Diabetes prevalence is increasing worldwide, especially through the increase of type 2 diabetes. Diabetic nephropathy occurs in up to 40% of diabetic patients and is the leading cause of end-stage ...renal disease. Various factors affect the development and progression of diabetic nephropathy. Hyperglycaemia increases free radical production, resulting in oxidative stress, which plays an important role in the pathogenesis of diabetic nephropathy. Free radicals have a short half-life and are difficult to measure. In contrast, oxidation products, including lipid peroxidation, protein oxidation, and nucleic acid oxidation, have longer lifetimes and are used to evaluate oxidative stress. In recent years, different oxidative stress biomarkers associated with diabetic nephropathy have been found. This review summarises current evidence of oxidative stress biomarkers in patients with diabetic nephropathy. Although some of them are promising, they cannot replace currently used clinical biomarkers (eGFR, proteinuria) in the development and progression of diabetic nephropathy.
Hyperuricemia is a state in which the serum levels of uric acid are elevated. As such it has a pronounced effect on vascular and renal function with their consequences, while also showing some ...antioxidant effects that show to be beneficial.
Hyperuricemia has shown to have a J-shaped relationship with mortality, is frequently associated with development and progression of heart and kidney disease, and is correlated with malnutrition-inflammation-atherosclerosis syndrome, although several Mendelian studies have failed to show an association with morbidity and mortality. Hyperuricemia is usually associated with gout flares and tophi development but can also present as asymptomatic hyperuricemia. It is still uncertain whether asymptomatic hyperuricemia is an independent risk factor for cardiovascular or renal disease and as such its treatment is questionable.
Some possible tools for future decision making are the use of noninvasive techniques such as pulse wave analysis, urinary sediment analysis, and joint ultrasound, which could help identify individuals with asymptomatic hyperuricemia that could benefit from urate lowering therapy most.
The prevalence of diabetes is increasing and has already reached pandemic proportions. Diabetes is a well-known risk factor for chronic kidney disease. Diabetic kidney disease (DKD) occurs in up to ...40% of people with type 1 or 2 diabetes and is nowadays the leading cause of end-stage renal disease (ESRD). Among several factors involved in the development and progression of DKD are also inflammation and oxidative stress. Unfortunately, there is a paucity of sensitive and specific biomarkers for the early prediction of patients who will develop DKD or will progress to ESRD. This review summarizes the evidence regarding the prognostic value and benefits of targeting markers of inflammation (pro-inflammatory cytokines, tumour necrosis factor-α (TNF-α) and TNF-α receptors, adhesion molecules, chemokines) and markers of oxidative stress. Some of these biomarkers are promising, but further studies are needed before they can be used in clinical practice.
Diabetic kidney disease is a frequent microvascular complication of diabetes and is currently the leading cause of chronic kidney disease and end-stage kidney disease worldwide. Although the ...prevalence of other complications of diabetes is falling, the number of diabetic patients with end-stage kidney disease in need of kidney replacement therapy is rising. In addition, these patients have extremely high cardiovascular risk. It is more than evident that there is a high unmet treatment need in patients with diabetic kidney disease. Finerenone is a novel nonsteroidal mineralocorticoid receptor antagonist used for treating diabetic kidney disease. It has predominant anti-fibrotic and anti-inflammatory effects and exhibits several renal and cardiac protective effects. This review article summarizes the current knowledge and future prospects of finerenone in treating patients with kidney disease.
Acute kidney injury and chronic kidney disease are among the most common non-communicable diseases in the developed world, with increasing prevalence. Patients with acute kidney injury are at an ...increased risk of developing chronic kidney disease. One of kidney injury’s most common clinical sequelae is increased cardiovascular morbidity and mortality. In recent years, new insights into the pathophysiology of renal damage have been made. Oxidative stress is the imbalance favoring the increased generation of ROS and/or reduced body’s innate antioxidant defense mechanisms and is of pivotal importance, not only in the development and progression of kidney disease but also in understanding the enhanced cardiovascular risk in these patients. This article summarizes and emphasizes the role of oxidative stress in acute kidney injury, various forms of chronic kidney disease, and also in patients on renal replacement therapy (hemodialysis, peritoneal dialysis, and after kidney transplant). Additionally, the role of oxidative stress in the development of drug-related nephrotoxicity and also in the development after exposure to various environmental and occupational pollutants is presented.
Diabetes mellitus is a global health issue and main cause of chronic kidney disease. Both diseases are also linked through high cardiovascular morbidity and mortality. Diabetic kidney disease (DKD) ...is present in up to 40% of diabetic patients; therefore, prevention and treatment of DKD are of utmost importance. Much research has been dedicated to the optimization of DKD treatment. In the last few years, mineralocorticoid receptor antagonists (MRA) have experienced a renaissance in this field with the development of non-steroidal MRA. Steroidal MRA have known cardiorenal benefits, but their use is limited by side effects, especially hyperkalemia. Non-steroidal MRA still block the damaging effects of mineralocorticoid receptor overactivation (extracellular fluid volume expansion, inflammation, fibrosis), but with fewer side effects (hormonal, hyperkalemia) than steroidal MRA. This review article summarizes the current knowledge and newer research conducted on MRA in DKD.
