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Cardiovascular disease poses the greatest risk of premature death seen among patients with chronic kidney disease (CKD). Up to 50% of mortality risk in the dialysis population is attributable to cardiovascular disease and the largest relative excess mortality is observed in younger patients. In early CKD, occlusive thrombotic coronary disease is co...
Citations
... For example, young adults with kidney transplants have a higher risk of graft failure than children and older adults (Dallimore et al., 2018). Furthermore, up to 50% of the mortality risk of people on dialysis is due to cardiovascular diseases, with a higher excess of deaths in young persons (Kumar et al., 2014). ...
Objective: To report the burden of young-onset chronic kidney disease (CKD) in Mexico from 1990 to 2019, and to assess the association between young-onset CKD burden with the Socio-Demographic Index (SDI), and the Healthcare Access and Quality Index (HAQ). Methods: Secondary analysis of data using the Global Burden of Disease, Injuries, and Risk Factors Study (GBD) by sex, age groups, states, and subcauses. Mortality, years of life lost (YLL), years lived with disability (YLD), and disability-adjusted life years (DALY), were obtained. Results: Between 1990 and 2019, the young-onset CKD mortality rate increased by 87.3% (126.3% for men and 48.1% for women). In 2019, this rate was highest in Tlaxcala, Estado de México, Puebla, Veracruz, Jalisco, and Guanajuato (all above 8 deaths per 100,000 inhabitants); Sinaloa and Quintana Roo had the lowest mortality rates (under 3.5 deaths per 100,000 inhabitants). While men had a higher rate of YLL, women were more likely to present YLD due to CKD. In 1990 there was a negative and statistically significant correlation between the HAQ Index and the young-onset CKD DALY rate. Conclusions: In the last 30 years, the burden of early-onset chronic CKD has had an unprecedented increase among the Mexican population, compromising the fulfillment of the Sustainable Development Goals. This will be unattainable if actions to promote healthy lifestyles and prevent kidney disease are not immediately established and articulated, starting with the youngest age groups.
... 20 The toxic effects of oxalate on renal epithelial and tubular cells cause oxalate nephropathy with persistent hyperoxaluria and, together with stone formation, constitute a major but rare contributor to the development of chronic kidney disease (CKD). 19,21 Uric acid supersaturation of the urine, which promotes uric acid stone formation, is aided by low urinary pH resulting from loss of alkali in diarrheal stool and diminished urine volumes (especially after colonic resection) in IBD. 10,18,22,23 Preventative measures include reduction in dietary purine intake, a high fluid intake to maintain a urine output of 2 to 3 litres, and alkalinization of the urine. ...
Renal and urinary tract complications related to inflammatory bowel disease (IBD) have been relatively understudied in the literature compared with other extraintestinal manifestations. Presentation of these renal manifestations can be subtle, and their detection is complicated by a lack of clarity regarding the optimal screening and routine monitoring of renal function in IBD patients. Urolithiasis is the most common manifestation. Penetrating Crohn’s disease involving the genitourinary system as an extraintestinal complication is rare but associated with considerable morbidity. Some biologic agents used to treat IBD have been implicated in progressive renal impairment, although differentiating between drug-related side effects and deteriorating kidney function due to extraintestinal manifestations can be challenging. The most common findings on renal biopsy of IBD patients with renal injury are tubulointerstitial nephritis and IgA nephropathy, the former also being associated with drug-induced nephrotoxicity related to IBD medication. Amyloidosis, albeit rare, must be diagnosed early to reduce the chance of progression to renal failure. In this review, we evaluate the key literature relating to renal and urological involvement in IBD and emphasize the high index of suspicion required for the prompt diagnosis and treatment of these manifestations and complications, considering the potential severity and implications of acute or chronic loss of renal function. We also provide suggestions for future research priorities.
... In particular, in the Korean population, the prevalence rate of patients with diabetes undergoing hemodialysis treatment has rapidly increased, from 23.8% in 2002 to 47.8% in 2017 [2]. Moreover, chronic kidney disease (CKD) is closely related to premature death [7], and the age-adjusted mortality rate of individuals with CKD is more than twice that of individuals without CKD (96.0 vs. 41.0 per 1,000 patients/year, respectively), according to the United States Renal Data System 2020 annual data report [3]. Additionally, in a nationwide study in Korea, the hazard ratio (HR) for mortality in patients with CKD who were not undergoing dialysis was 4.88 (95% confidence interval [CI], 4.36 to 5.47; p < 0.001) compared with that in ageand sex-matched controls [8]. ...
