e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 5 (2010) e54–e57

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e-SPEN, the European e-Journal of

Clinical Nutrition and Metabolism
journal homepage: http://www.elsevier.com/locate/clnu

Educational Paper

Basics in Clinical Nutrition: Nutritional support in renal disease

Wilfred Druml
University of Vienna and Vienna General Hospital, Vienna, Austria

a r t i c l e i n f o

Article history:
Received 4 June 2009
Accepted 4 June 2009

Keywords:
Pathophysiology
Chronic renal failure (CRF)
Acute renal failure (ARF)

Learning objectives substrates, such as amino acids and water soluble vitamins, but also
systemic effects, such as activation of protein catabolism and
– To understand the metabolic abnormalities in patients with increase in lipid peroxidation as a consequence of bioincompatibility.
renal disease In patients with acute renal failure (ARF) continuous renal replace-
– To know the determinants of nutritional state and the causes of ment therapies (CRRT) have become the standard treatment
malnutrition in uraemia modalities, the metabolic side effects of which are clinically relevant
– To be aware of the aims of nutritional support and the type and because of the continuous mode of therapy and the high fluid turn-
composition of diets in renal disease over. These effects have to be considered in designing a nutritional
program for a patient with ARF (see below).

1. Pathophysiology Nutritional treatment can be considered under 3 main headings:

Patients with renal failure comprise an extremely heteroge-
neous group of subjects with differing – and sometimes contra-
dictory – aims of nutritional support, nutritional requirements and
composition of nutritional regimes.
Renal failure is a pan-metabolic and pan-endocrine abnormality
affecting more or less every metabolic pathway of the body. Despite
differences in metabolic presentation (and nutritional needs) in
various forms of renal failure and during the course of disease in the
individual patient, there are some common features in their
metabolic changes (Table 1). Energy metabolism is not grossly
affected by renal dysfunction (which rather decreases than
increases oxygen consumption) and is more determined by asso-
ciated complications.
2. Metabolic and nutritional consequences of renal
replacement therapies
Renal replacements therapies are associated with multiple
metabolic side effects. Among those are the loss of nutritional
E-mail address: espenjournals@espen.org (Editorial Office).
– The patient with stable chronic renal failure
– The patient on renal replacement therapy
– The patient with acute renal failure
3. Nutritional therapy of patients with renal disease
3.1. Non-catabolic patients with stable chronic renal failure (CRF)
3.1.1. Additional metabolic aspects
In the absence of concurrent disease and compensation for
metabolic acidosis the patients are usually not (grossly) catabolic.
3.1.2. Nutritional state
The patients however, are at a high risk of malnutrition, because
of uraemia associated factors, metabolic acidosis and concurrent
disease, impaired appetite and oral food intake, gastrointestinal
side effect of uraemia, and potentially ill directed dietary regimens.
3.1.3. Aims of nutritional management
The purpose of nutritional management is to prevent malnu-
trition at an early stage of renal disease and/or to maintain an

1751-4991/$36.00 Ó 2009 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.eclnm.2009.06.006
 W. Druml / e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 5 (2010) e54–e57 e55

Table 1 Table 3
Main metabolic abnormalities in patients with renal failure. Causes of malnutrition in haemodialysis patients

Metabolic abnormalities in patients with renal failure Malnutrition in haemodialysis patients

Peripheral insulin resistance Anorexia – reduced oral nutrient intake
Impairment of lipolysis Gastrointestinal consequences of uraemia
Low grade inflammatory state  activation of protein catabolism Restrictive diets
Augmented catabolic response to intercurrent disease Uremic toxicity – inadequate dialysis prescription
Metabolic acidosis Metabolic acidosis
Hyperparathyroidisms, uremic bone disease Endocrine factors (PTH, insulin resistance etc.)
Impairment of vitamin D3 activation Dialysis-associated factors (loss of nutrients, induction of protein catabolism)
Intercurrent disease (infections, etc.)

