 per 100,000 people in children aged 0–18 years. The 5–9-year age group was the most affected 43.7% (95% CI 38–51%). Of these children, 56.2% (95% confidence interval 40–70%) lived in single-parent households, and 35% (95% CI 23–57%) of the parents had a primary education. Of the children, 29% (95% CI 21–42%) were from families with no resources. Diabetes was diagnosed by ketoacidosis in 56% (95% CI 38–74%) of the patients. Forty percent (95% CI 35–66%) of the patients had an HbA1c > 9%. There was an imbalance in the prevalence of children with higher Hba1c (>9%), with 18.7% (95% CI 10–29%, p < 0.001) of children whose parents had a low level of education having an Hba1c > 9% compared with only 6% (95% CI 3–10%) of children whose parents had a university degree, and a marked imbalance in the prevalence of children with High Hba1c (>9%) among children from single-parent families (22.9%, 95% CI 17–30%) compared with children whose parents lived in couples (8%, 95% CI 5–12%). The 10–14-year age group (18.7%, 95% CI 11–25%) had the highest imbalance in the prevalence of poor diabetes control between children whose parents had lower versus higher education levels. Diabetic retinopathy and diabetic nephropathy were the only reported complications. The multivariate analysis showed that a low level of parental education (Odds ratio 2.9 [95% CI 2.1–4.5], p < 0.001) and single-parent families (Odds ratio 3.1 [95% CI 2.6–4.3], p < 0.001) were predictors of poor control of T1DM. However, the lack of social insurance coverage at diagnosis was not associated with poor T1DM control (p = 0.4). In conclusion, these sociodemographic factors should be considered when caring for children with T1DM in French Guiana. Full article

Background/Objectives: Diabetic nephropathy (DN) is a serious complication of diabetes mellitus. This clinical condition is diagnosed through the detection of microalbuminuria. Molecular biomarkers such as MicroRNA-192 may play a role in the early diagnosis of this condition. This study aims to compare the serum concentrations of MicroRNA-192 in diabetic patients with and without DN and in healthy individuals. Methods: This study was a retrospective case-control study that included three groups. Group I included diabetic patients without DN, Group II included patients with DN, and Group III included healthy control subjects. Blood samples were obtained from each participant and subjected to a full biochemical study including creatinine, albumin, and the detection of MicroRNA-192 by real-time polymerase chain reaction. Results: There were significant differences among the MicroRNA-192 levels in the three groups (p-0.001). There was a significant increase in the MicroRNA-192 level in Group I (1.35 ± 7 0.5) compared with Group II (0.65 ± 7 0.2, p3 = 0.001) and Group III (0.83 ± 7 0.3, p1-0.001). There was a significant reduction in the MicroRNA-192 level in Group II compared with Group III (p2-0.001). Conclusions: This study highlights the potential role of serum miR-192 as a noninvasive biomarker for the early detection of DN in patients with type 2 DM. Our findings demonstrated that serum miR-192 levels were significantly reduced in patients with DN compared with diabetic patients without nephropathy and healthy controls, suggesting the possible protective role of miR-192 in early disease stages. Full article

Background: Acute phosphate nephropathy (APN) is an underrecognized cause of acute kidney injury (AKI), typically associated with the use of oral sodium phosphate (OSP)-based bowel preparations. It is characterized by calcium phosphate crystal deposition within the renal tubules and may result in permanent renal impairment. Despite known risks, phosphate-containing solutions are still widely used without sufficient risk stratification. Methods: We retrospectively evaluated 517 native kidney biopsies performed in our nephrology clinic between 2017 and 2022. Among these, 12 patients with unexplained AKI and recent colonoscopy history were identified. In nine cases, non-specific tubular deposits on routine staining prompted further histochemical analysis. All had a history of recent OSP-based bowel cleansing. The use of von Kossa staining confirmed calcium phosphate deposition, consistent with APN. Results: Out of 517 kidney biopsies performed during the study period, 9 patients were diagnosed with APN based on histopathological findings following recent colonoscopy and OSP-based bowel cleansing. The mean age was 58.7 years, and three were female. Hypertension was present in seven patients, diabetes mellitus in three, and epilepsy in two; one patient had no comorbidities. Baseline renal function was normal (mean serum creatinine 0.86 mg/dL) and increased to 1.76 mg/dL at three months post-exposure. All biopsies revealed tubulointerstitial calcium phosphate deposits and interstitial inflammation; mesangial hypercellularity was observed in five cases, tubular atrophy in three, and acute tubular necrosis in one. All samples stained positive with von Kossa staining. Over time, all patients developed chronic kidney disease, and one progressed to end-stage renal disease requiring dialysis. Conclusions: In patients presenting with unexplained AKI and recent OSP-based bowel preparation, APN should be considered in the differential diagnosis. When routine histology is inconclusive, definitive diagnosis may require special histochemical staining. Risk-based restrictions on phosphate-containing agents are warranted to reduce preventable kidney injury. Full article

