Chronic kidney disease is defined as a reduced glomerular filtration rate, increased urinary albumin excretion, or both, and is an increasing public health issue. Prevalence is estimated to be 8–16% ...worldwide. Complications include increased all-cause and cardiovascular mortality, kidney-disease progression, acute kidney injury, cognitive decline, anaemia, mineral and bone disorders, and fractures. Worldwide, diabetes mellitus is the most common cause of chronic kidney disease, but in some regions other causes, such as herbal and environmental toxins, are more common. The poorest populations are at the highest risk. Screening and intervention can prevent chronic kidney disease, and where management strategies have been implemented the incidence of end-stage kidney disease has been reduced. Awareness of the disorder, however, remains low in many communities and among many physicians. Strategies to reduce burden and costs related to chronic kidney disease need to be included in national programmes for non-communicable diseases.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Abstract
Chronic kidney disease (CKD) in heart failure (HF) patients is common, present in 49%, and is associated with a higher mortality hazard ratio 2.34 (95% confidence interval 2.20–2.50); P < ...0.001 and multiple hospital admissions. The management of HF in CKD can be challenging due to drug-induced electrolyte and creatinine changes, resistance to diuretics and infections related to device therapy. Evidence for improvement in mortality and HF hospitalizations exists in HF with reduced ejection fraction (HFrEF) in Stage 3 CKD patients from randomized controlled trials of angiotensin-converting enzyme inhibitor (ACEi) and mineralocorticoid receptor antagonist therapy but not in dialysis patients, where higher doses can cause hyperkalaemia. Evidence of improvement in cardiovascular death and HF hospitalizations has emerged with the angiotensin receptor neprilysin inhibitor ivabradine and more recently with sodium–glucose cotransporter inhibitors in HFrEF patients with CKD Stages 1–3. However, these studies have excluded CKD Stages 4 and 5 patients. Evidence for β-blocker therapy exists in CKD Stages 1–3 and separately in haemodialysis patients. Cardiac resynchronization therapy reduces HF hospitalizations and mortality in patients with CKD Stages 1–3 but has not been shown to do so in CKD Stages 4 and 5 or dialysis patients. Internal cardioverter and defibrillator therapy in HFrEF patients has been shown to be beneficial in CKD 3 patients but not in dialysis patients, where it is associated with high rates of infection. For HFpEF patients with CKD, therapy is symptomatic, as there is no proven therapy for improvement in survival or hospitalizations. HF patients with end-stage kidney disease with fluid overload may benefit from peritoneal dialysis. A multidisciplinary, personalized approach has been associated with better care and improved patient satisfaction.
Protein energy wasting (PEW) is common in patients with chronic kidney disease (CKD) and is associated with adverse clinical outcomes, especially in individuals receiving maintenance dialysis ...therapy. A multitude of factors can affect the nutritional and metabolic status of CKD patients requiring a combination of therapeutic maneuvers to prevent or reverse protein and energy depletion. These include optimizing dietary nutrient intake, appropriate treatment of metabolic disturbances such as metabolic acidosis, systemic inflammation, and hormonal deficiencies, and prescribing optimized dialytic regimens. In patients where oral dietary intake from regular meals cannot maintain adequate nutritional status, nutritional supplementation, administered orally, enterally, or parenterally, is shown to be effective in replenishing protein and energy stores. In clinical practice, the advantages of oral nutritional supplements include proven efficacy, safety, and compliance. Anabolic strategies such as anabolic steroids, growth hormone, and exercise, in combination with nutritional supplementation or alone, have been shown to improve protein stores and represent potential additional approaches for the treatment of PEW. Appetite stimulants, anti-inflammatory interventions, and newer anabolic agents are emerging as novel therapies. While numerous epidemiological data suggest that an improvement in biomarkers of nutritional status is associated with improved survival, there are no large randomized clinical trials that have tested the effectiveness of nutritional interventions on mortality and morbidity.
In chronic kidney disease, anemia and disordered iron homeostasis are prevalent and associated with significant adverse consequences. In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) issued ...an anemia guideline for managing the diagnosis, evaluation, and treatment of anemia in chronic kidney disease. Since then, new data have accrued from basic research, epidemiological studies, and randomized trials that warrant a re-examination of previous recommendations. Therefore, in 2019, KDIGO decided to convene 2 Controversies Conferences to review the latest evidence, explore new and ongoing controversies, assess change implications for the current KDIGO anemia guideline, and propose a research agenda. The first conference, described here, focused mainly on iron-related issues, including the contribution of disordered iron homeostasis to the anemia of chronic kidney disease, diagnostic challenges, available and emerging iron therapies, treatment targets, and patient outcomes. The second conference will discuss issues more specifically related to erythropoiesis-stimulating agents, including epoetins, and hypoxia-inducible factor-prolyl hydroxylase inhibitors. Here we provide a concise overview of the consensus points and controversies resulting from the first conference and prioritize key questions that need to be answered by future research.