3.2.1. Aims of nutritional treatment during renal replacement

optimal nutritional status, to reduce or control accumulation of therapy
waste products, to prevent cardiovascular disease by treating The purpose of nutritional management is to prevent or treat
hyperlipidemia, bone disease by treating vitamin D deficiencies and malnutrition, to reduce accumulation of fluid, waste products,
hyperparathyreoidismus and to retard progression of renal potassium and phosphorus, and to prevent complications of urae-
dysfunction. mia (cardiovascular disease, bone disease etc.)
Note: In nutrition of patients with CRF there is a delicate balance Nutrient requirements are shown in Table 2. Special attention
between induction of toxic effects by giving excess and inducing must be paid to potassium, phosphorus, and fluids (but not protein
malnutrition by giving too little. or energy intake).
Nutrient requirements are summarized in Table 2. Special During dietary treatment patients must be maintained on an
attention must be given to protein, phosphorus, potassium, and adequate energy and protein intake. Vitamins (including active
bicarbonate and also to active vitamin D3 analogues. vitamin D3) must be supplied. Potassium and phosphate intake
During dietary treatment the most controversial question is should be reduced. If necessary, oral phosphate binders must be
related to protein intake. There is some agreement that there should given to the patients. Parenteral and enteral nutrition are usually
be (at least) a moderate protein restriction (0.7–1.0 g kg1 day1). If given in acutely ill patients (see below).
protein intake is reduced below 0.6 g kg1 day1 a supplement of
essential amino acids and/or keto-analogues of amino acids must be 3.2.2. Intradialytic parenteral nutrition (IDPN)
provided. The extent of electrolyte restriction is variable in the If alternative strategies for improving nutrient intake or nutri-
individual patient. Bicarbonate supplementation must not be tional state (Table 4) have failed, an IDPN should be considered:
forgotten in these patients. Parenteral and enteral nutrition is
usually only given in acutely ill patients (see below). Composition:
– A mixture of glucose (50–100 g), amino acids (50–70 g),
lipids (20–40 g) and water soluble vitamins should be given
3.2. Patients on chronic renal replacement therapy
instead of a single nutrient.
– The parenteral nutrition solution should be infused during
Patients on chronic renal replacement therapy (haemodialysis –
the whole dialysis period into the drip chamber of the
HD, chronic ambulatory peritoneal dialysis – CAPD) are frequently
venous blood line.
malnourished or at extreme risk of developing malnutrition. This
is because HD per se is a catabolic event with 10–13 g of amino
acids lost per day in the dialysate (see »Impact of renal replace- 3.3. Patients with acute renal failure (ARF) and HD/CAPD – patients
ment therapies«). In CAPD 8–9 g of protein are lost daily in the with acute catabolic disease
dialysate, although up to 125 g of glucose may be gained. The
problem in these patients is not that they eat too much but too 3.3.1. Aims of nutritional therapy
little (Table 3). In ARF the aim of nutritional treatment is not the alleviation of
Note: In HD patients there is a high prevalence of malnutrition uremic toxicity and retardation of progression of renal disease (as
(10–30%) and a tight correlation between nutritional state, morbidity in CRF), but – as in other acute disease – the stimulation of
and mortality. immunocompetence, of wound healing and other reparative
functions. In most clinical situations, requirements will exceed the
Table 2 minimal intake recommended for stable CRF patients or the rec-
Daily nutritional requirements in (stable) patients with CRF, on HD or CAPD. ommended daily allowances (RDA) for normal subjects.
Conservative therapy Haemodialysis Peritoneal
Table 4
dialysis
Strategies to treat malnutrition in haemodialysis patients
1 a
Energy (kcal kg ) >35 >35 >35
Protein (g kg1) 0.6–1.0 1.1–1.4 1.2–1.5 Treatment of malnutrition in haemodialysis patients
Phosphorus (mg) 600–1000 800–1000 800–1000 Treatment of potential causes – inadequate dialysis prescription
(mmol) 19–31 25–32 25–32 – metabolic acidosis
Potassium (mg) 1500–2000b 2000–2500 2000–2500 – hyperparathyroidisms
(mmol) 38–40 40–63 40–63 – intercurrent acute illness
Sodium (g) 1.8–2.5b 1.8–2.5 1.8–2.5 Dietetic counselling – modifications of the diet
(mmol) 77–106 77–106 77–106 – enteral supplements
Fluid (ml) Not restricted 1000 ml þ DO 1000 – tube feeding
ml þ UF þ DO – nocturnal
– nursing homes
DO ¼ daily (urine) output.
a Parenteral nutrition – intradialytic parenteral nutrition (IDPN)
Included energy (glucose) from the dialysate.
b Therapy with growth factors – anabolic steroids, rHGH, rIGF-1??
Individual requirements can differ considerably.
e56 W. Druml / e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 5 (2010) e54–e57
Table 5
Substrate requirements in patients with ARF
Energy
Carbohydrates
Lipids
Amino acids
- conservative therapy
- extracorporal therapy þ hypercatabolism
Vitamins
Water soluble vitamins
Fat soluble vitamins
Trace elements
Electrolytes
3.3.2. Metabolic aspects and nutritional requirements
