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Background Recent data pose the question whether conservative management of chronic kidney disease (CKD) by means of a low‐protein diet can be a safe and effective means to avoid or defer transition to dialysis therapy without causing protein‐energy wasting or cachexia. We aimed to systematically review and meta‐analyse the controlled clinical trials with adequate participants in each trial, providing rigorous contemporary evidence of the impact of a low‐protein diet in the management of uraemia and its complications in patients with CKD. Methods We searched MEDLINE (PubMed) and other sources for controlled trials on CKD to compare clinical management of CKD patients under various levels of dietary protein intake or to compare restricted protein intake with other interventions. Studies with similar patients, interventions, and outcomes were included in the meta‐analyses. Results We identified 16 controlled trials of low‐protein diet in CKD that met the stringent qualification criteria including having 30 or more participants. Compared with diets with protein intake of >0.8 g/kg/day, diets with restricted protein intake (<0.8 g/kg/day) were associated with higher serum bicarbonate levels, lower phosphorus levels, lower azotemia, lower rates of progression to end‐stage renal disease, and a trend towards lower rates of all‐cause death. In addition, very‐low‐protein diets (protein intake <0.4 g/kg/day) were associated with greater preservation of kidney function and reduction in the rate of progression to end‐stage renal disease. Safety and adherence to a low‐protein diet was not inferior to a normal protein diet, and there was no difference in the rate of malnutrition or protein‐energy wasting. Conclusions In this pooled analysis of moderate‐size controlled trials, a low‐protein diet appears to enhance the conservative management of non‐dialysis‐dependent CKD and may be considered as a potential option for CKD patients who wish to avoid or defer dialysis initiation and to slow down the progression of CKD, while the risk of protein‐energy wasting and cachexia remains minimal.

This study examined risk associations calibrated to the U.S. population-level incidence of end-stage renal disease and death and projected long-term incidences of ESRD. Risk projections among nondonors were lower than 15-year observed risks after donation. Nearly 30,000 people worldwide become living kidney donors each year. 1 – 3 Traditionally, living donors have been selected on the basis of an absence of risk factors for poor outcomes after donation and without a comprehensive assessment of individualized long-term risk. Although kidney donation is considered to be safe in healthy, low-risk persons, donation has lifelong implications, and the most direct effect may be an increased long-term risk of end-stage renal disease (ESRD). 4 – 7 A tool to predict a donor candidate’s long-term risk of ESRD that incorporates the combined effect of multiple demographic and health characteristics before donation could help make . . .

In the USA, mortality among patients with chronic kidney disease (CKD) and end-stage renal disease has declined over the past two decades. By contrast, new data indicate that the rate of CKD-associated deaths is increasing worldwide. This important finding highlights CKD as a major contributor to global morbidity and mortality.

Proteinuria poses a substantial risk for the progression of chronic kidney disease (CKD) and its related complications. Kidneys excrete hundreds of individual proteins, some with a potential impact on CKD progression or as a marker of the disease. However, the available data on specific urinary proteins and their relationship with CKD severity remain limited. Therefore, we aimed to investigate the urinary proteome and its association with kidney function in CKD patients and healthy controls. The proteomic analysis of urine samples showed CKD stage-specific differences in the number of detected proteins and the exponentially modified protein abundance index for total protein (p = 0.007). Notably, specific urinary proteins such as B2MG, FETUA, VTDB, and AMBP exhibited robust negative associations with kidney function in CKD patients compared to controls. Also, A1AG2, CD44, CD59, CERU, KNG1, LV39, OSTP, RNAS1, SH3L3, and UROM proteins showed positive associations with kidney function in the entire cohort, while LV39, A1BG, and CERU consistently displayed positive associations in patients compared to controls. This study suggests that specific urinary proteins, which were found to be negatively or positively associated with the kidney function of CKD patients, can serve as markers of dysfunctional or functional kidneys, respectively.