Renal artery stenosis (RAS) is a vascular condition characterized by narrowing of one or both renal arteries, leading to reduced blood flow to the kidneys, activation of the renin–angiotensin–aldosterone system (RAAS), and subsequent renovascular hypertension. Overactivation of the same cascade potentiates the production of angiotensin II, which induces systemic vasoconstriction, increases sodium and water retention via aldosterone, and activates the sympathetic nervous system. Angiotensin II is also implicated in endothelial dysfunction, oxidative stress, and chronic inflammation, thus impairing vascular remodeling and arterial stiffness, all of which serve to accelerate cardiovascular complications, such as left ventricular hypertrophy, heart failure, and myocardial infarction. RAS is usually due in at least 90% of cases to atherosclerosis, which typically affects older people with diabetes and smoking as risk factors. There are two types of RAS: unilateral and bilateral. Bilateral RAS is commonly associated with flash pulmonary edema, a life-threatening emergency condition in which alveolar space flooding can occur within minutes. RAS typically remains asymptomatic until the late stage with complications of hypertension, ischemic nephropathy, or chronic kidney disease. FMD tends to create structural abnormalities of the artery, whereas atherosclerosis causes plaque formation and endothelial dysfunction of the artery. Epidemiological surveys have revealed that the prevalence of RAS ranges from 4% to 53% and is especially high among patients with hypertension, cardiovascular disease, or CKD. Diagnosis is based on clinical suspicion and supported by imaging studies, including Doppler ultrasound, computed tomography angiography, and magnetic resonance angiography. Early detection also relies on certain laboratory biomarkers, especially in identifying high-risk patients. These markers would include increased plasma renin activity, elevated aldosterone-renin ratio, and inflammatory markers, including C-reactive protein and endothelin-1. Treatment would also involve pharmacological approaches, including RAAS inhibitors, beta-blockers, and statins, and interventional treatments, including angioplasty and stenting in patients with severe forms of the disease. However, the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) Trial showed that most patients would likely require medical therapy, and that intervention should be reserved for those with uncontrolled hypertension, progressive renal dysfunction, or recurrent episodes of pulmonary edema. Other emerging therapies include drug-eluting balloons, bioresorbable stents, and gene-editing techniques, all of which have shown great promise in the few studies that have been conducted, although further evaluation is needed. Despite these advances, there are still gaps in knowledge regarding patient stratification, biomarker validation, and the development of personalized treatment strategies. This article reviews the complexities of RAAS and its systemic impact on cardiovascular and renal health. Future research can therefore focus on improving early diagnosis, optimizing patient selection for intervention, and developing new therapies to slow disease progression and mitigate complications. Full article

Background: Metabolic syndrome is a complex disorder characterized by the coexistence of multiple risk factors, including dysglycemia, hypertension, dyslipidemia, and visceral obesity. Both metabolic syndrome and diabetes mellitus are closely associated with the onset of microvascular complications such as retinopathy, polyneuropathy, and nephropathy. Methods: This narrative review analyzed 137 studies published up to 2025, retrieved from PubMed and Crossref databases. The objective was to identify and evaluate potential biomarkers that could facilitate the early detection of microvascular complications in patients with metabolic syndrome. Results: Several biomarkers demonstrated a strong correlation with microvascular complications in individuals with metabolic syndrome. These findings suggest their potential role in early diagnosis and risk assessment. Conclusions: The identification of reliable biomarkers may enhance early detection and targeted interventions for microvascular complications in metabolic syndrome. Further research is essential to validate these markers and establish their clinical applicability in routine medical practice. Full article