In most patients ARF is a complication of another condition such as
sepsis, trauma or multiple-organ failure. Metabolic changes will
therefore be determined by the uremic state plus the underlying
disease process, by its complications such as severe infection and
organ dysfunction, or by the type and intensity of renal replacement
therapy. The acute loss of excretory renal function affects not only
water, electrolyte and acid base metabolism but has a profound effect
on protein and amino acid, carbohydrate and lipid metabolism.
Thus, the optimal intake of nutrients in ARF is influenced more
by the nature of the illness causing ARF, the extent of catabolism
and type and frequency of renal replacement therapy rather than
renal dysfunction. Patients with ARF present an extremely
heterogeneous group of subjects with widely differing nutrient
requirements and individual requirements can vary considerably
during the course of disease (Table 5).
3.3.3. Energy metabolism and energy requirements
Again, energy metabolism is determined more by the under-
lying disease and associated complications than by ARF and energy
requirements are usually not higher than 25–30 kcal kg1 day1
even in patients with sepsis or MODS.
Note: With the well defined side effects and complications of over-
feeding energy intake must not exceed actual oxygen consumption.
3.3.4. Amino acid and protein requirements
ARF is characterized by a profound activation of protein catab-
olism of 1.3–1.8 g protein kg1 day1 with stimulation not only of
hepatic gluconeogenesis and ureagenesis but also of protein
synthesis. Amino acid utilization is altered and several amino acids
designated as non-essential in healthy subjects, such as tyrosine,
arginine, cysteine and serine can become conditionally essential in
renal failure.
Protein/amino acid requirements in patients without renal
replacement therapy usually will range between 0.8 and
1.2 g kg1 day1, and with daily haemodialysis/CRRT increase to
between 1.2 and 1.5 kg1 day1.
3.3.5. Carbohydrate metabolism
Hyperglycaemia is usually present in patients with ARF. The
major cause is insulin resistance, plasma insulin concentrations
being elevated and insulin-stimulated glucose transport being
reduced by 50%. A second feature is accelerated hepatic gluco-
neogenesis mainly from conversion of amino acids, which can be
reduced but not suppressed by exogenous glucose infusion.
Moreover insulin metabolism becomes abnormal in ARF.
Glucose is still an important energy substrate but intake should
not exceed 4–6 g kg1 day1. Adverse effects of excessive glucose
25–30 (Max. 35) kcal kg1 day1
3–5 (Max. 7) g kg1 day1
0.8–1.2 (Max. 1.5) g kg1 day1
Essential þ non-essential amino acids!!
0.6–0.8 (Max. 1.0) g kg1 day1
0.8–1.2 (Max. 1.5) g kg1 day1
Multivitamin preparations (Cave: vitamin C < 200 mg/day)
1–2 amp. (2RDA) Daily
2–4 amp. Weekly
Multi-trace-element preparations (Cave: toxic effects)
2–4 amp Weekly
Requirements must be calculated individually
(Cave: hypokalaemia and/or hypophosphataemia after start of TPN or EN)
intake are well characterized. Hyperglycaemia must be prevented
and insulin is often necessary to maintain normoglycaemia. Insulin,
however, does not improve oxidative glucose disposal and if
possible, energy requirements should be met by a combination of
glucose and lipid in ARF patients.
3.3.6. Lipid metabolism
ARF is also associated with profound alterations in lipid
metabolism. The triglyceride (TG) content of lipoproteins is
increased and HDL cholesterol is decreased. The major cause of
these disturbances is impairment of lipolysis.
As a consequence, elimination of intravenously infused lipids is
delayed in ARF (half life is doubled) and clearance is reduced by
>50%. These changes in lipid metabolism should not however
prevent the use of lipids in nutritional therapy in patients with ARF.
Instead, the amount of lipids infused must be adjusted to meet the
patient’s capacity to utilize lipids and usually 1 g kg1 day1 will
not increase plasma TG substantially.
3.3.7. Micronutrients
Requirements for water soluble vitamins are increased in ARF
mainly because of losses associated with renal replacement therapy.
Despite the fact that fat soluble vitamins are not lost during renal
replacement therapy, plasma concentrations with the exception of
vitamin K are low in ARF. Similarly, loss of trace elements is negli-
gible during haemodialysis/CRRT but plasma concentrations of
several elements, such as selenium, zinc or iron are decreased.
Several micronutrients such as vitamin A, vitamin C, vitamin E, and
selenium are components of the oxygen radical scavenger system of
the body, depletion of which can contribute to impaired immuno-
competence and induce/promote tissue injury in critically ill patients.
3.3.8. Electrolytes
Electrolyte requirements can vary profoundly between ARF
patients but also during the course of disease and must be deter-
mined individually on a day-to-day basis.
Note: Many patients with ARF can present with hypokalemia/
hypophosphataemia, which can also develop during nutritional
therapy or during CRRT with low electrolyte solutions.
4. Solution used for nutritional support
4.1. Enteral nutrition
Enteral nutrition has become the main type of nutritional