While chronic kidney disease (CKD) is regularly evaluated among patients with diabetes, kidney function may be significantly impaired before diabetes is diagnosed. Moreover, disparities in the severity of CKD in such a population are likely. This study evaluated the extent of CKD in a national cohort of 36,764 US veterans first diagnosed with diabetes between 2003 and 2013 and prior to initiating oral antidiabetic therapy. Evidence of CKD (any stage) at the time of diabetes diagnosis was determined using eGFR and urine-albumin-creatinine ratios, the odds of which were assessed using logistic regression controlling for patient characteristics. CKD was evident in 31.6% of veterans prior to being diagnosed with diabetes (age and gender standardized rates: 241.8 per 1,000 adults [overall] and 247.7 per 1,000 adult males), over half of whom had at least moderate kidney disease (stage 3 or higher). The odds of CKD tended to increase with age (OR: 1.88; 95% CI: 1.82-1.93), hemoglobin A1C (OR: 1.05; 95% CI: 1.04-1.06), systolic blood pressure (OR: 1.04; 95% CI: 1.027-1.043), and BMI (OR: 1.016; 95% CI: 1.011-1.020). Both Asian Americans (OR: 1.53; 95% CI: 1.15-2.04) and African Americans (OR: 1.11; 95% CI: 1.03-1.20) had higher adjusted odds of CKD compared to whites, and prevalence was highest in the Upper Midwest and parts of the Mid-South. Results suggest that evidence of CKD is common among veterans before a diabetes diagnosis, and certain populations throughout the country, such as minorities, may be afflicted at higher rates.

Heart failure and renal dysfunction frequently coexist. The term cardiorenal syndrome (CRS) is frequently used to describe this scenario, but the definition of CRS has been a matter of debate and has evolved over time. Here, the authors review the concept of CRS and its evolution and classification, and describe current and future targets for the clinical management of CRS. In addition, they propose a new classification system with seven distinct categories. Combined dysfunction of the heart and the kidneys, which can be associated with haemodynamic impairment, is classically referred to as cardiorenal syndrome (CRS). Cardiac pump failure with resulting volume retention by the kidneys, once thought to be the major pathophysiologic mechanism of CRS, is now considered to be only a part of a much more complicated phenomenon. Multiple body systems may contribute to the development of this pathologic constellation in an interconnected network of events. These events include heart failure (systolic or diastolic), atherosclerosis and endothelial cell dysfunction, uraemia and kidney failure, neurohormonal dysregulation, anaemia and iron disorders, mineral metabolic derangements including fibroblast growth factor 23, phosphorus and vitamin D disorders, and inflammatory pathways that may lead to malnutrition–inflammation–cachexia complex and protein–energy wasting. Hence, a pathophysiologically and clinically relevant classification of CRS based on the above components would be prudent. With the existing medical knowledge, it is almost impossible to identify where the process has started in any given patient. Rather, the events involved are closely interrelated, so that once the process starts at a particular point, other pathways of the network are potentially activated. Current therapies for CRS as well as ongoing studies are mostly focused on haemodynamic adjustments. The timely targeting of different components of this complex network, which may eventually lead to haemodynamic and vascular compromise and cause refractoriness to conventional treatments, seems necessary. Future studies should focus on interventions targeting these components. Key Points The so-called cardiorenal syndrome is a complex phenomenon involving multiple organ systems; traditional understanding of the mechanisms involved forms only a small part of the big picture Any overt or covert involvement of heart or kidney can affect the other organ and usually by the time of clinical manifestation, multiple components of the interconnected network of events are involved It is not usually practically possible to specify whether kidney or heart was the initiator of the events Besides haemodynamic interactions, many other components are involved in the pathophysiology of cardiorenal syndrome; these components can be potential targets for management Most studies, particularly major clinical trials, have targeted and are still focusing on the 'haemodynamic' mechanisms of cardiorenal syndrome; future studies need to concentrate further on the other elements of this complex pathophysiology