Background and Objective: Diabetic peripheral neuropathy (DPN) is a prevalent complication of type 2 diabetes mellitus (T2DM), with nerve conduction studies (NCSs) serving as the diagnostic gold standard. Early diagnosis is critical for effective management, yet many cases are detected late due to the gradual onset of symptoms. This study explores the relationship between hematological tests and NCS outcomes in T2DM patients to improve the early detection of DPN. Material and Methods: This retrospective study involved T2DM patients exhibiting neuropathic symptoms, and patients were divided based on NCS findings into groups with normal and abnormal results to assess the diagnostic value of various hematological markers, clinical, and demographic data for DPN. Results: Among 400 participants, 57% (n = 228) had abnormal NCS results indicative of DPN. Significant differences were observed in the abnormal-NCS group, including older age, longer diabetes duration, higher levels of fasting plasma glucose, HbA1c, and apolipoprotein B, along with lower eGFR, HDL-C, and Apo A-I levels. Notably, negative correlations were found between HDL-C, Apo A-I, vitamin B12, and specific NCS measurements, while positive correlations existed with sural sensory nerve amplitudes. Multivariate analysis highlighted the importance of age, diabetes duration, hyperglycemia, and specific hematologic markers in predicting DPN. Conclusions: The findings confirm that NCSs, combined with hematologic testing, can effectively identify DPN in T2DM patients. Consistent with prior research, prolonged hyperglycemia and nephropathy progression are strongly linked to DPN development. Additionally, lower levels of HDL-C, Apo A-I, and vitamin B12 are associated with the condition, suggesting their potential utility in early diagnostic protocols. Full article

Advanced glycation end products (AGEs) represent a class of toxic and irreversible compounds formed through non-enzymatic reactions between proteins or lipids and carbonyl compounds. AGEs can arise endogenously under normal metabolic conditions and in pathological states such as diabetes, kidney disease, and inflammatory disorders. Additionally, they can be obtained exogenously through dietary intake, particularly from foods high in fat or sugar, as well as grilled and processed items. AGEs accumulate in various organs and have been increasingly recognized as significant contributors to the progression of numerous diseases, particularly kidney disease. As the kidney plays a crucial role in AGE metabolism and excretion, it is highly susceptible to AGE-induced damage. In this review, we provide a comprehensive discussion on the role of AGEs in the onset and progression of various kidney diseases, including diabetic nephropathy, chronic kidney disease, and acute kidney injury. We explore the potential biological mechanisms involved, such as AGE accumulation, the AGEs-RAGE axis, oxidative stress, inflammation, gut microbiota dysbiosis, and AGE-induced DNA damage. Furthermore, we discuss recent findings on the metabolic characteristics of AGEs in vivo and their pathogenic impact on renal function. Additionally, we examine the clinical significance of AGEs in the early diagnosis, treatment, and prognosis of kidney diseases, highlighting their potential as biomarkers and therapeutic targets. By integrating recent advancements in AGE research, this review aims to provide new insights and strategies for mitigating AGE-related renal damage and improving kidney disease management. Full article

New onset diabetes mellitus after organ transplantation (NODAT) is a frequent and serious complication of solid organ transplantation. It significantly impacts graft function, patient survival, and quality of life. NODAT is diagnosed based on the criteria for type 2 diabetes, with the oral glucose tolerance test (OGTT) serving as the gold standard for diagnosis. The development of NODAT is influenced by a range of risk factors, which are classified into modifiable and non-modifiable categories. Post-transplant, regular glycemic monitoring at specific intervals is essential for timely diagnosis and initiation of therapy. Early intervention can help prevent or delay the onset of diabetes-related complications. The treatment strategy for NODAT involves lifestyle modifications and pharmacological interventions. These include medications such as metformin, sulfonylureas, glinides, thiazolidinediones, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and insulin. Adjusting immunosuppressive therapy—either by reducing dosages or substituting drugs with lower diabetogenic potential—is a common preventative and therapeutic measure. However, this must be performed cautiously to avoid acute graft rejection, which poses a greater risk to the patient compared to NODAT itself. In addition to managing diabetes, addressing comorbidities such as hypertension and dyslipidemia is crucial, as they elevate the risk of cardiovascular events and mortality. Patients with NODAT are also prone to developing common diabetes-related complications, including diabetic nephropathy, neuropathy, retinopathy, and peripheral vascular disease. Therefore, regular follow-ups and appropriate treatment are vital to maintaining quality of life and improving long-term outcomes. Full article

