Rationale: Idiopathic pulmonary fibrosis (IPF) is a chronic dysregulated response to alveolar epithelial injury with differentiation of epithelial cells and fibroblasts into matrix-secreting myofibroblasts resulting in lung scaring. The prognosis is poor and there are no effective therapies or reliable biomarkers. Galectin-3 is a β-galactoside binding lectin that is highly expressed in fibrotic tissue of diverse etiologies.Objectives: To examine the role of galectin-3 in pulmonary fibrosis.Methods: We used genetic deletion and pharmacologic inhibition in well-characterized murine models of lung fibrosis. Further mechanistic studies were performed in vitro and on samples from patients with IPF.Measurements and Main Results: Transforming growth factor (TGF)-β and bleomycin-induced lung fibrosis was dramatically reduced in mice deficient in galectin-3, manifest by reduced TGF-β1–induced EMT and myofibroblast activation and collagen production. Galectin-3 reduced phosphorylation and nuclear translocation of β...

Regulation of Transforming Growth Factor-beta 1-driven Lung Fibrosis by Galectin-3

Hemodialyzed type I and type II diabetic patients in the US : Characteristics, glycemic control, and survival. Commentary

Diabetic kidney disease (DKD), as the most common complication of diabetes mellitus (DM), is the major cause of end-stage renal disease (ESRD). Renal interstitial fibrosis is a crucial metabolic change in the late stage of DKD, which is always considered to be complex and irreversible. In this review, we discuss the pathological mechanisms of diabetic renal fibrosis and discussed some signaling pathways that are closely related to it, such as the TGF-β, MAPK, Wnt/β-catenin, PI3K/Akt, JAK/STAT, and Notch pathways. The cross-talks among these pathways were then discussed to elucidate the complicated cascade behind the tubulointerstitial fibrosis. Finally, we summarized the new drugs with potential therapeutic effects on renal fibrosis and listed related clinical trials. The purpose of this review is to elucidate the mechanisms and related pathways of renal fibrosis in DKD and to provide novel therapeutic intervention insights for clinical research to delay the progression of renal fibrosis.

/pdf/signaling-pathways-involved-in-diabetic-renal-fibrosis-54jiyo2c7g.pdf

Signaling Pathways Involved in Diabetic Renal Fibrosis.

Mechanisms of Autonomic Nervous System Dysfunction in Uremia

Objective:

Galectins (Gal) exert many activities, including regulation of inflammation and adipogenesis. We evaluated modulation of Gal-1, -3, -9 and -12 in visceral (VAT) and subcutaneous (SAT) adipose tissue in mice.



Design and Methods:

We used two mouse models of obesity, high-fat diet induced obesity (DIO) and ob/ob mice. We also evaluated the response of Gal-1 KO mice to DIO.



Results:

Both age and diet modulated expression of galectins, with DIO mice having higher serum Gal-1 and Gal-3 versus lean mice after 13-17 weeks of high-fat diet. In DIO mice there was a progressive increase in expression of Gal-1 and Gal-9 in SAT, whereas Gal-3 increased in both VAT and SAT. Expression of Gal-12 declined over time in VAT of DIO mice, similar to adiponectin. Obesity lead to increased production of Gal-1 in adipocytes, whereas the increased Gal-3 and Gal-9 of obesity mostly derived from the stromovascular fraction. Expression of Gal-12 was restricted to adipocytes. There was increased production of Gal-3 and Gal-9, but not Gal-1, in CD11c− and CD11c+ macrophages from VAT of DIO versus lean mice. Expression of Gal-1, -3 and -12 in VAT and SAT of ob/ob mice followed a trend comparable to DIO mice. Rosiglitazone reduced serum Gal-1, but not Gal-3 and modulated expression of Gal-3 in VAT and Gal-9 and Gal-12 in SAT of DIO mice. High-fat feeding lead to increased adiposity in Gal-1 KO versus WT mice, with loss of correlation between leptin and adiposity and no alterations in glucose and insulin levels.



Conclusions:

Obesity leads to differential modulation of Gal-1, 3, 9 and 12 in VAT and SAT, with Gal-1 acting as a modulator of adiposity.

/pdf/adipose-tissue-specific-modulation-of-galectin-expression-in-2h0alvv5j1.pdf

Adipose tissue‐specific modulation of galectin expression in lean and obese mice: Evidence for regulatory function

Objective We conducted a cohort study to identify the risk factors for vitamin D deficiency in predialyzed patients with chronic kidney disease (CKD) Methods An observational study of 135 outpatients with stage 3-5 CKD was undertaken Clinical and biochemical parameters were analyzed in terms of nutritional status, inflammation, and mineral metabolism in relation to serum levels of 25-hydroxyvitamin D [25(OH)D] Levels of 25(OH)D lower than 15 ng/mL were considered to be deficient Results The 25(OH)D-deficient group had a higher body mass index (241±42 kg/m2 vs 225±40 kg/m2, p=00322), and had more diabetic patients (279% vs 36%, p=00003) The multivariate analysis revealed that body mass index (odds ratio=2758; 95% CI, 1048-7721; p=00398), the presence of diabetes (odds ratio=7792; 95% CI, 1808-55439; p=00043), lower hemoglobin concentration (odds ratio=0297; 95% CI, 0099-8732; p=0821), higher serum levels of non-HDL cholesterol (odds ratio=3570; 95% CI, 1449-9442; p=00053) and triglyceride (odds ratio=2447; 95% CI, 0779-1776; p=00258) were the factors associated with low 25(OH)D levels Conclusion Vitamin D deficiency was common among the predialysis CKD patients, and the factors identified as being associated with vitamin D deficiency were diabetes and obesity

Risk factors for vitamin D deficiency in patients with chronic kidney disease.

