Review on Inflammation Markers in Chronic Kidney Disease

Petreski, Tadej; Piko, Nejc; Ekart, Robert; Hojs, Radovan; Bevc, Sebastjan

doi:10.3390/biomedicines9020182

Cited by 38 publications

(39 citation statements)

References 153 publications

(173 reference statements)

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“…Moreover, POx may trigger inflammation and atherosclerosis in pa-tients with kidney stones or end-stage kidney disease [3,[26][27][28]. Consistent with the published data [21,22], we observed no differences in serum IL-6 and MCP-1 concentrations between healthy volunteers and the GN group since the average eGFR in our patients consisted of 64.1 (34.7-84.3) mL/min/1.73 m 2 . However, the elevation of both pro-inflammatory mediators was significantly associated with increased POx levels.…”

supporting

confidence: 89%

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Crosstalk between proteinuria, plasma oxalic acid and inflammation in glomerulonephritis patients: an exploratory study

Stepanova

Snisar

Lebid

et al. 2021

Ukr. J. Nephrol. and Dial.

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Abstract. In the present exploratory cross-sectional cohort study, we evaluated whether plasma and urine oxalate concentrations in patients with primary glomerulonephritis depend not only on the glomerular filtration rate but also on the proteinuria level and influence the inflammatory response. Methods. We enrolled 100 participants, including 76 patients with glomerulonephritis having chronic kidney disease stage (CKD) 1–3b (69.7% of them with nephrotic syndrome) and 24 healthy volunteers. We excluded patients with diabetes, cardiovascular disease and those with glomerulonephritis with an estimated GFR (eGFR) < 30 mL/min/1.73 m2. In addition to routine hematological and biochemical tests, plasma oxalate concentration, urinary oxalate excretion, and serum interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1) levels were assessed in all study participants. Results. We observed that plasma oxalic acid concentration was significantly higher in patients with glomerulonephritis (19.0 [5.9–45.2] µmol/L) than in healthy volunteers (5.5 [3.8–7.3] µmol/L, p < 0.0001). Moreover, nephrotic proteinuria was significantly associated with plasma oxalic acid elevation independent of the patients’ age, sex, glomerular filtration rate, and body mass index (odds ratio = 1.42, 95% confidence interval = 1.13–1.77, p = 0.002). In turn, the increased plasma oxalic acid concentration was associated with high levels of serum IL-6 and MCP-1, which may be cardiovascular risk factors in patients with primary glomerulonephritis. Conclusions. Nephrotic proteinuria was significantly associated with the elevation of plasma oxalic acid concentration and hyperoxaluria in glomerulonephritis patients with CKD stages 1–3b. Plasma oxalate at least partly promotes inflammation, which may be a cardiovascular risk factor in patients with glomerulonephritis in the early stages of CKD. Future studies should recruit at least 156 participants to confirm our preliminary results, validate nephrotic proteinuria as a risk factor for oxalate metabolism violation or determine the role of impaired oxalate homeostasis in clinical outcomes in patients with glomerulonephritis.

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supporting

confidence: 89%

“…Atherosclerosis has been described as the pivotal mechanism of serum IL-6 and MCP-1 elevation in CKD, which may explain the lack of changes in serum IL-6 and MCP-1 concentrations in early CKD stages [21][22][23]. In turn, the expression of these pro-inflammatory markers is induced by oxalate in HK-2 cells, resulting in hyperoxaluria [24,25].…”

mentioning

confidence: 99%

Crosstalk between proteinuria, plasma oxalic acid and inflammation in glomerulonephritis patients: an exploratory study

Stepanova

Snisar

Lebid

et al. 2021

Ukr. J. Nephrol. and Dial.

