scholarly journals Circulating Expression Level of LncRNA Malat1 in Diabetic Kidney Disease Patients and Its Clinical Significance

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Lian-ji Zhou ◽  
Da-wei Yang ◽  
Li-Na Ou ◽  
Xing-Rong Guo ◽  
Biao-liang Wu
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Clinical Significance ◽  
Diabetic Kidney Disease ◽  
Glycosylated Hemoglobin ◽  
Expression Level ◽  
Diabetic Kidney ◽  
Lncrna Malat1 ◽  
Prediction Probability

Background. Long noncoding RNA MALAT1 is closely related to diabetes and kidney diseases and is expected to be a new target for the diagnosis and treatment of diabetic nephropathy. Objective. This study aimed to explore the circulating expression level and significance of lncRNA Malat1 in patients with type 2 diabetes mellitus (T2DM) and diabetic kidney disease (DKD). Methods. Quantitative real-time PCR (qPCR) was conducted to assess the expression of lncRNA Malat1 in 20 T2DM patients, 27 DKD patients, and 14 healthy controls, and then, the clinical significance was analyzed. Results. LncRNA MALAT1 expression in peripheral blood mononuclear cells (PBMC) was significantly upregulated in T2DM and DKD groups when compared to control. Pearson’s correlation analysis showed correlation of lncRNA MALAT1 levels with ACR, urine β2-microglobulin (β2-MG), urine α1-microglobulin (α1-MG), creatinine (Cr), and glycosylated hemoglobin (HbA1c), while negative with superoxide dismutase (SOD) (r=−0.388, P<0.05). Binary regression analysis showed that ACR, creatinine, α1-MG, and LncRNA Malat1 were the risk factors for diabetic nephropathy with OR value of 1.166, 1.031, 1.031, and 2.019 (P<0.05). The area under ROC curve (AUC) of DKD identified by the above indicators was 0.914, 0.643, 0.807, and 0.797, respectively. The AUC of Joint prediction probability of DKD recognition was 0.914, and the sensitivity and specificity of DKD diagnosis were 1.0 and 0.806, respectively. (Take ≥0.251 as the diagnostic cutoff point). Conclusion. LncRNA Malat1 is highly expressed in DKD patients, and the combined detection of ACR, creatinine, α1-MG, and LncRNA Malat1 with diabetes mellitus may be the best way to diagnose diabetic nephropathy.

scholarly journals Urolithiasis as a Result of Secondary Hyperuricemia in Patients with Diabetic Kidney Affection

2021 ◽  
Vol 6 (3) ◽  
pp. 170-174
Author(s):  
S. M. Kolupayev ◽  
◽  
N. M. Andonieva ◽  
M. Ya. Dubovik ◽  
E. A. Huts
Keyword(s):  
Diabetes Mellitus ◽  
Uric Acid ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Metabolic Disorders ◽  
Glycosylated Hemoglobin ◽  
Kidney Damage ◽  
Urinary Stones ◽  
Comparative Approach ◽  
Diabetic Kidney

Urolithiasis is currently one of the most pressing problems of modern urology and medicine in general. The pathogenesis of urolithiasis is multifactorial and caused by various metabolic disorders, in particular carbohydrate, the main manifestation of which is diabetes mellitus. In connection with the above, a comparative approach to the study of metabolic disorders in patients with diabetic kidney damage, in particular hyperuricemia, is relevant in order to identify possible causes of lithogenesis. The purpose of the study is to study the effect of secondary hyperuricemia on the formation of urinary stones in patients with diabetic kidney damage, compared with non-diabetic nephropathies. Materials and methods. The study included 59 patients with chronic kidney disease, including 27 with diabetic nephropathy and 32 with non-diabetic nephropathy. All patients underwent a comprehensive clinical and laboratory study, which included glycosylated hemoglobin, glycemic profile, lipid complex, C-reactive protein, serum creatinine, urea, electrolytes, uric acid, uric acid clearance, glomerular filtration rate, and ultrasound examination of the urinary system. Results and discussion. Urolithiasis was detected in 70.3 % patients with diabetic kidney disease and in 29.6% patients with non-diabetic pathology. The stones had a renal localization: pelvic stones occurred in 38.9% patients, stones in calyces – in 61.1% patients. When assessing the biochemical parameters, the average level of uric acid in the blood serum of patients with diabetes mellitus significantly exceeded the same indicator in the group of patients with non-diabetic pathology. Also, the level of hyperuricemia was higher in diabetic patients with a glycosylated hemoglobin content of more than 8.5%, compared with patients with an HbA1 concentration of less than 7.5%. In patients of both groups compared with serum uric acid concentrations exceeding the level of 498.5 mmol/l in men and 384.2 mmol/L in women, there was a progression of arterial hypertension. In patients with diabetic nephropathy, there was a significant increase in the level of cholesterol, low-density lipoproteins and triglycerides, which provided an increase in the value of the atherogenicity index to 5.7±1.2. Conclusion. In patients with diabetic kidney damage, there are prerequisites for the development of urolithiasis, due to the development of a number of metabolic disorders that affect kidney function and the composition of urine. The key links in the pathogenesis of more frequent development of urolithiasis in this category of patients are secondary hyperuricemia, as well as disorders of carbohydrate and lipid metabolism in the form of hyperglycemia and hyperlipidemia

