scholarly journals Uric acid and inflammation in kidney disease

2020 ◽  
Vol 318 (6) ◽  
pp. F1327-F1340 ◽  
Author(s):  
Su Woong Jung ◽  
Su-Mi Kim ◽  
Yang Gyun Kim ◽  
Sang-Ho Lee ◽  
Ju-Young Moon
Keyword(s):  
Uric Acid ◽  
Immune System ◽  
Kidney Disease ◽  
Biological Effects ◽  
Experimental Studies ◽  
Epidemiologic Studies ◽  
Causative Role ◽  
Immune System Activation ◽  
Progression Of Kidney Disease ◽  
System Activation

Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune system activation and alters the characteristics of resident kidney cells, such as tubular epithelial cells, endothelial cells, and vascular smooth muscle cells, toward a proinflammatory and profibrotic state. These findings have led to an increased awareness of uric acid as a potential and modifiable risk factor in kidney disease. Here, we discuss the effects of uric acid on the immune system and subsequently review the effects of uric acid on the kidneys mainly in the context of inflammation.

scholarly journals Balloon cells promote immune system activation in focal cortical dysplasia type 2B

2021 ◽  
Author(s):  
Till S. Zimmer ◽  
Diede W.M. Broekaart ◽  
Mark Luinenburg ◽  
Caroline Mijnsbergen ◽  
Jasper J. Anink ◽  
...  
Keyword(s):  
Immune System ◽  
Focal Cortical Dysplasia ◽  
Cortical Dysplasia ◽  
Balloon Cells ◽  
Immune System Activation ◽  
System Activation

scholarly journals Expression of Phosphocitrate-Targeted Genes in Osteoarthritis Menisci

2014 ◽  
Vol 2014 ◽  
pp. 1-17 ◽  
Author(s):  
Yubo Sun ◽  
David R. Mauerhan ◽  
Nury M. Steuerwald ◽  
Jane Ingram ◽  
Jeffrey S. Kneisl ◽  
...  
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Fibroblast Growth Factor Receptor ◽  
Collagen Type ◽  
Skeletal Development ◽  
Growth Factor Receptor ◽  
Type Ii ◽  
Immune System Activation ◽  
System Activation ◽  
Disease Modifying

Phosphocitrate (PC) inhibited calcium crystal-associated osteoarthritis (OA) in Hartley guinea pigs. However, the molecular mechanisms remain elusive. This study sought to determine PC targeted genes and the expression of select PC targeted genes in OA menisci to test hypothesis that PC exerts its disease modifying activity in part by reversing abnormal expressions of genes involved in OA. We found that PC downregulated the expression of numerous genes classified in immune response, inflammatory response, and angiogenesis, including chemokine (C-C motif) ligand 5, Fc fragment of IgG, low affinity IIIb receptor (FCGR3B), and leukocyte immunoglobulin-like receptor, subfamily B member 3 (LILRB3). In contrast, PC upregulated the expression of many genes classified in skeletal development, including collagen type II alpha1, fibroblast growth factor receptor 3 (FGFR3), and SRY- (sex determining region Y-) box 9 (SOX-9). Immunohistochemical examinations revealed higher levels of FCGR3B and LILRB3 and lower level of SOX-9 in OA menisci. These findings indicate that OA is a disease associated with immune system activation and decreased expression of SOX-9 gene in OA menisci. PC exerts its disease modifying activity on OA, at least in part, by targeting immune system activation and the production of extracellular matrix and selecting chondroprotective proteins.

A mechanistic study of immune system activation by fusion of antigens with the ligand-binding domain of CTLA4

2006 ◽  
Vol 55 (12) ◽  
pp. 1504-1514 ◽  
Author(s):  
Dhanalakshmi Chinnasamy ◽  
Matt Tector ◽  
Nachimuthu Chinnasamy ◽  
Kate Dennert ◽  
Karen M. Kozinski ◽  
...  
Keyword(s):  
Immune System ◽  
Ligand Binding ◽  
Binding Domain ◽  
Ligand Binding Domain ◽  
Mechanistic Study ◽  
Immune System Activation ◽  
System Activation

scholarly journals Deoxycorticosterone acetate-salt hypertension activates placental growth factor in the spleen to couple sympathetic drive and immune system activation

2018 ◽  
Vol 114 (3) ◽  
pp. 456-467 ◽  
Author(s):  
Marialuisa Perrotta ◽  
Andrea Lori ◽  
Lorenzo Carnevale ◽  
Stefania Fardella ◽  
Giuseppe Cifelli ◽  
...  
Keyword(s):  
Immune System ◽  
Growth Factor ◽  
Placental Growth Factor ◽  
Deoxycorticosterone Acetate ◽  
Immune System Activation ◽  
Acetate Salt ◽  
Salt Hypertension ◽  
System Activation

Abstract P145: Renal Inflammation and Injury is Associated with Increased Lymphangiogenesis in Hypertension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sterling C Kneedler ◽  
Lauren Phillips ◽  
Kayla R Hudson ◽  
Katharine M Beckman ◽  
Alan R Parrish ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Immune System ◽  
Immune Cells ◽  
Lymphatic Vessels ◽  
Macrophage Infiltration ◽  
Shr Rats ◽  
Renal Inflammation ◽  
Immune System Activation ◽  
System Activation ◽  
Fischer Rats

