Nutrition in renal disease

Attaa A Ali

Acute renal failure Chronic renal failure

◦ Stable◦ With critical illness

Patients on renal replacement therapy (RRT)◦ Intermittent haemodialysis (IHD)◦ Continuous renal replacement therapy (CRRT)

Groups of renal failure

Malnutrition is a risk factor for death Patient are hypercatabolic due to

◦ The primary disease ◦ ARF

Loose nutrients in dialysis Renal failure affects GIT

◦ Motility and absorption are impaired◦ Increased risk for GIT bleeding

Nutritional effect on regeneration of renal function

Why nutrition in renal failure patients

A prospective cohort study in 309 patients (ARF)◦ Severe malnutrition (By SGA) was present in 42%◦ LOS and Mortality was increased◦ Malnutrition appeared to be an independent

factor of in-hospital mortality French series of 7000 HD patients

◦ Albumin < 3.5 mg/dl, prealbumin < 0.3 mg/dl, nPNA < 1 g/kg/d in 20%, 36%, 35% resp.

DOPPS II (HD patients)◦ 20.5% of patients had albumin < 3.5 mg/dl

Malnutrition in renal disease

Fiaccadori E et al, J Am Soc Nephrol (1999) 10, 581-593Aparico M et al, Nephrol Dial Transplant (1999) 14, 1679-1686Port FK et al, Blood Purif (2000) 22, 175-180

Water content Electrolytes imbalance Alteration of protein metabolism, amino acids Alteration of carbohydrate metabolism Alteration of lipid metabolism Proinflammatory action Profound effect on antioxidant system Underlying disease process Comorbidity, different organ dysfunction Method and intensity of RRT

ARF effect on nutrition

Cano et al, Clinical Nutrition (2006) 25, 295-310

Insulin resistance causes release of amino acids from muscles increasing gluconeogensis and ureagensis

Tyrosine and other amino acids becomes essential

Decrease renal synthesis of amino acids Acidosis activates proteases Release of cytokines (TNF-α and others) Loss in RRT (0.2g/L of filtrate)

Protein metabolism

Increase available amino acids causes increase gluconeogensis uncontrolled by hyperglycaemia feedback

Insulin resistance Inhibited glycogen synthesis in muscles All will cause persistent hyperglycaemia Heat loss in RRT increases caloric

requirements

Carbohydrate metabolism

Impairment of lipolysis with delayed fat clearance following enteral and parentral nutrition is a characteristic of renal failure that will lead to hypertriglyceridaemia.

This will manifest by elevated LDL and VLDL-cholesterol with decreased levels of HDL-cholesterol.

Lipid metabolism

Increased proteolysis◦ Loss of substrates 0.2g/L filtrate ◦ 10-15g amino acids per day◦ Increase catabolic mediators

Increase lipid oxidation with decreased carbohydrate oxidation ◦ Glucose losses 25g / session

Water and electrolyte disturbances◦ Hypophosphataemia, hypomagnesaemia, hyponatraemia◦ Hyperlactacidaemia, metabolic alkalosis

Loss of water soluble substrates◦ Vitamin B, C◦ L-carnitine

Renal Replacement Therapy

CAPD usually have better residual renal function Peritoneal losses of various nutrients are significant

◦ Protein 10 g/d ◦ Amino acids 3-4 g/d 30% essential amino acids◦ Peritonitis increases losses to15 g/d reaching100 g/d◦ Protein bound micronutrients are also lost

Absorption of glucose from the dialysate is enhanced ◦ 100-200 g/d that increases with peritonitis

Induction or aggravation of diabetes, hypertriglyceridemia with increased body weight and decreased lean body weight

Patients on CAPD

Prevent PEM Preserve lean body mass Maintenance of nutritional status Avoidance of further metabolic derangement Enhancement of wound healing Support of immune function Reduction of mortality Attenuation of inflammatory status Improvement of the oxygen radical

scavenging system and endothelial system

Nutritional goals (ARF)

Cano et al, Clinical Nutrition (2009) 28, 1-14

Prevent and treat PEM leading to cachexia Ensuring the provision of optimal levels of

energy, essential nutrients and trace elements

Attenuation of CKD progression through protein or phosphate restriction

Nutritional goals (CKD, RRT)

Cano et al, Clinical Nutrition (2006) 25, 295-310

No specific indications GIT is the primary route Data on influence of PN on acute renal

failure are inconclusive and there is a possible that nutritional support disregarding the route and associated kidney injury could explain the reduction of mortality and morbidity

Balance on the toxic effects of nutrients (excess nitrogen and pro-oxidants) and the need to prevent PEM is crucial

When to provide nutritional support

Cano et al, Clinical Nutrition (2009) 28, 1-19

GIT functioning◦ Increase dietary intake by augmenting energy

and protein intake either by kitchen food or ONS◦ If targets not reached start tube feeding (TF)◦ If goals not reached start PN

GIT not functioning ◦ Peripheral PN: in cases of short-term therapy with

or without fluid restriction ◦ Central PN: in cases of long-term therapy with

fluid restriction◦ When GIT function is recovered tapper PN to EN

How to provide nutritional support

Nutritional requirements in patients with ARF

Energy (non-protein calories) 20-30 kcal/kg/d OR other estimating formula

Carbohydrates 3-5 (max. 7) g/kg/d

Fat 0.8 -1.2 (max 1.5) g/kg/d

Protein (essential and non-essential amino acids)