scholarly journals Estimation and correlation of sirtuin1 with Carboxy Methyl Lysine in type 2 diabetic and its microvascular complication

2020 ◽  
Author(s):  
Sai Deepika ◽  
KN Shashidhar ◽  
A. Raveesha ◽  
C. Muninarayana
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Microvascular Complication ◽  
Diabetic Kidney ◽  
Chronic Hyperglycemia ◽  
Group 3

Background: Increase in Diabetes Mellitus increases incidence of its Microvascular complications such as diabetic retinopathy, diabetic kidney disease (DKD), neuropathy, stroke and cardio vascular diseases (CVD). Advanced glycation end products promotes Type 2 Diabetes to its major Microvascular complication; diabetic kidney disease or diabetic nephropathy leading to increase in expression of sirtuin1; a regulatory protein mediating deacetylation of histone proteins. In addition to diet and nutrition, environmental changes may increase incidence of disorders, one such factor considered in this study is Fluoride. Objective: Estimation of Sirtuin1 in type 2 diabetes mellitus and diabetic kidney disease and interpreting the outcome by diabetic profiling of patients with controls. Participants: 150 study subjects were recruited for this cross- sectional study divided into 3groups with 50 subjects in each group. Methods: Diabetic and renal profiling was carried by fully automated analyzer available in our hospital facility, eGFR was calculated, sirtuin1 and CML were measured by ELISA, serum and urine fluoride were estimated by Ion Selective Electrode. Results: Significant differences observed in FBS, PPBS and CML of deceased with controls. Least median of sirt1 was observed in diabetic nephropathy (36.9). Also, urine and serum fluoride levels were proportionally balanced in group 1& 2 in contrast with group 3 [0.28 (0.2- 0.54) & 0.2 (0.15- 0.26)]. Conclusion: Decrease in Sirtuin1 in group 3 may be due to chronic hyperglycemia and oxidative stress in diabetes hence, further research on large cohort may aid considering sirtuin1 as a biomarker or therapeutic target in aging disorders.

Angiopoietin 2 and Neuropeptide Y are Associated with Diabetic Kidney Disease in Type 1 Diabetes Mellitus

2020 ◽  
Vol 128 (10) ◽  
pp. 654-662 ◽  
Author(s):  
Jelizaveta Sokolovska ◽  
Juris Stefanovics ◽  
Gita Gersone ◽  
Leonora Pahirko ◽  
Janis Valeinis ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Neuropeptide Y ◽  
Type 1 Diabetes Mellitus ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney ◽  
Angiopoietin 2

Abstract Background Serum angiopoietin 2 levels have been associated with endothelial dysfunction and diabetic kidney disease. Derangements in autonomous nervous system lead to increased production of vasoconstrictory and angiogenic mediators such as norepinephrine and neuropeptide Y and are associated with increased risk of microvascular complications. Aim To investigate associations between angiopoietin 2, neuropeptide Y and diabetic kidney disease in patients with type 1 diabetes mellitus. Methods 289 patients with type 1 diabetes mellitus duration > 1 year were included. Patients were stratified according to presence of diabetic nephropathy (macroalbuminuria, estimated glomerular filtration rate<60 ml/min/1.73 m2 or end-stage renal disease). Angiopoietin 2 was measured by Luminex technology. Neuropeptide Y was measured by ELISA. Results Patients with diabetic nephropathy had significantly increased levels of angiopoietin 2 (4020.5 (2172.4–5778.1) pg/ml vs. 2001.0 (1326.7–2862.7) pg/ml) and neuropeptide Y (18.22 (14.85–21.85) ng/ml vs. 12.91 (9.96–17.07) ng/ml). Higher levels of angiopoietin 2 and neuropeptide Y were observed also in patients with arterial hypertension. Angiopoietin 2 and neuropeptide Y correlated significantly (ρ=0.245, p<0.001). Both biomarkers were significant predictors of estimated glomerular filtration rate and diabetic nephropathy in univariate regression models. In the fully adjusted regression models and after application of a stepwise selection regression method, angiopoietin 2 demonstrated a stronger predictive power for diabetic nephropathy compared to neuropeptide Y. Conclusion Diabetic nephropathy is associated with increased serum concentrations of angiopoietin 2 (marker of endothelial dysfunction) and neuropeptide Y (marker of sympathetic activity) in type 1 diabetes. Angiopoietin 2 is a more potent predictor of diabetic nephropathy compared to neuropeptide Y.