Key Points Hyperkalaemia is common in patients with chronic kidney disease (CKD), especially when CKD is accompanied by exacerbating factors Hyperkalaemia is associated with adverse outcomes in patients with CKD, and can restrict the use of beneficial medications, such as renin–angiotensin–aldosterone-system (RAAS) inhibitors Current therapeutic paradigms for hyperkalaemia emphasize intermittent acute interventions and the elimination of exacerbating factors (including RAAS inhibitors) Proactive treatment strategies to prevent the development of hyperkalaemia could also benefit patients by enabling more liberal use of RAAS inhibitors The emergence of new potassium binders may result in more widespread implementation of strategies for hyperkalaemia prevention Hyperkalaemia is common in patients with chronic kidney disease and is associated with adverse outcomes. Here, Csaba Kovesdy gives an overview of the mechanisms underlying hyperkalaemia and its clinical consequences in this patient population, and discusses current treatment regimens, as well as emerging therapies that might enable the more-liberal use of beneficial therapeutics in specific populations of patients at risk of hyperkalaemia. Hyperkalaemia is common in patients with chronic kidney disease (CKD), in part because of the effects of kidney dysfunction on potassium homeostasis and in part because of the cluster of comorbidities (and their associated treatments) that occur in patients with CKD. Owing to its electrophysiological effects, severe hyperkalaemia represents a medical emergency that usually requires prompt intervention, whereas the prevention of hazardous hyperkalaemic episodes in at-risk patients requires measures aimed at the long-term normalization of potassium homeostasis. The options for effective and safe medical interventions to restore chronic potassium balance are few, and long-term management of hyperkalaemia is primarily limited to the correction of modifiable exacerbating factors. This situation can result in a difficult trade-off in patients with CKD, because drugs that are beneficial to these patients (for example, renin–angiotensin–aldosterone-system antagonists) are often the most prominent cause of their hyperkalaemia. Maintaining the use of these beneficial medications while implementing various strategies to control potassium balance is desirable; however, discontinuation rates remain high. The emergence of new medications that specifically target hyperkalaemia could lead to a therapeutic paradigm shift, emphasizing preventive management over ad hoc treatment of incidentally discovered elevations in serum potassium levels.

To determine whether dry weight gain accompanied by an increase in muscle mass is associated with a survival benefit in patients receiving maintenance hemodialysis (HD). In a nationally representative 5-year cohort of 121,762 patients receiving HD 3 times weekly from July 1, 2001, through June 30, 2006, we examined whether body mass index (BMI) (calculated using 3-month averaged post-HD dry weight) and 3-month averaged serum creatinine levels (a likely surrogate of muscle mass) and their changes over time were predictive of mortality risk. In the cohort, higher BMI (up to 45) and higher serum creatinine concentration were incrementally and independently associated with greater survival, even after extensive multivariate adjustment for available surrogates of nutritional status and inflammation. Dry weight loss or gain over time exhibited a graded association with higher rates of mortality or survival, respectively, as did changes in serum creatinine level over time. Among the 50,831 patients who survived the first 6 months and who had available data for changes in weight and creatinine level, those who lost weight but had an increased serum creatinine level had a greater survival rate than those who gained weight but had a decreased creatinine level. These associations appeared consistent across different demographic groups of patients receiving HD. In patients receiving long-term HD, larger body size with more muscle mass appears associated with a higher survival rate. A discordant muscle gain with weight loss over time may confer more survival benefit than weight gain while losing muscle. Controlled trials of muscle-gaining interventions in patients receiving HD are warranted.

Background Higher muscle mass is associated with better outcomes and longevity in patients with chronic disease states. Imaging studies such as dual-energy X-ray absorptiometry (DEXA) are among the gold standard methods for assessing body fat and lean body mass (LBM), approximately half of which is comprised of skeletal muscle mass. Elaborate imaging devices, however, are not commonly available in routine clinical practice and therefore easily accessible and cost-effective, but reliable muscle mass biomarkers are needed. One such marker is serum creatinine, derived from muscle-based creatine, which is inexpensive and ubiquitously available, and it can serve as a biomarker of skeletal muscle mass in human subjects. Methods and results In 118 hemodialysis patients, we found that the 3-month averaged serum creatinine concentration correlated well with DEXA-measured LBM. The recent literature regarding serum creatinine as a surrogate of muscle mass is summarized, as is the literature concerning the use of other measures of muscle mass, such as plasma gelsolin and actin, and urinary creatinine excretion. We have also reviewed the role of dietary meat intake in serum creatinine variability along with several biomarkers of dietary meat intake (creatine, carnitine, carnosine, ophidine, anserine, 3-methyl- l -histidine and 1-methylhistidine). Conclusion In summary, none of these biomarkers was studied in CKD patients. We advance the hypothesis that in both health and disease, under steady state, serum creatinine can serve as a reliable muscle mass biomarker if appropriate adjustment for full or residual kidney function and dietary meat intake is undertaken.