Common goals of nutritional therapy across the spectrum of pediatric and adult chronic kidney disease (CKD) include maintaining normal body mass and composition and reducing associated morbidity and ...mortality. Adult nephrologists caring for children and adolescents may be challenged by the existing complexities in identifying and interpreting the nutritional status and growth in children. Pediatric nephrologists may face situations that call for a sound knowledge of assessing nutritional status and providing nutrition therapy for adolescents and young adults. One important additional nutrition goal in children is to achieve normal growth and development. Children are growing and therefore need more calories and nutrients than just maintaining their body weight and composition. Lack of weight and height gain actually is considered failure to thrive in children. Some fundamental differences in approaches to nutritional therapy in CKD are necessitated based on the etiology of CKD. A large proportion of adults with CKD are diabetics, so the approach would be a low-carbohydrate diet. Children with CKD, especially young ones, often are anorexic, so calorie supplements that could include quite a lot of carbohydrates often are prescribed. More adults with CKD have hypertension and atherosclerotic comorbidities, which result in recommendations for low-salt and low-fat diets. Children with CKD often have salt and electrolyte wasting disease states and would require normal- or even high-salt diets, and fats often are included in supplements to bolster calorie intake. Low-protein diets often are recommended in adults with predialysis CKD to slow disease progression. Children are growing and have a higher protein daily requirement. Low-protein diets have not been found to be efficacious in children with CKD, in achieving normal growth, or in slowing disease progression. Adult nephrologists caring for children and adolescents may be challenged by the existing complexities in identifying and interpreting nutritional status and growth in children. Pediatric nephrologists may face situations that call for a sound knowledge of assessing nutritional status and providing nutrition therapy for adolescents and young adults. This article discusses the differences in the assessment of nutritional status between children and adults, as well as provides a comprehensive approach to nutritional management for CKD across the age spectrum.
Abstract
Renin–angiotensin–aldosterone system inhibitors (RAASi) are now a standard treatment in most patients with cardiovascular disease, especially in those with heart failure (HF). The European ...Society of Cardiology and the American College of Cardiology/American Heart Association gave a Class IA recommendation for the use of RAASi in the treatment of Classes II–IV symptomatic HF with reduced ejection fraction (HFREF), based on their strong clinical benefits of lowering all-cause mortality and HF hospitalizations in these subjects. However, RAASi therapy or adding mineralocorticoid receptor antagonists in subjects receiving background angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be associated with an increased risk of hyperkalemia (HK), especially in those with reduced kidney function. As a result, a significant proportion of these subjects either have RAASi dose reduced or more often discontinued when they develop HK. Discontinuation of RAASi in patients hospitalized with HFREF was associated with higher postdischarge mortality and rehospitalization rates, while optimal dosing of RAASi significantly reduced median hospital stays, outpatient visits and related costs. Thus, effective treatment is required to lower potassium level and maintain normokalemia in subjects with HF and reduced kidney disease who develop or are at risk of HK, thus enabling them to continue their RAASi therapy and maximize benefits from RAASi. In this review, we provide an up-to-date review of the prevalence and significance of HK in patients with cardiorenal syndrome, as well as their optimal management of HK with recent novel therapies.
Vitamin D seems to protect against cardiovascular disease, but the reported effects of vitamin D on patient outcomes in CKD are controversial. We conducted a prospective, double blind, randomized, ...placebo-controlled trial to determine whether oral activated vitamin D reduces left ventricular (LV) mass in patients with stages 3-5 CKD with LV hypertrophy. Subjects with echocardiographic criteria of LV hypertrophy were randomly assigned to receive either oral paricalcitol (1 μg) one time daily (n=30) or matching placebo (n=30) for 52 weeks. The primary end point was change in LV mass index over 52 weeks, which was measured by cardiac magnetic resonance imaging. Secondary end points included changes in LV volume, echocardiographic measures of systolic and diastolic function, biochemical parameters of mineral bone disease, and measures of renal function. Change in LV mass index did not differ significantly between groups (median interquartile range, -2.59 -6.13 to 0.32 g/m(2) with paricalcitol versus -4.85 -9.89 to 1.10 g/m(2) with placebo). Changes in LV volume, ejection fraction, tissue Doppler-derived measures of early diastolic and systolic mitral annular velocities, and ratio of early mitral inflow velocity to early diastolic mitral annular velocity did not differ between the groups. However, paricalcitol treatment significantly reduced intact parathyroid hormone (P<0.001) and alkaline phosphatase (P=0.001) levels as well as the number of cardiovascular-related hospitalizations compared with placebo. In conclusion, 52 weeks of treatment with oral paricalcitol (1 μg one time daily) significantly improved secondary hyperparathyroidism but did not alter measures of LV structure and function in patients with severe CKD.
Patients with chronic kidney disease and severely decreased glomerular filtration rate (GFR) are at high risk for kidney failure, cardiovascular disease (CVD) and death. Accurate estimates of risk ...and timing of these clinical outcomes could guide patient counseling and therapy. Therefore, we developed models using data of 264,296 individuals in 30 countries participating in the international Chronic Kidney Disease Prognosis Consortium with estimated GFR (eGFR)s under 30 ml/min/1.73m2. Median participant eGFR and urine albumin-to-creatinine ratio were 24 ml/min/1.73m2 and 168 mg/g, respectively. Using competing-risk regression, random-effect meta-analysis, and Markov processes with Monte Carlo simulations, we developed two- and four-year models of the probability and timing of kidney failure requiring kidney replacement therapy (KRT), a non-fatal CVD event, and death according to age, sex, race, eGFR, albumin-to-creatinine ratio, systolic blood pressure, smoking status, diabetes mellitus, and history of CVD. Hypothetically applied to a 60-year-old white male with a history of CVD, a systolic blood pressure of 140 mmHg, an eGFR of 25 ml/min/1.73m2 and a urine albumin-to-creatinine ratio of 1000 mg/g, the four-year model predicted a 17% chance of survival after KRT, a 17% chance of survival after a CVD event, a 4% chance of survival after both, and a 28% chance of death (9% as a first event, and 19% after another CVD event or KRT). Risk predictions for KRT showed good overall agreement with the published kidney failure risk equation, and both models were well calibrated with observed risk. Thus, commonly-measured clinical characteristics can predict the timing and occurrence of clinical outcomes in patients with severely decreased GFR.
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