Diabetes has reached epidemic proportions, both in Korea and worldwide and is associated with an increased risk of chronic kidney disease and kidney failure (KF). The natural course of kidney function among people with diabetes (especially type 2 diabetes) may be complex in real-world situations. Strong evidence from observational data and clinical trials has demonstrated a consistent association between decreased estimated glomerular filtration rate (eGFR) and subsequent development of hard renal endpoints (such as KF or renal death). The disadvantage of hard renal endpoints is that they require a long follow-up duration. In addition, there are many patients with diabetes whose renal function declines without the appearance of albuminuria, measurement of the eGFR is emphasized. Many studies have used GFR-related parameters, such as its change, decline, or slope, as clinical endpoints for kidney disease progression. In this respect, understanding the trends in GFR changes could be crucial for developing clinical management strategies for the prevention of diabetic complications. This review focuses on the clinical implication of the eGFR-related parameters that have been used so far in diabetic kidney disease. We also discuss the use of recently developed new antidiabetic drugs for kidney protection, with a focus on the GFR as clinical endpoints.
... However, n-3 alone or a combination of PUFA and vitamin E did not exhibit a beneficial effect. An increase in the serum LDL level and increases in the proportion of oxidized LDL and small, dense LDL particles contribute to an acceleration of atherosclerosis in such patients [49][50][51][52]. Basically, previous studies suggested that PUFA intake can lower serum LDL in general patients, but studies of dialysis patients are still limited [53,54]. ...
Numerous randomized controlled trials (RCTs) and meta-analyses have assessed the effects of supplemental dietary polyunsaturated fatty acids (PUFAs) on levels of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) and the LDL/HDL ratio in patients receiving renal replacement therapy (RRT). However, results are ambiguous due to mixed reports of various nutrients used in the intervention group. We performed a network meta-analysis of RCTs to assess the effects of PUFAs on lipid profiles in patients undergoing RRT. RCTs performed before November 2021 were gathered from three databases. The means, standard deviations and the number of cases for each arm were independently extracted by two authors to form a network meta-analysis of LDL and HDL levels and the LDL/HDL ratio in a random effects model. Twenty-eight RCTs (n = 2017 subjects) were included in this study. The pooled results revealed that the combination of omega-3 fatty acids (n-3) and omega-6 fatty acids (n-6) produced significantly lower LDL (standardized mean difference (SMD) = −1.43, 95% confidence interval: −2.28 to −0.57) than the placebo. Both n-3 fatty acids (SMD = 0.78) and the combination of n-3 + n-6 (SMD = 1.09) benefited HDL significantly compared with placebo. Moreover, n-3 alone also exhibited a significantly lower LDL/HDL ratio than placebo. Collectively, PUFAs seem to be adequate nutrients for controlling lipoproteins in patients undergoing RRT. Specifically, n-3 + n-6 supplementation improved LDL levels, while n-3 improved HDL levels and the LDL/HDL ratio. However, our data provide limited information on specific dosages of PUFAs to form a concrete recommendation.
... С этим, в частности, связывают вероятность участия Umо в формировании тубулоинтерстициальных изменений [3,5], а также артериальной гипертензии [6][7][8][9]. Одним из механизмов последней полагают активацию Na, K, 2Cl-котранспортера [10] Прогрессирование хронической болезни почек (ХБП) сопровождается увеличением распространенности, а также выраженности нарушений ионного гомеостаза и артериальной гипертензии [11 ]. В соответствии с современными рекомендациями препаратами первого ряда, используемыми для не только для нормализации артериального давления, но и для нефропротекции, являются ингибиторы ангиотензинпревращающего фермента (иАПФ) [12]. ...