Microcirculation is an essential system that regulates oxygen and nutrients to cells and tissues in response to various environmental stimuli and pathophysiological conditions. Diabetes mellitus can cause microvascular complications including nephropathy, neuropathy, and retinopathy. The pathogenesis of microvascular dysfunction in diabetes is associated with hyperglycemia and the result of an interplay of various factors. Research studies have demonstrated that functional microvascular dysfunction appears much earlier than structural alterations in vasculature in diabetes. This finding of the progression from microvascular dysfunction to macrovascular disease establishes a foundation for the screening and early diagnosis of diabetes by assessing the microvascular function. This comprehensive review discusses technologies (laser Doppler, transcutaneous oximetry, infrared thermography and near-infrared spectroscopy) with computational methods (linear (time and frequency domains), nonlinear and machine learning approaches) for diagnosing microvascular dysfunction in diabetes. Pathophysiological changes of microvascular dysfunction leading to impaired vasomotion and blood flow oscillations in diabetes are reviewed. Recent findings in managing microvascular dysfunction using lifestyle modifications and force-based modulations are evaluated. A consensus endorsed by the American Diabetes Association has been reached that an effective exercise program would greatly slow down the progression of microvascular dysfunction and its impact on diabetic foot ulcers, muscle fatigue and weakness and peripheral neuropathy. However, it is imperative to determine the dose–response relationship of exercise and microvascular responses in patients with diabetes. Research studies have demonstrated that local vibration and whole-body vibration can improve microcirculation in various pathological conditions, including diabetes. Due to the complex nature of microvascular regulation, various computational methods have been developed to shed light on the influence of diabetes on microvascular dysfunction. This comprehensive review will contribute to the diagnosis and management of microvascular dysfunction in diabetes. Full article

Background/Objectives: The increase in patients with type 2 diabetes, coupled with the development of complications caused by the same disease is an alarming aspect for the health sector. One of the main complications of diabetes is nephropathy, which is also the main cause of kidney failure. Once diagnosed, in Mexican patients the kidney damage is already highly compromised, which is why acting preventively is extremely important. The aim of this research is to compare distinct methodologies of feature selection to identify discriminant risk factors that may be beneficial for early treatment, and prevention. Methods: This study focused on evaluating a Mexican dataset collected from 22 patients containing 32 attributes. To reduce the dimensionality and choose the most important variables, four feature selection algorithms: Univariate, Boruta, Galgo, and Elastic net were implemented. After selecting suitable features detected by the methodologies, they are included in the random forest classifier, obtaining four models. Results: Galgo with Random Forest achieved the best performance with only three predictors, “creatinine”, “urea”, and “lipids treatment”. The model displayed a moderate classification performance with an area under the curve of 0.80 (±0.3535 SD), a sensitivity of 0.909, and specificity of 0.818. Conclusions: It is demonstrated that the proposed methodology has the potential to facilitate the prompt identification of nephropathy and non-nephropathy patients, and thereby could be used in the clinical area as a preliminary computer-aided diagnosis tool. Full article

Despite numerous studies conducted by various research teams, predicting long-term outcomes (known as Post-COVID-19 Syndrome, PCS) that may result from Coronavirus Disease 2019 (COVID-19) remains challenging. PCS affects over a million people, primarily those with comorbid conditions. Therefore, it is crucial to undertake research aimed at developing a predictive model for early diagnosis of PCS, which in turn would enable faster preventive actions. The aim of this study was to assess the value of measuring and attempt a quantitative evaluation using Enzyme-Linked Immunosorbent Assay (ELISA) tests of three non-serum proteins, whose presence in the blood during COVID-19 was associated with severe disease progression: neutrophil elastase (NE), calcium-binding protein S100B, and neuron-specific enolase (NSE). The concentrations of these proteins were measured in blood serum samples collected before the COVID-19 pandemic from (1) patients with type 2 diabetes (T2DM); (2) advanced stage diabetic nephropathy (NfT2DM); (3) a healthy group; and in blood serum samples collected two years after recovering from COVID-19 from patients with (4) T2DM and (5) NfT2DM. It was found that elevated levels of NE and NSE were significantly more common (p < 0.05) in patients with NfT2DM after recovering from COVID-19 compared to the other groups, while elevated levels of S100B were significantly more frequently observed in patients with T2DM after recovering from COVID-19 (p < 0.05). Demonstrating differences in the prevalence of NE, NSE, and S100B in individuals who recovered from COVID-19 with T2DM and NfT2DM makes these proteins important components of the developing predictive model for early detection of PCS. To our knowledge, this is the first study showing the significance of NE, NSE, and S100B in PCS in the context of T2DM and NfT2DM. Full article