support used in patients with renal failure despite the fact that little
is known of the impact of renal disease on gastrointestinal function.
Three types of enteral diets have been used:
 W. Druml / e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism 5 (2010) e54–e57
– (Semi) – elemental powder diets developed for CRF patients
(should no longer be used)
– Standard polymeric ready-to-use liquid diets developed for
non-uremic patients can also be used for subjects with ARF
(Cave: development of hyperkalaemia)
– Polymeric «nephro&raquo diets (ready-to-use liquid
preparations):
 with reduced protein and electrolyte (potassium, phosphorus)
content designed for patients with CRF (without renal
replacement therapy)
 with a moderate protein content, electrolyte reduced, with
variable additions, such as carnitine for patient on renal
replacement therapy (also suited for patients with ARF)
4.2. Parenteral nutrition
4.2.1. Amino acid solutions
Solutions of exclusively essential amino acids should no longer
be used in ARF. Use solutions including all essential and non-
essential amino acids in standard proportions or in a special
composition to counteract metabolic changes in renal failure
(«nephro»-solutions). Some of the latter contain tyrosine (which is
conditionally essential in renal failure) as a dipeptide (because
tyrosine has a low-water solubility).
4.2.2. Lipid emulsions
Emulsions containing LCT only or a mixture of LCT and MCT can
be used safely in renal failure patients. Because of the impairment
of lipolysis, TG infusion has to be adapted to the patient’s ability to
utilize lipids and usually has to be restricted to 1 g kg1 day1.
Monitor plasma clearance after infusion.
4.2.3. Parenteral nutrition administration
Solutions including amino acids, glucose, lipids plus vitamins,
trace elements and electrolytes contained in a single bag (All-in-
One Solutions) have become the standard. Insulin can be added to
the solution or be administered separately.
4.2.4. Complications and monitoring of nutritional support
Complications of nutritional support are similar in non-uremic
and renal failure subjects but because of impairment of gastro-
intestinal function, reduced tolerance to volume load and elec-
trolytes and alterations in utilization of various nutrients, the
frequency of metabolic complications is high. Thus, nutritional
therapy in patients with renal failure requires a tight schedule of
monitoring.
Note: By starting nutrition (both enteral and parenteral) at a low
infusion rate and by gradually increasing intake, utilization of
e57
nutrients can be ensured and development of metabolic complications
can be minimized.
5. Summary
The aims of nutritional support in patients with renal failure are
dependent on the degree and character of kidney impairment,
degree of malnutrition and associated disease.
Patients with chronic renal insufficiency but without concurrent
disease are at a high risk of malnutrition due to uraemia associated
factors, metabolic acidosis, impaired appetite and oral food intake
and the gastrointestinal side effect of uraemia. The main purpose of
nutritional management is to prevent malnutrition, to reduce or
control the accumulation of waste products, and to prevent bone
and cardiovascular disease.
Chronic renal replacement therapy leads to the loss of some
nutritional substrates, such as amino acids and water soluble
vitamins, but also to activation of protein catabolism. An adequate
supply of energy, protein and vitamins amount must therefore be
given to these patients.
In patients with renal insufficiency complicated by an acute
catabolic disease and/or in patients with acute renal failure the
stimulation of immunocompetence, wound healing and other
reparative functions is the principal goal of nutritional therapy. In
most clinical situations, requirements exceed the minimal intake
recommended for stable CRF patients or normal subjects. Intensive
nutritional support must be provided to these patients and
potential accumulation of waste and toxic products must be pre-
vented by more intensive renal replacement therapy.
Renal failure is a pan-metabolic and pan-endocrine abnormality
affecting more or less every metabolic pathway of the body and in
no other patient group there is such a narrow range between
induction of toxic effects and the development of malnutrition.
Conflict of interest
There is no conflict of interest.
Further reading
1. Druml W. Nutritional support in acute renal failure. In: Mitch WE, Klahr S, editors.
Nutrition and the kidney. Philadelphia: Lippincott Williams & Wilkins; 2002. p. 191.
2. Druml W. Nutritional support in patients with acute renal failure. In:
Molitoris BA, Finn WF, editors. Acute renal failure (a companion to Brenner &
Rectoŕs THE KIDNEY). Philadelphia: WB Saunders Company; 2001. p. 465.
3. Druml W. Metabolic effects of continuous renal replacement therapies. Kidney
Int 1999;56(Suppl.):S-56.
4. Druml W, Mitch WE. Enteral nutrition in renal disease. In: Rolandelli RH, editor.
Enteral and tube feeding. 4th ed. Philadelphia: WB Saunders; 2003.
5. Kopple JD. Renal disorders and nutrition. In: Shils ME, Olson JA, Balado D,
editors. Modern nutrition in health and disease. Baltimore: William & Wilkins;
1999. p. 1439.