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Chronic kidney disease (CKD) is an irreversible and progressive disease state leading to renal dysfunction and related morbidity [ 1 ]. According to the National Kidney Foundation (NKF) Kidney Disease Outcome Quality Initiative (K/DOQI) guidelines, CKD is defined as a chronic disease state in that irreversible, structural, or functional abnormalities of the kidney, with or without a decreased glomerular filtration rate (GFR), are present for at least three consecutive months [ 1 ]. The degree of renal insufficiency, based on the magnitude of the estimated GFR for 1.73 m^2 body surface, is used to classify the CKD into five stages: (1) GFR > 90 ml/min, (2) GFR 60-89 ml/min, (3) GFR 30-59 ml/min, (4) GFR 15-29 ml/min, and (5) GFR < 15 ml/min [ 1 ]. If they survive long enough, CKD patients eventually reach stage 5 CKD, also known as end-stage renal disease (ESRD), in which life prolongation is exclusively dependent upon renal replacement therapy, i.e. maintenance haemodialysis or peritoneal dialysis treatment and/or kidney transplantation.

The pathophysiology, evaluation, and treatment of malnutrition have been extensively investigated in recent years, and knowledge has accumulated gradually. As a result, it is now well-known that several benign digestive diseases may cause malnutrition. This chapter reviews recent clinical aspects of malnutrition related to common digestive diseases, such as Crohn’s disease, short bowel syndrome, chronic liver diseases, and chronic pancreatitis. In addition, recent progress in nutritional support in the treatment of these diseases is discussed.

The association between weight loss and severe chronic obstructive pulmonary disease (COPD) has long been recognised. Fowler and Godlee [ 1 ] first described the association of weight loss and emphysema in the late nineteenth century. Attempts to establish different COPD classifications led to the realisation that body weight might be an important disease determinant [ 2 ]. This led to the classical description of the pink puffer (emphysematous type) and the blue bloater (bronchitic type). The pink puffing patient is characteristically thin, breathless, and with marked hyperinflation of the chest. The blue and bloated patient may not be particularly breathless, at least when at rest, but has severe central cyanosis. In the 1960s, several studies reported that low body weight and weight loss are negatively associated with survival in COPD [ 3 ]. Nevertheless, therapeutic management of weight loss and muscle wasting in patients with COPD has become of interest only recently, since these features were generally considered as terminal progression in the disease process and therefore inevitable and irreversible.

Cachexia (body wasting) in patients with cardio-vascular illness usually develops when patients have chronic heart failure (CHF). As an increasing public health problem and a leading cause of morbidity and mortality worldwide, CHF is associated with a poor prognosis [ 1 ]. The onset of cachexia in CHF patients (cardiac cachexia) is a serious complication of their disease and even worsens the prognosis of the underlying disease [ 2 ]. This connection between advanced heart failure and significant weight loss has long been recognised. The earliest report dates back to the school of medicine of Hippocrates some 2300 years ago. The term ‘cachexia’ is of Greek origin and derives from the words kakos (bad) and hexis (condition). The term ‘cardiac cachexia’ was first used in 1860 by Mauriac [ 3 ].

Weight loss among geriatric patients is not unusual. In fact, 30–50% of nursing-home residents have substandard body weight, substandard mid-arm muscle circumference, and low serum albumin levels [ 1 ] [ 8 ]. The incidence of weight loss has been reported to be 5–15% in the elderly community overall [ 9 ]. Morley and Kraenzle [ 10 ] found that among 156 nursing home residents, 15–21% had weight loss of 5 lbs. or more over 3–6 months.

Aging is associated with changes in body composition that have important consequences on health and physical function. Thus, studying body composition changes is of increasing interest in geriatric research, and measures are being developed to favourably influence body composition in old age, in addition to exercise and diet.

The word cachexia is derived from the Greek words kakòs , meaning ‘bad,’ and hexis , meaning ‘condition’ [ 1 ]. From an epidemiological point of view, while patients with haematological malignancies and breast cancer seldom have this syndrome, most other solid tumours are associated with a high frequency of cachexia [ 2 ]. Indeed, its prevalence increases from 50% to more than 80% before death, and in more than 20% of patients cachexia is the main cause of death [ 3 ].

The physiological decline in food intake that occurs with aging is an appropriate response to the reduced physical activity of this population. This physiological decline is termed the ‘anorexia of aging’ [ 1 ]; however, cachexia in the elderly seems to be reaching epidemic levels, with 30–40% of men and women over age 75 being 10% underweight or more [ 2 ]. There is no agreed upon definition for cachexia, which means ‘poor condition’ in Greek [ 3 ]. While it has traditionally been thought that chronic illness fully explains the pathogenesis of cachexia, this concept is proving inadequate [ 4 ]. In general, cachexia is characterised by weight loss due to loss of fat and skeletal muscle mass [ 5 ].

A decline in functional status is a profound predictor of morbidity and mortality [ 1 ]. The mortality rate increases from 15% in individuals with only one impairment in an instrumental activity of daily living (IADL) to 21% in persons with one or two IADL impairments. In subjects with five or six IADL impairments, the mortality rate reaches 37% [ 2 ]. Disabled older adults are four to six times more likely to die than the nondisabled [ 3 ]. Up to half of the geriatric patients admitted to a hospital have either loss of or a diminished performance in at least one ADL during admission. This decline in functional status occurs as early as the second day of hospital admission [ 4 , 5 ].

Protein energy malnutrition (PEM) is, alone or associated with other diseases, the first step in the development of cachexia [ 1 ] [ 3 ]. An insufficient amount of food is the leading cause of malnutrition and infectious diseases are the second. In developing countries, 20% of the population — more than 800 million people — eats a quantity of food only sufficient to supply energy for a sedentary life, i.e. 1.2–1.4 times the resting energy expenditure (REE).More than 192 million children suffer from PEM and 2 billion people lack different micronutrients (vitamins, minerals, essential fatty and amino-acids) [ 4 ] [ 7 ]. Even in Western countries, where an enormous surplus of food is produced, many groups of people, especially the poor, the elderly, drug addicts, pregnant women, patients with liver, kidney and gastro-intestinal (GI)-tract diseases, cancer, AIDS, show nutritional defects. In general, 60% of the world’s population (41% in developing countries) consumes less than 2600 Kcal/person/day, an amount of energy considered barely sufficient for limited activity.