scholarly journals Twenty years after ACEIs and ARBs: emerging treatment strategies for diabetic nephropathy

2015 ◽  
Vol 309 (10) ◽  
pp. F807-F820 ◽  
Author(s):  
Stacy A. Johnson ◽  
Robert F. Spurney
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Angiotensin Receptor Blockers ◽  
Treatment Strategies ◽  
Renin Angiotensin System ◽  
Developed Countries ◽  
Converting Enzyme Inhibitors ◽  
Diabetic Kidney

Diabetic nephropathy (DN) is a serious complication of both type 1 and type 2 diabetes mellitus. The disease is now the most common cause of end-stage kidney disease (ESKD) in developed countries, and both the incidence and prevalence of diabetes mellitus is increasing worldwide. Current treatments are directed at controlling hyperglycemia and hypertension, as well as blockade of the renin angiotensin system with angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor blockers. Despite these therapies, DN progresses to ESKD in many patients. As a result, much interest is focused on developing new therapies. It has been over two decades since ACEIs were shown to have beneficial effects in DN independent of their blood pressure-lowering actions. Since that time, our understanding of disease mechanisms in DN has evolved. In this review, we summarize major cell signaling pathways implicated in the pathogenesis of diabetic kidney disease, as well as emerging treatment strategies. The goal is to identify promising targets that might be translated into therapies for the treatment of patients with diabetic kidney disease.

scholarly journals Early Renoprotective Effect of Ruxolitinib in a Rat Model of Diabetic Nephropathy

2021 ◽  
Vol 14 (7) ◽  
pp. 608
Author(s):  
Mohamed M. El-Kady ◽  
Reham A. Naggar ◽  
Maha Guimei ◽  
Iman M. Talaat ◽  
Olfat G. Shaker ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Kidney Disease ◽  
Rat Model ◽  
Diabetic Kidney Disease ◽  
Tubulointerstitial Fibrosis ◽  
Favorable Effect ◽  
Glomerular Sclerosis ◽  
Diabetic Kidney ◽  
Renoprotective Effect ◽  
Tgf Β1

Diabetic kidney disease (DKD) is still one of the unresolved major complications of diabetes mellitus, which leads ultimately to end-stage renal disease in both type 1 and type 2 diabetes patients. Available drugs that suppress the renin–angiotensin system have partially minimized the disease impact. Yet, there is an unmet need for new therapeutic interventions to protect the kidneys of diabetic patients. In DN, glomerular sclerosis and tubulointerstitial fibrosis are mediated through several pathways, of which JAK/STAT is a key one. The current study explored the potential renoprotective effect of the JAK1/JAK2 inhibitor ruxolitinib (at doses of 0.44, 2.2, and 4.4 mg·kg−1) compared to that of enalapril at a dose of 10 mg·kg−1, in a rat model of streptozotocin-induced diabetes mellitus over 8 weeks. The effect of ruxolitinib was assessed by determining urinary albumin/creatinine ratio, serum level of cystatin, and levels of TGF-β1, NF-κB, and TNF-α in renal tissue homogenates by biochemical assays, the glomerular sclerosis and tubulointerstitial fibrosis scores by histological analysis, and fibronectin, TGF-β1, and Vimentin levels by immunohistochemical staining with the respective antibodies. Our results revealed a significant early favorable effect of a two-week ruxolitinib treatment on the renal function, supported by a decline in the proinflammatory biomarkers of DKD. This pre-clinical study suggests that the renoprotective effect of ruxolitinib in the long term should be investigated in animals, as this drug may prove to be a potential option for the treatment of diabetic kidney disease.

scholarly journals Diabetic kidney disease in patients with type 2 diabetes mellitus: a cross-sectional study

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Randa I. Farah ◽  
Mohammed Q. Al-Sabbagh ◽  
Munther S. Momani ◽  
Asma Albtoosh ◽  
Majd Arabiat ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Laboratory Data ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Diabetic Kidney ◽  
Type 2 Dm