Abstract
Background
Obesity is associated with several neurohumoral changes that play an essential role in organ damage. Increased arterial stiffness causes functional vessel wall changes and can ...therefore lead to accelerated target organ damage as well. Whether obesity causes an independent increase in central arterial stiffness is, however, not yet fully known.
Methods
One hundred thirty-three patients (63.2% male) were included. Body Mass Index (BMI) was defined as body weight in kilograms, divided by the square of body height in meters. Chronic Kidney Disease Epidemiology Collaboration creatinine 2009 equation was used to estimate the glomerular filtration rate (eGFR). Non-invasive applanation tonometry was used for arterial stiffness measurements (Sphygmocor Atcor Medical, Sydney, Australia). All patients underwent coronarography.
Results
The mean age of our patients was 65.0 ± 9.2 years. Their mean BMI was 28.5 ± 4.4 kg/m
2
, eGFR 75.5 ± 17.2 ml/min/1.73 m
2
and ankle-brachial index (ABI) 1.0 ± 0.1. Their arterial stiffness measurements showed mean carotid-femoral pulse wave velocity (cfPWV) 10.3 ± 2.7 m/s, subendocardial viability ratio (SEVR) 164.4 ± 35.0%, and pulse pressure (PP) 47.8 ± 14.5 mmHg. Spearman's correlation test revealed a statistically significant correlation between BMI and SEVR (
r
= -0.193;
p
= 0.026), BMI and cfPWV (
r
= 0.417;
p
< 0.001) and between BMI and PP (
r
= 0.227;
p
= 0.009). Multiple regression analysis confirmed an independent connection between BMI and cfPWV (B = 0.303;
p
< 0.001) and between BMI and SEVR (B = -0.186;
p
= 0.040). There was no association between BMI and kidney function, ABI, or coronary artery disease.
Conclusion
Increased BMI is independently associated with augmented central arterial stiffness and reduced subendocardial perfusion but not with coronary artery disease, kidney function, or ABI.
The atherosclerotic state of haemodialysis (HD) patients may be influenced by heavy metals. The purpose of our study was to assess the relationship between serum zinc (Zn) ankle brachial index (ABI) ...as a non-invasive diagnostic tool for atherosclerosis, and mortality in chronic haemodialysis (HD) patients.
Sixty one HD patients were included (mean age 61.2 ± 13.8 years). The ABI was measured with an automated measuring device (ABPI MD, MESI®, Slovenia). Two groups of patients were formed based on the median value of Zn (14.1 mcmol/l). The average observation time was 2.8 years. Comorbidities (arterial hypertension (AH), diabetes mellitus (DM), dyslipidaemia), smoking and oral nutritional supplements (ONS) consumption were noted. Survival rates were analysed by Kaplan-Meier and Cox regression was used to determine the influence of Zn, ABI, AH, DM, dyslipidaemia, smoking and ONS.
Zn values were between 9.2 and 23.5 mcmol/l (14.4 ± 2.34), ABI values ranged from 0.8 to 1.4 (1.14 ± 0.12). Patients with lower Zn values had lower ABI (p = 0.036). Mean survival time of patients with higher Zn values was 985 days ± 277 days and with lower Zn values 1055 ± 143 days. Six (19.4%) patients with lower Zn and five (16.7%) patients with higher Zn died. We found statistically insignificant lower survival in patients with higher Zn. We failed to find any predictor of all-cause mortality, except for ONS consumption (95% CI 1.6-33.3; p = 0.012).
Lower Zn is associated with lower ABI in HD patients, but we found no impact of Zn on patient survival.
Chronic kidney disease (CKD) is one of the major health problems of the modern age. It represents an important public health challenge with an ever-lasting rising prevalence, which reached almost 700 ...million by the year 2017. Therefore, it is very important to identify patients at risk for CKD development and discover risk factors that cause the progression of the disease. Several studies have tackled this conundrum in recent years, novel markers have been identified, and new insights into the pathogenesis of CKD have been gained. This review summarizes the evidence on markers of inflammation and their role in the development and progression of CKD. It will focus primarily on cytokines, chemokines, and cell adhesion molecules. Nevertheless, further large, multicenter studies are needed to establish the role of these markers and confirm possible treatment options in everyday clinical practice.
The global increase in chronic kidney disease (CKD) parallels the obesity epidemic. Obesity conveys a gradual but independent risk of progression of CKD that seems irrespective of the underlying ...nephropathy. Obesity has been associated with a secondary focal segmental glomerulosclerosis coined obesity-related glomerulopathy (ORG). Pathways through which obesity might cause renal disease are not well understood, and early clinical biomarkers for incipient ORG or renal relevant obesity are currently lacking. Recent human and experimental studies have associated ectopic lipid accumulation in the kidney (fatty kidney) with obesity-related renal disease. There is enough growing insight that ectopic lipid--the accumulation of lipid in non-adipose tissue--is associated with structural and functional changes of mesangial cells, podocytes, and proximal tubular cells to propose the development of ORG as a maladaptive response to hyperfiltration and albuminuria. Recent advances in metabolic imaging might validate ectopic lipid as a biomarker and research aid, to help translate novel therapeutics from experimental models to patients.
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