Dr Joanne Reid and Dr Helen Noble, Lecturers, from Queens University Belfast, will be hosting this week’s ENB twitter chat on Wednesday the 17th of December between 8-9pm focusing on ‘cachexia in renal disease’ Participating in the twitter chat requires a Twitter account; if you do not already have one you can create an account at www.twitter.com. Once you have an account contributing is straightforward – follow the discussion by searching links to #ebnjc @EBNursingBMJ, or better still, create a tweet (tweets are text messages limited to 140 characters) to @EBNursingBMJ and add #ebnjc (the EBN chat hash tag) at the end of your tweet, this allows everyone taking part to view your tweets.
Cachexia is diagnosed when a person loses weight, suffers muscle atrophy, fatigue, weakness, and significant loss of appetite. It is defined as loss of body mass that cannot be reversed nutritionally. This loss in lean body mass indicates a primary pathology is in place. Cachexia occurs in many chronic conditions such as cancer, acquired immune deficiency syndrome, chronic obstructive pulmonary disease, chronic heart failure, rheumatoid arthritis and chronic kidney disease (CKD). Chronic kidney disease denotes abnormal kidney function and/or structure. The definition of CKD is based on the presence of kidney damage or decreased kidney function indicated by a glomerular filtration rate <60 ml/minute per 1·73 m² for three months or more, irrespective of clinical diagnosis.
In patients with chronic kidney disease (CKD) managed with or without dialysis, the prevalence of cachexia has been reported to range from 30-60%. The pathophysiology of cachexia in CKD is known to be multifactorial. Previous research has established that while reduced food intake may contribute to cachexia, additional factors such as dysregulated appetite controlling hormones, inflammation, abnormal neuropeptide signaling, insulin resistance, and metabolic acidosis may also be associated with its pathogenesis in CKD. Most notably, cachexia is manifested by weight loss and specifically loss of lean muscle mass. It is this amplified loss of lean muscle mass that distinguishes cachexia from weight loss due solely to reduced food intake. Starvation and cachexia represent two distinct types of malnutrition that may be present in people who have advanced CKD. These discrete nutritional deficits have very different pathophysiologies. Central to this distinction, is that starvation is typically not associated with inflammation or reduced serum albumin levels, whereas cachexia is characterized by systemic inflammation and low serum albumin concentrations. Adequate dialysis and intensive dietary support often reverse deteriorating nutritional parameters in persons with CKD who have starvation. It is much more challenging to improve the nutritional status and body composition in people who have renal cachexia. This is because cachexia results not only from a combination of reduced nutritional intake (similar to starvation) but also profound metabolic alterations.
A number of potential treatment modalities for cachexia in advanced CKD have been examined including exercise, nutritional supplements, appetite stimulants, growth hormones, and ghrelin agonists. However, research has not determined the most effective means of anti-cachectic therapy. No research to date has examined the subjective experiences of individuals who have advanced CKD and cachexia and there are no data to delineate the patients’ experience of this phenomenon and that of those caring for them (See Reid et al http://www.ncbi.nlm.nih.gov/pubmed/23432742 ).The current emphasis is largely placed on the anatomical, physiological and pathological issues central to cachexia in advanced CKD. Qualitative research methods can provide a more holistic exploration of the complexities of renal cachexia associated with CKD and interpretation of the data can help to shape future care delivery to address unmet psychosocial needs in this client group. The twitter blog on Wednesday evening aims to discuss cachexia in a renal population and how we can commence research looking at the impact of this syndrome on patients their lay and professional carers with a view to understanding this state of ill health.