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“…Other identified shared pathways are TNF-α signaling via NF-kB, TLR signaling, AGE-RAGE signaling, and Fc epsilon RI signaling. From these pathways, IFNA1 and C3 were found to be suitable therapeutic candidates, but the role of IFNA1 in CDK is not well understood [ 95 ]. However, it has been reported that inborn errors of type I IFN immunity are associated with severe COVID-19 [ 96 ] since the low type I IFN activity triggers IL6 and NF-α mediated pro-inflammatory responses and cytokine storm [ 97 ].…”

Section: Discussionmentioning

confidence: 99%

Predicting COVID-19—Comorbidity Pathway Crosstalk-Based Targets and Drugs: Towards Personalized COVID-19 Management

et al. 2021

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It is well established that pre-existing comorbid conditions such as hypertension, diabetes, obesity, cardiovascular diseases (CVDs), chronic kidney diseases (CKDs), cancers, and chronic obstructive pulmonary disease (COPD) are associated with increased severity and fatality of COVID-19. The increased death from COVID-19 is due to the unavailability of a gold standard therapeutic and, more importantly, the lack of understanding of how the comorbid conditions and COVID-19 interact at the molecular level, so that personalized management strategies can be adopted. Here, using multi-omics data sets and bioinformatics strategy, we identified the pathway crosstalk between COVID-19 and diabetes, hypertension, CVDs, CKDs, and cancers. Further, shared pathways and hub gene-based targets for COVID-19 and its associated specific and combination of comorbid conditions are also predicted towards developing personalized management strategies. The approved drugs for most of these identified targets are also provided towards drug repurposing. Literature supports the involvement of our identified shared pathways in pathogenesis of COVID-19 and development of the specific comorbid condition of interest. Similarly, shared pathways- and hub gene-based targets are also found to have potential implementations in managing COVID-19 patients. However, the identified targets and drugs need further careful evaluation for their repurposing towards personalized treatment of COVID-19 cases having pre-existing specific comorbid conditions we have considered in this analysis. The method applied here may also be helpful in identifying common pathway components and targets in other disease-disease interactions too.

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“…In the present study, alamandine reduced renal TGF-β 1 levels. TGF-β 1 expression in the kidneys is considered to be the final common pathway leading to structural damage and fibrosis in various glomerular diseases [ 51 , 52 ]. Urinary TGF-β1 appears to be a marker of glomerular damage severity.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of alamandine on doxorubicin‑induced nephrotoxicity in rats

Hekmat

Chenari

Alipanah

et al. 2021

BMC Pharmacol Toxicol

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Background This study aimed to evaluate the protective effects of alamandine, a new member of the angiotensin family, against doxorubicin (DOX)-induced nephrotoxicity in rats. Methods Rats were intraperitoneally injected with DOX (3.750 mg/kg/week) to reach a total cumulative dose of 15 mg/kg by day 35. Alamandine (50 µg/kg/day) was administered to the rats via mini-osmotic pumps for 42 days. At the end of the experiment, rats were placed in the metabolic cages for 24 h so that their water intake and urine output could be measured. After scarification, the rats’ serum and kidney tissues were collected, and biochemical, histopathological, and immunohistochemical studies were carried out. Results DOX administration yielded increases in pro-inflammatory cytokines, including interleukin (IL)-1β and IL-6, pro-fibrotic proteins transforming growth factor-β (TGF-β), pro-inflammatory transcription factor nuclear kappa B (NF-κB), kidney malondialdehyde (MDA), creatinine clearance, blood urea nitrogen (BUN), and water intake. On the other hand, the DOX-treated group exhibited decreased renal superoxide dismutase (SOD), renal glutathione peroxidase (GPx) activity, and urinary output. Alamandine co-therapy decreased these effects, as confirmed by histopathology and immunohistochemical analysis. Conclusions The results suggest that alamandine can prevent nephrotoxicity induced by DOX‎ in rats.

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Review on Inflammation Markers in Chronic Kidney Disease

Cited by 38 publications

References 153 publications

Crosstalk between proteinuria, plasma oxalic acid and inflammation in glomerulonephritis patients: an exploratory study

Crosstalk between proteinuria, plasma oxalic acid and inflammation in glomerulonephritis patients: an exploratory study

Predicting COVID-19—Comorbidity Pathway Crosstalk-Based Targets and Drugs: Towards Personalized COVID-19 Management

Protective effect of alamandine on doxorubicin‑induced nephrotoxicity in rats

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