Suppression of renal fibrosis by galectin-1 in high glucose-treated renal epithelial cells

Non-high-density lipoprotein cholesterol (non-HDL-C) has been proposed as a predictor of cardiovascular disease (CVD) in the general population. The aim of this study was to evaluate the utility of non-HDL-C in predicting CV mortality in chronic hemodialysis (HD) patients. We calculated the serum non-HDL-C level of 259 HD patients by subtracting their HDL-C levels from their total cholesterol. Cox proportional hazards models were used to estimate the hazards ratio (HR) for CV mortality and the 95% confidence interval (CI). A receiver-operating characteristic (ROC) analysis was performed to estimate the relationship between sensitivity and specificity of a diagnostic parameter. There were 44 deaths (17.0%) during the follow-up period, 33 (12.7%) of which were due to CVD. A multivariate Cox analysis with adjustments for age, diabetes, dialysis vintage, systolic blood pressure, serum albumin, and lipid levels showed that non-HDL-C was an independent predictor of CV mortality (HR 1.015, 95% CI 1.004–1.025, p = 0.0083). An ROC analysis showed that the plots of the non-HDL-C levels yielded significant specificity and sensitivity for predicting the risk of CVD mortality in HD patients [area under the curve (AUC) 0.62416; p = 0.0366; cutoff value 111.0 mg/dl]. The Kaplan–Meier survival curves of HD patients showed significant differences in CV mortality according to their tertiles with respect to serum non-HDL-C levels (p = 0.0165). The results of this study suggest that serum non-HDL-C level is a significant CV mortality predictor of chronic HD patients.

Serum non-high-density lipoprotein cholesterol (non-HDL-C) levels and cardiovascular mortality in chronic hemodialysis patients

Glycated albumin (GA) has been reported to be a better indicator of glycemic control than hemoglobin A1c (HbA1c) in diabetic hemodialysis (HD) patients. We performed a cross-sectional study to evaluate associations between daily glucose profiles based on blood glucose measurements at seven different times a day and their GA, HbA1c, and pre-dialysis glucose levels in 90 HD patients with (n = 46) and without (n = 44) diabetes. The results of a univariate analysis showed that the GA, HbA1c, and pre-dialaysis glucose levels were significantly correlated with the daily glucose profiles. In a multivariate analysis, the GA levels were found to be independently correlated with maximum glucose levels (F = 9.448, P = 0.0028) and mean amplitude of glucose excursion (MAGE, F = 5.169, P = 0.0255), but no significant correlation was found between the HbA1c levels and daily glucose profiles. The pre-dialysis glucose levels were independently correlated with minimum glucose levels (F = 8.336, P = 0.0049). In a stratified analysis, the identical trend was seen in the diabetic HD patients, but an independent correlation was found only between HbA1c values and mean glucose levels in nondiabetic HD patients. GA levels may be a better indicator of glycemic control than HbA1c and pre-dialysis glucose levels, especially as a means of evaluating the glucose excursions in diabetic HD patients.

/pdf/glycated-albumin-is-a-better-indicator-of-the-glucose-5e6e1aj949.pdf

Glycated albumin is a better indicator of the glucose excursion than predialysis glucose and hemoglobin A1c in hemodialysis patients

Background: New bone metabolic markers have become available clinically for evaluating chronic kidney disease mineral and bone disorders (CKD-MBD). The aim of this study was to correlate these new bone metabolic markers with conventional markers in regular hemodialysis (HD) patients. 

Methods: One hundred forty three HD patients underwent cross-sectional assessment. Two bone formation markers, bone-specific alkaline phosphatase (BAP) and osteocalcin (OC), and one bone resorption marker, amino-terminal telopeptides of type 1 collagen (NTx), were selected for study. 

Results: Both circulating OC and NTx levels showed positive correlations with serum intact parathyroid hormone (iPTH) levels. The levels of NTx and OC showed a strongly positive correlation, although they are known to be markers of different aspects of bone metabolism: bone formation and resorption. Patients with high iPTH (≥300pg/mL) had significantly higher levels of all the three bone markers compared with patients with low or normal iPTH .

Conclusion: Serum OC and NTx levels may be useful markers of serum iPTH levels for evaluating bone turnover in HD patients and may eventually prove useful in the management of patients with CKD-MBD.

https://cimonline.ca/index.php/cim/article/download/15669/12790

Correlation of new bone metabolic markers with conventional biomarkers in hemodialysis patients.

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