BACKGROUND. Uromodulin (UMO) is a multifunctional glycoprotein expressed in epithelial cells of the thick ascending part of the loop of Henle. Currently, enough information has been accumulated about the participation of this glycoprotein in a number of important physiological and pathological processes. THE AIM: to evaluate the relationship between the level of urine uromodulin (Umo) and the intake of angiotensin converting enzyme (ACE) inhibitors in chronic kidney disease. PATIENTS AND METHODS. 96 patients aged 43.6±15.4 years were examined. (M:W = 46:50). The presence of kidney disease in all cases is confirmed morphologically. The main criterion for the inclusion of patients in the study was the presence of CKD C1-C3. The exclusion criteria were age over 70 years, the presence of diabetes mellitus, immunosuppressive therapy at the time of examination, taking diuretics. Umo concentrations in blood serum (SUmo) and urine (UUmo) were measured by enzyme immunoassay. Serum and urinary concentrations of creatinine, potassium, sodium, chlorine, calcium, and inorganic phosphorus, as well as protein levels in urine, were also determined. The glomerular filtration rate (eGFR) was calculated using the formula CKD-EPI. The values of daily excretion, clearance, and fractional excretion were calculated for all ions. RESULTS. The patients were divided into two groups: group 1 – 20 people who did not take ACE inhibitors; group 2 – 78 people who took ACE inhibitors. The content of Umo in urine correlated in the first group with the value of systolic and diastolic blood pressure and serum Umo. In the second group, associations of the concentration of Umo in urine with age, eGFR, the excreted fraction of sodium and chlorine, and serum Umo were noted. CONCLUSION . The data obtained suggest that the nephroprotective properties of ACE inhibitors are broader than is commonly thought. Our data allow us to talk about their protective effect at the level of the tubular apparatus. The authors believe that the information currently available is quite sufficient to discuss the need to introduce the definitions of SUmo and UUmo into real clinical practice.
... Individuals with end-stage kidney disease (ESKD) are at increased risk for cardiovascular disease (CVD), which has been considered an important predictor for allcause mortality and cardiovascular mortality [1,2]. Cardiac valve calcification (CVC) is tightly associated with cardiovascular complications [3]. ...
... This study showed that ESKD patients with CVC had 1.4-2.5 times increased prevalence of arrhythmia, heart failure and CHD compared with those without CVC, and CVC was correlated with heart failure, suggesting that CVC may be a marker of cardiovascular events. Similarly, some studies [1,2] have indicated that CVC itself is a superior predictor of clinical outcomes in ESKD patients and is closely associated with an increased risk of cardiovascular events and all-cause mortality. Taken together, these findings indicated that CVC might reflect a poor clinical prognosis in ESKD patients. ...
Background
Cardiac valve calcification (CVC) is an important risk factor for cardiovascular complications. However, limited data are available concerning the prevalence, clinical features and risk factors for CVC in end-stage kidney disease (ESKD) patients. In this study, we aimed to assess these parameters in Chinese ESKD patients receiving combination therapy with hemodialysis and hemodiafiltration.
Methods
We conducted a cross-sectional study on 293 ESKD patients undergoing combination therapy of hemodialysis and hemodiafiltration at the First Affiliated Hospital of Chongqing Medical University from October 2014 to December 2015. CVC was evaluated via echocardiography.
Results
ESKD patients with CVC had a higher prevalence of diabetes mellitus, aortic and/or coronary artery calcification, arrhythmia, heart failure and coronary heart disease; increased systolic, diastolic and pulse pressure; longer duration of hemodialysis and hypertension; reduced hemoglobin, albumin and high-density lipoprotein cholesterol levels; and increased serum calcium and calcium-phosphorus product levels compared with those without CVC. Logistic regression analysis showed that increased dialysis duration (p = 0.006, OR = 2.25), serum calcium levels (p = 0.046, OR = 2.04) and pulse pressure (p < 0.001, OR = 3.22), the presence of diabetes (p = 0.037, OR = 1.81) and decreased serum albumin levels (p = 0.047, OR = 0.54) were risk factors for CVC. The correlation analysis indicated a significantly increased CVCs prevalence with an increase prevalence of heart failure, aortic and coronary artery calcification.
Conclusions
CVC represents a common complication and a danger signal for cardiovascular events in ESKD patients undergoing combination therapy of hemodialysis and hemodiafiltration. The presence of diabetes, increased pulse pressure, long dialysis duration, hypoalbuminemia and high serum calcium levels were independent risk factors for CVC.
... Vascular calcifications (VC) are very common in chronic kidney disease (CKD) and are associated with high morbidity and mortality caused by cardiovascular (CV) events (RUSSO et al., 2004;KUMAR et al., 2014;KRAMER et al., 2005;KESTENBAUM et al., 2009;COVIC et al.,2010;SCHIFFRIN et al., 2007;ORTIZ et al., 2014). They are strong predictors of CV disease and all-cause mortality in hemodialysis (EDDINGTON et al., 2009;RAGGI et al., 2002;MATSUOKA et al., 2004) peritoneal dialysis and renal transplant (RT) patients (SEYAHI et al., 2011;LIEFELDT et al., 2010). ...