Abstract Aim Diabetic kidney disease (DKD) is a major long-term complication of diabetes mellitus (DM). Given the paucity of data on DKD in Jordan, we aimed to evaluate the prevalence, characteristics and correlates of DKD in Jordanian patients with type 2 DM. Methods This cross-sectional study included 1398 adult patients with type 2 DM who sought medical advice in the endocrinology clinic between March and September 2019. Demographic, clinical and laboratory data were reviewed. DKD was defined as reduced eGFR, and/or albuminuria. Three regression models were constructed to identify factors associated with CKD stages, albuminuria and DKD. Results Overall, 701 (50.14%) patients had DKD, with a median age of 59.71 ± 11.36  years. Older age, high triglycerides, and low high-density lipoprotein were associated with DKD (multivariable odds ratio [OR]: 1.02, 95% confidence interval [CI]: 1.01–1.03, p < 0.01; OR: 1.1, 95% CI: 1.01–1.2; and OR: 0.98, 95% CI: 0.97–0.99, p < 0.01 respectively). Metformin and renin-angiotensin system blockers were negatively associated with albuminuria and chronic kidney disease stages (p < 0.01). Conclusion Our study demonstrated that approximately one half of patients with type 2 DM had DKD. Further studies are necessary to understand this high prevalence and the underlying factors. Future research are needed to assess implementing targeted community-based intervention.

Diabetic kidney disease in thedb/dbmouse

2003 ◽  
Vol 284 (6) ◽  
pp. F1138-F1144 ◽  
Author(s):  
Kumar Sharma ◽  
Peter McCue ◽  
Stephen R. Dunn
Keyword(s):  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Mouse Model ◽  
Renal Disease ◽  
Mouse Models ◽  
Diabetic Kidney Disease ◽  
Diabetic Kidney ◽  
Matrix Expansion ◽  
Stage Renal Disease ◽  
End Stage

Diabetic nephropathy is increasing in incidence and is now the number one cause of end-stage renal disease in the industrialized world. To gain insight into the genetic susceptibility and pathophysiology of diabetic nephropathy, an appropriate mouse model of diabetic nephropathy would be critical. A large number of mouse models of diabetes have been identified and their kidney disease characterized to various degrees. Perhaps the best characterized and most intensively investigated model is the db/ db mouse. Because this model appears to exhibit the most consistent and robust increase in albuminuria and mesangial matrix expansion, it has been used as a model of progressive diabetic renal disease. In this review, we present the findings from various studies on the renal pathology of the db/ db mouse model of diabetes in the context of human diabetic nephropathy. Furthermore, we discuss shortfalls of assessing functional renal disease in mouse models of diabetic kidney disease.

scholarly journals Effects of Dapagliflozin on Circulating Markers of Phosphate Homeostasis

2018 ◽  
Vol 14 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Maarten A. de Jong ◽  
Sergei I. Petrykiv ◽  
Gozewijn D. Laverman ◽  
Antonius E. van Herwaarden ◽  
Dick de Zeeuw ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Glycosylated Hemoglobin ◽  
Fibroblast Growth Factor 23 ◽  
Serum Phosphate ◽  
Phosphate Homeostasis ◽  
Double Blind ◽  
Diabetic Kidney ◽  
Albumin Excretion

Background and objectivesThe sodium glucose cotransporter 2 (SGLT-2) inhibitor dapagliflozin is a novel drug for the treatment of diabetes mellitus. Recent studies suggest that SGLT-2 inhibitors affect phosphate homeostasis, but their effects on phosphate-regulating hormones in patients with diabetic kidney disease are still unclear.Design, setting, participants, & measurementsWe performed a post-hoc analysis of a double-blind, randomized, crossover trial in patients with type 2 diabetes with early-stage diabetic kidney disease on stable renin–angiotensin–aldosterone system blockade, with an albumin-to-creatinine ratio between 100 and 3500 mg/g, eGFR≥45 ml/min per 1.73 m2, and glycosylated hemoglobin≥7.2% and <11.4%. Patients were randomized to dapagliflozin 10 mg/d or placebo during consecutive 6-week study periods, separated by a 6-week wash-out. We investigated effects on circulating phosphate, calcium, parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), 25-hydroxyvitamin D (25[OH]D), and 1,25-dihydroxyvitamin D (1,25[OH]2D) levels.ResultsThirty-one patients (age 62 years; 23% female) were analyzed. Compared with placebo, dapagliflozin increased serum phosphate by 9% (95% confidence interval, 4% to 15%; P=0.002), PTH increased by 16% (3% to 30%; P=0.01), FGF23 increased by 19% (0.3% to 42%; P=0.05), and serum 1,25(OH)2D decreased by −12% (−25% to 4%; P=0.12). Calcium and 25(OH)D were unaffected. We found no correlation between changes in markers of phosphate homeostasis and changes in eGFR or 24-hour albumin excretion during dapagliflozin treatment.ConclusionsDapagliflozin increases serum phosphate, plasma PTH, and FGF23. This effect was independent of concomitant changes in eGFR or 24-hour albumin excretion.

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