Background and Objectives: Diabetes is a global health issue, with approximately 50% of patients developing diabetic nephropathy (DN) and 25% experiencing early and severe forms of the disease. The genetic factors contributing to rapid disease progression in a subset of these patients are unclear. This study investigates genetic variations in the GLO-1, CBR-1, and ACE genes associated with early and severe DN. Materials and Methods: Sanger DNA sequencing of the exons of CBR1, GLO1, and ACE genes was conducted in 113 patients with early and severe DN (defined as occurring within 10 years of the diagnosis of diabetes and with eGFR < 45 mL/min/1.73 m²) and 100 controls. The impact of identified genetic variations was analyzed using computational protein models created in silico with SWISS-Model and SWISS-Dock for ligand binding interactions. Results: In GLO1, two heterozygous missense mutations, c.102G>T and c.147C>G, and one heterozygous nonsense mutation, c.148G>T, were identified in patients. The SNP rs1049346 (G>A) at location 6:38703061 (GRCh38) was clinically significant. The c.147C>G mutation (C19S) was associated with ligand binding disruption in the GLO1 protein, while the nonsense mutation resulted in a truncated, non-functional protein. In CBR1, two heterozygous variations, one missense c.358G>A, and one silent mutation c.311G>C were observed, with the former (D120N) affecting the active site. No significant changes were noted in ACE gene variants concerning protein structure or function. Conclusions: The study identifies four novel and five recurrent mutations/polymorphisms in GLO1, ACE, and CBR1 genes associated with severe DN in Pakistani patients. Notably, a nonsense mutation in GLO1 led to a truncated, non-functional protein, while missense mutations in GLO1 and CBR1 potentially disrupt enzyme function, possibly accelerating DN progression. Full article

Maturity-onset diabetes of the young (MODY; OMIM # 606391) comprises a cluster of inherited disorders within non-autoimmune diabetes mellitus (DM), typically emerging during adolescence or young adulthood. We report a novel in-frame deletion of HNF1B in a family with renal cysts and MODY, furthering our understanding of HNF1B-related phenotypes. We conducted sequential genetic testing to investigate the glucose intolerance, renal cysts, hepatic cysts, and agenesis of the dorsal pancreas observed in the proband. A comprehensive clinical exome sequencing approach using a Celemics G-Mendeliome Clinical Exome Sequencing Panel was employed. Considering the clinical manifestations observed in the proband, gene panel sequencing identified a heterozygous HNF1B variant, c.36_38delCCT/p.(Leu13del) (reference transcript ID: NM_000458.4), as the most likely cause of MODY in the proband. The patient’s clinical presentation was consistent with MODY caused by the HNF1B variant, showing signs of glucose intolerance, renal cysts, hepatic cysts, and agenesis of the dorsal pancreas. Sanger sequencing confirmed the same HNF1B variant and established the paternally inherited autosomal dominant status of the heterozygous variant in the patient, as well as in his father and sister. The presence of early-onset diabetes, renal cysts, a family history of the condition, and nephropathy appearing before or after the diagnosis of diabetes mellitus (DM) suggests a diagnosis of HNF1B-MODY5. Early diagnosis is crucial for preventing complications of DM, enabling family screening, providing pre-conceptional genetic counseling, and monitoring kidney function decline. Full article

Glomerular kidney diseases typically begin insidiously and can progress to end stage kidney failure. Early onset of therapy can slow down disease progression. Early diagnosis is required to ensure such timely therapy. The goal of our study was to evaluate protein biomarkers (BMs) for common nephropathies that have been described for children with Alport syndrome. Nineteen candidate BMs were determined by commercial ELISA in children with congenital anomalies of the kidneys and urogenital tract, inflammatory kidney injury, or diabetes mellitus. It is particularly essential to search for kidney disease BMs in children because they are a crucial target group that likely exhibits early disease stages and in which misleading diseases unrelated to the kidney are rare. Only minor differences in blood between affected individuals and controls were found. However, in urine, several biomarker candidates alone or in combination seemed to be promising indicators of renal injury in early disease stages. The BMs of highest sensitivity and specificity were collagen type XIII, hyaluronan-binding protein 2, and complement C4-binding protein. These proteins are unrelated to inflammation markers or to risk factors for and signs of renal failure. In conclusion, our study evaluated several strong candidates for screening for early stages of kidney diseases and can help to establish early nephroprotective regimens. Full article

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. Full article