Hypertension is associated with immune system activation and inflammation. Renal infiltration of both innate and adaptive immune cells contributes to injury, dysfunction, and increased blood pressure. Activated immune cells that exit blood vessels into the interstitium then travel through lymphatic vessels to draining lymph nodes where they signal to other immune cells to increase the immune response. It is unknown how renal lymphatic vessels change in the context of hypertension, immune system activation, inflammation, and injury. We hypothesized that renal macrophage infiltration, inflammation, and injury would significantly increase lymphangiogenesis in various strains of rats. SHR rats that exhibit hypertension and renal injury (SHR-A3 strain) had significantly increased numbers of renal lymphatic vessels at 40 weeks of age compared to WKY controls (total of 3 fields of view: 52 ± 1 vs. 28 ± 1; p<0.05). This was associated with increased renal macrophage infiltration. SHR rats that exhibit hypertension but minimal renal injury (SHR-B2 strain) had significantly less renal lymphatic vessel numbers compared to WKY controls (25 ± 2 vs. 28 ± 1; p<0.05) and normal levels of macrophages. The signals for lymphangiogenesis, VEGF-C and its receptor VEGF-R3, were both increased significantly at the protein level in the kidneys of SHR-A3 rats at 18 weeks but not different in the kidneys of SHR-B2 rats compared to WKY controls. To test whether the increased lymphangiogensis is due to hypertension and/or renal inflammation and injury, we obtained kidneys from Fischer 344 rats that exhibit normal blood pressure but develop renal inflammation and injury as they age. Compared to kidneys from control 4-month old Fischer rats, kidneys from 20-month and 24-month old Fischer rats had significantly increased numbers of lymphatic vessels (32 ± 3 vs. 74 ± 1 vs. 110 ± 6, respectively; p<0.05) and this was also associated with increased macrophage infiltration. Protein levels of VEGF-C and VEGF-R3 were increased significantly in 20-month old Fischer rats compared to 4-month old controls. These data together demonstrate that renal immune cell infiltration, inflammation, and injury increases lymphangiogenesis.

Immune System Activation in Perioperative Thrombectomy Patients: Preliminary Retrospective Study

2019 ◽  
Vol 128 ◽  
pp. e966-e969
Author(s):  
Skylar Trott ◽  
Olga Vsevolozhskaya ◽  
Keith Pennypacker ◽  
Abdulnasser Alhajeri ◽  
Justin F. Fraser
Keyword(s):  
Immune System ◽  
Retrospective Study ◽  
Immune System Activation ◽  
System Activation

P0751METFORMIN, A CLASSIC TREATMENT FOR TYPE 2 DIABETES WITH POSSIBLE RENOPROTECTIVE EFFECTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Adriana Acosta Barrios ◽  
Marian Goicoechea ◽  
Eduardo Verde ◽  
Ángela González-Rojas ◽  
Andres Delgado ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Kidney Disease ◽  
Experimental Studies ◽  
Diabetic Patients ◽  
Metformin Treatment ◽  
End Point ◽  
Progression Of Kidney Disease

Abstract Background and Aims Metformin is the antidiabetic of choice in patients with type 2 diabetes mellitus. Experimental studies and clinical observations have shown that metformin could have a beneficial effect on the progression of kidney disease through the activation of cAMP due to its anti-inflammatory, antifibrotic, and anti-oxidative action. The objective was to compare the progression of CKD in diabetic patients with or without metformin as antidiabetic in their treatment and the prevalence of cardiovascular events in both groups. Method Unicentric retrospective observational analysis. Inclusion criteria: outpatients seen in nephrology consultation during the year of 2012 with diabetes mellitus and stage 3 CKD. Renal, cardiovascular outcomes and mortality were analyzed between patients treated with / without metformin. Median follow-up of 76.5 months (41-84). Renal end-point: estimated glomerular filtration rate drop (MDRD-4) by 50% and / or start of dialysis program. Cardiovascular end-point: ischemic heart disease, stroke, arterial revascularization and / or amputation. Cardiovascular or any cause mortality. Results 148 patients (96M, 52W) with a mean age of 75±9 years and an eGFR of 40±9 ml / min / 1.73 m2 were included. In relation to hypoglycemic therapy: 45 received metformin, 61 insulin and 31 DPP4i. 80% received treatment with RAAS blockers. After the follow-up, the progression of the renal disease was greater in patients who did not receive metformin: eGFR fall of -7.0±16 vs -0.15±16 ml / min in those treated with metformin (p = 0.019). 25 patients in the group without metformin suffered a renal event vs. 5 in the metformin group (logRank: 4.186, p = 0.045). In the Cox analysis, metformin treatment decreases the progression of kidney disease in a model adjusted for baseline renal function and treatment with RAASB (HR 0.368, p = 0.043), losing its predictive power in a proteinuria-adjusted model. During the follow-up, 45 patients died (20 metformin, 25 non-metformin) and 45 patients suffered a cardiovascular event (15 metformin, 30 non-metformin), with no differences between the two groups. Conclusion Metformin treatment in patients with stage 3 CKD could slow the progression of CKD, this effect should be demonstrated in randomized studies with larger sample size.

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