Fetuin A is a major systemic inhibitor of vascular calcifications. The aim of this study was to examine association of single nucleotide polymorphisms (SNP) in the gene for fetuin-A with fetuin-A serum levels, coronary arteries calcification (CAC) and mortality in renal transplant (RT) and chronic kidney (CKD) patients. This study included 88 patients (42 stable RT patients at least 6 months after transplantation and 46 CKD patients, stage 2-5 not requiring dialysis) followed five years. Detection and analysis of fetuin A gene polymorphisms in positions C742T (Thr248Met; rs4917) and C766G (Thr256Ser; rs4918) were performed using PCR method. Respondents with allele 742T had at the same time 766G. Combined genotypes TT/GG had lower serum fetuin A levels than CT /CG and CC/CC. Predictors of CAC in univariate analysis were age (p=0,000), serum fetuin-A levels (p=0.011) and rs 4917 polymorphism (p=0.021) while multivariate determined age (p=0.001) and fetuin-A levels (p=0.031). Patients who were homozygous for variant 742T and 766G (combined genotype TT/GG) had lowest survival rate. Our results suggest that allele 742T and 766G in gene for fetuin-A were associated with lower serum fetuin-A levels, higher CAC occurrence and higher mortality rate in RT and CKD patients.
... CKD and end-stage renal disease (ESRD) patients have a 5-to 10-fold higher risk for developing cardiovascular diseases (CVDs) compared to the age-matched control population [6]. Large population studies have reported that all stages of CKD predispose to premature death, mainly from cardiovascular diseases (CVDs), and this is not restricted to ESRD [7]. Interestingly, the incidence of cardiovascular mortality is much higher in CKD patients at stages G2 and G3 than in ESRD patients [6,8]. ...
... The severity and persistence of LVH are strongly associated with cardiovascular events and mortality risk in CKD and ESRD patients [6]. Macrovascular disease seems to be more important in the early stages of CKD, and microvascular injury could play a major role in the late stages of CKD [7]. Therefore, AMI is a common cause of death in the early stages of CKD. ...
... Therefore, AMI is a common cause of death in the early stages of CKD. In contrast, ESRD patients are more prone to sudden cardiac death due to arrhythmias and heart failure related to LVH, coronary calcification, and electrolyte disturbances [7]. ...
Background:
Uremic cardiomyopathy is a common cardiovascular complication of chronic kidney disease (CKD) characterized by left ventricular hypertrophy (LVH) and fibrosis enhancing the susceptibility of the heart to acute myocardial infarction. In the early stages of CKD, approximately 60% of patients are women. We aimed to investigate the influence of sex on the severity of uremic cardiomyopathy and the infarct size-limiting effect of ischemic preconditioning (IPRE) in experimental CKD.
Methods:
CKD was induced by 5/6 nephrectomy in 9-week-old male and female Wistar rats. Two months later, serum and urine laboratory parameters were measured to verify the development of CKD. Transthoracic echocardiography was performed to assess cardiac function and morphology. Cardiomyocyte hypertrophy and fibrosis were measured by histology. Left ventricular expression of A- and B-type natriuretic peptides (ANP and BNP) were measured by qRT-PCR and circulating BNP level was measured by ELISA. In a subgroup of animals, hearts were perfused according to Langendorff and were subjected to 35 min global ischemia and 120 min reperfusion with or without IPRE (3 × 5 min I/R cycles applied before index ischemia). Then infarct size or phosphorylated and total forms of proteins related to the cardioprotective RISK (AKT, ERK1,2) and SAFE (STAT3) pathways were measured by Western blot.
Results:
The severity of CKD was similar in males and females. However, CKD males developed more severe LVH compared to females as assessed by echocardiography. Histology revealed cardiac fibrosis only in males in CKD. LV ANP expression was significantly increased due to CKD in both sexes, however, LV BNP and circulating BNP levels failed to significantly increase in CKD. In both sexes, IPRE significantly decreased the infarct size in both the sham-operated and CKD groups. IPRE significantly increased the phospho-STAT3/STAT3 ratio in sham-operated but not in CKD animals in both sexes. There were no significant differences in phospho-AKT/AKT and phospho-ERK1,2/ERK1,2 ratios between the groups.