Conservative therapy mild catabolism 0.6-0.8 (max 1) g/kg/d

RRT, moderate catabolism 1-1.5 g/kg/d

CRRT, Severe hypercatabolism Up to max. 1.7 g/kg/d

Substrate requirements (ARF)

Cano et al, Clinical Nutrition (2009) 28, 1-14

Micronutrients should be supplemented as recommended for ICU patients◦ Vitamin A toxicity should be monitored if supplied◦ Limit Vitamin C to 30-50 mg/day◦ Selenium and thiamine should be supplied at double

recommended doses in patients on prolonged CCRT Electrolytes should be monitored and intake

tailored according Slandered enteral formula are adequate except if

major electrolyte derangement is present NO disease specific IV formula has shown to

improve patients outcome

Substrate requirements (ARF)

Cano et al, Clinical Nutrition (2009) 28, 1-14

Nutritional requirements in patients with Stable stage III-V CKD

Energy (non-protein calories) >30-35 kcal/kg/day

Protein

GFR = 25-70 ml/min 0.55-0.6 g/kg/d (2/3 HBV)

GFR < 25 ml/min (ESPEN) 0.55-0.6 g/kg/d (2/3 HBV)OR 0.28+EAA OR EAA+KA

GFR < 25 ml/min (NKF) 0.6-0.7 g/kg/d (intolerance or inadequate energy intake)

Proteinuria IBW kg × 0.6-0.8 × proteinuria

Electrolytes

Phosphate 600-1000 mg/d

Potassium 1500-2000 mg/d

Sodium 1.8-2.5 g/d

Fluid Unlimited

Substrate requirements (CKD)

Adapted from: Cano et al, Clinical Nutrition (2009) 28, 1-14

Overweight and undernorished patients may need adjustments of energy supply

Thiamine needed to be supplied at 0.5-1.5 mg/d especially with infection, surgery and glucose rich infusions

Vitamin E should be prescribed to patients with high cardiovascular risk at a daily dose of 800 IU alpha-tocopherol

Substrate requirements (CKD)

Cano et al, Clinical Nutrition (2006) 25, 295-310

Nutritional requirements in patients with Stable stage III-V CKD

Energy (non-protein calories)

ESPEN 35 kcal/kg/day

NKF <60 y 35 kcal/kg/day> 60y 30 kcal/kg/day

EBPG-ERA 30-40 kcal/kg/dayAdjust to age, gender and acitivity

Protein

Haemodialysis (ESPEN) 1.2-1.4 g/kg/d (>50% HBV)

Haemodialysis (NKF) 1.2 g/kg/d (>50% HBV)

Haemodialysis (EBPG-ERA) ≥1.1 g/kg/d

CAPD (ESPEN) 1.2-1.5 g/kg/d (>50% HBV)

CAPD (NKF) 1.2-1.3 g/kg/d (>50% HBV)

Substrate requirements (RRT)

Adapted from: Cano et al, Clinical Nutrition (2009) 28, 1-14

Nutritional requirements in patients on

Minerals

Phosphate 800-1000 mg/d9-11 mmol/d

Potassium 2000-2500 mg/d25-30 mmol/d

Sodium 1.8 – 2.5 g/d75-110 mmol/dIndividual requirements may differ in acute conditions

Fluids 1000+urine volume /d40 + urine volume /hr

Substrate requirements (RRT)

Adapted from: Cano et al, Clinical Nutrition (2006) 25, 295-310

Phosphorus intake should be limited to 10-15 mg/kg/day ◦ Nutrients contain phosphorus protein ratio of 10-

13 mg: 1g so phosphate binders are usually needed (e.g. Calcium carbonate)

Thiamine needed to be supplied at 0.5-1.5 mg/d especially with infection, surgery and glucose rich infusions

Vitamin E should be prescribed to patients with high cardiovascular risk at a daily dose of 800 IU alpha-tocopherol

Substrate requirements (RRT)

Cano et al, Clinical Nutrition (2006) 25, 295-310

Indication◦ If nutritional counseling and oral nutritional

supplements (ONS) fail to prevent or treat PEM Content

◦ 800-1200 kcal and 30-60 g protein three times per week

Route◦ Venous site of dialysis catheter

Evidence◦ No controlled randomized studies are available◦ Retrospective studies suggest improved survival and

decreased hospitalization rate

Intradialytic Parentral nutrition (IDPN)

Indication◦ If nutritional counseling and oral nutritional

supplements (ONS) fail to maintain nutritional goals in patients on CAPD

Mechanism◦ Dialysate containing a 1.1% amino acids

Adverse effects◦ Hypokalaemia ◦ Hypophosphataemia◦ Mild acidosis

Intraperitoneal parentral nutrition (IPPN)

Evidence◦ 11 studies including 4 randomized studies◦ Improvement of nitrogen balance and nutritional

parameters in 4 cohort studies◦ In one randomized study benefit was only

observed in hypoalbumenic patients ◦ Another should improvement of nutritional

biochemical markers which was more prominent in women (no effect on survival)

Intraperitoneal parentral nutrition (IPPN)