Conclusion:
The infarct size-limiting effect of IPRE was preserved in both sexes in CKD despite the more severe uremic cardiomyopathy in male CKD rats. Further research is needed to identify crucial molecular mechanisms in the cardioprotective effect of IPRE in CKD.
... Notably, kidney function is often decreased in HFpEF and HFrEF patients, and chronic heart failure aggravates renal dysfunction mutually. This bidirectional interaction of renal and heart failure is the key concept in cardio-renal syndrome 53,54 . Dysfunction of each organ can induce and perpetuate injury in the other via complex hemodynamic, neurohormonal, and biochemical pathways such as over-activated RAAS and sympathetic nervous system, increased nitro-oxidative stress, and inflammatory pathways 6 . ...
Uremic cardiomyopathy is characterized by diastolic dysfunction (DD), left ventricular hypertrophy (LVH), and fibrosis. Angiotensin-II plays a major role in the development of uremic cardiomyopathy via nitro-oxidative and inflammatory mechanisms. In heart failure, the beta-3 adrenergic receptor (β3-AR) is up-regulated and coupled to endothelial nitric oxide synthase (eNOS)-mediated pathways, exerting antiremodeling effects. We aimed to compare the antiremodeling effects of the angiotensin-II receptor blocker losartan and the β3-AR agonist mirabegron in uremic cardiomyopathy. Chronic kidney disease (CKD) was induced by 5/6th nephrectomy in male Wistar rats. Five weeks later, rats were randomized into four groups: (1) sham-operated, (2) CKD, (3) losartan-treated (10 mg/kg/day) CKD, and (4) mirabegron-treated (10 mg/kg/day) CKD groups. At week 13, echocardiographic, histologic, laboratory, qRT-PCR, and Western blot measurements proved the development of uremic cardiomyopathy with DD, LVH, fibrosis, inflammation, and reduced eNOS levels, which were significantly ameliorated by losartan. However, mirabegron showed a tendency to decrease DD and fibrosis; but eNOS expression remained reduced. In uremic cardiomyopathy, β3-AR, sarcoplasmic reticulum ATPase (SERCA), and phospholamban levels did not change irrespective of treatments. Mirabegron reduced the angiotensin-II receptor 1 expression in uremic cardiomyopathy that might explain its mild antiremodeling effects despite the unchanged expression of the β3-AR.
... We found that the impact of the duration of EEE on CKD among younger women is even stronger than in older counterparts, an important finding with high clinical utility given the higher morbidity and mortality of younger women with CKD [35].In addition to early menopause or late age at menarche, other physiological situations such as increased parity and longer duration of lactation may result in a decrease of EEE. Furthermore, pathologic causes of low estrogen levels in young women including excessive exercise, eating disorders, and low-functioning pituitary gland needs to be considered [34,[36][37][38]. ...
Background
Despite strong evidence demonstrating the role of estrogen as a protective factor for kidney function in women, limited data are available regarding the influence of endogenous estrogen exposure (EEE) on chronic kidney disease (CKD). The present study aimed to assess the incidence of CKD in women with various levels of EEE.
Methods
In a prospective population-based study over a 15-year follow-up, a total of 3043 eligible women aged 30–70 years, participating in Tehran-Lipid and Glucose-Study were recruited and divided into two groups (EEE < 11 and EEE ≥ 11 years). EEE calculated based on age at menarche, age at menopause, number and duration of pregnancies, lactation, and duration of oral contraceptive use after excluding the progesterone dominant phase of the menstrual cycle. Cox’s proportional hazards model was applied to estimate the hazard ratio of CKD between the study groups, after adjusting for confounders.
Results
The total cumulative incidence rate of CKD was 50.1 per 1000 person years; 95% CI: 47.7–52.6); this was 53.9 (95%CI, 50.2–57.8) and 47.1 (95%CI, 44.0–50.4) per 1000 person years in women with EEE < 11 and EEE ≥ 11 years, respectively. The model adjusted for age, BMI, smoking, hypertension, and diabetes showed that the hazard ratio (HR) of incidence CKD in women with EEE < 11 compare to those with EEE ≥ 11 years in the subgroup of women aged< 45 years was 2.66(95% CI, 2.2, 3.2), whereas, in the subgroup aged ≥45 years, it was 1.22 (95% CI, 1.04, 1.4).
Conclusion
This study shows a higher HR of CKD incidence in women with low EEE levels in their later life. Screening of these women for CKD may be recommended.
