Creatinine 5700 700, 1200 41200 (mmol/l) small muscle normal levels in dialysis depends on size of (55, 125) mass (check patients patient. May be BMI) underdialysed residual function
Potassium 53.5 3.5, 5.5 (PD) 6.0 (PD), 6.5 (HD) (mmol/l) residual 3.5, 6.00 (HD) check diet, drugs, blood (3.5, 5.5) function transfusion diarrhoea underdialysed vomiting hyperglycaemic malnourished acidotic re-feeding
Phosphate 50.8 0.8, 1.8 1.8, 2.0 42.0 (mmol/l) too many check diet and (0.8, 1.4) binders binders malnourished check Ca and PTH re-feeding levels
Calcium 52.15 2.15, 2.6 2.6, 2.8 42.8 (mmol/l) check adjusted check CaCO3 adjusted for albumin tablets (2.15, 2.6) bone disease active vitamin D high PTH
Albumin (g/l) 530 33, 45 45 445 (35, 55) infection NB: 30, 34 may underdialysed (CRP) indicate constipated nephritic malnutrition acidotic malnourished NB: Use pre-dialysis HD bloods. This information is not applicable to other groups of renal patients.
DIABETES AND RENAL REPLACEMENT THERAPY 237
Energy Gains and Losses from Glucose Fluxes During Dialysis Energy requirements for CAPD patients are partially met from absorbed dialysate glucose.
Requirements from dietary intake are therefore lower at 30 kcal/kg body weight (25 kcal/kg if obese) and 25, 30 kcal/kg body weight if older than 65 years (21).
Patients absorb approximately 70% of dialysate glucose, amounting to 300, 600 kcal or 2.5, 17 g of glucose per hour during dwell times (22) (See table 15.4).
Bag volumes range from 1 to 3 litres, with higher dextrose concentrations and larger volumes used to maximize solute clearance and ultrafiltration.
The exact amount of glucose absorbed will depend on the dialysate glucose concentration and volume, the number of exchanges, the dwell time between each exchange and the permeability of the patient’s peritoneal membrane.
Membrane permeability is likely to be increased in people with diabetes.
Increasing glucose loads can predispose to hyperglycaemia, hyperinsulinaemia, hyper- lipidaemia, and obesity.
On the basis of a 70% absorption rate of glucose from dialysate fluid, between 2.5, 17 g of glucose can be absorbed per hour during dwell times.
This glucose load can predispose to hyperglycaemia, leading in turn to hyper- insulinaemia, hyperlipidaemia and obesity.
During HD blood values frequently fall below 4.0 mmol/l when patients are dialysed against a glucose-free dialysate (23).
Such patients should be advised to either eat a snack before or during dialysis.
The choice of a slowly absorbed, low-glycaemia snack is ideal for this purpose.
Due to the metabolic problems associated with glucose as the main osmotic agent for inducing ultrafiltration in PD, alternative osmotic agents are now becoming available.
High molecular weight glucose polymer solutions such as Icodextrin appear to be safe and effective.
Icodextrin has the advantage of a reduced glucose and calorific load but requires dwell times of between 8, 12 h and is therefore often left in situ overnight.
No studies of use in diabetic patients have so far been published (24).
Table 15.4 Approximate energy provided by glucose-containing dialysate
Dialysate (1 l) Grams of absorbed glucose Energy provided (kcal)
1.36% dextrose 10 40 2.27% dextrose 16 60 3.86% dextrose 27 100
238 NUTRITIONAL MANAGEMENT OF DIABETES MELLITUS
NUTRITIONAL REQUIREMENTS IN DIALYSIS PATIENTS
The general principles surrounding the nutritional requirements of patients with ESRF receiving dialysis are generally applicable to both diabetic and non- diabetic subjects and are briefly outlined below.
DIETARY PROTEIN Protein requirements are increased in dialysis patients due to protein losses during dialysis (20) (see Table 15.5) and can be as high as 20 g albumin daily in CAPD with peritonitis.
These losses are further increased in the diabetic patient (25) due to greater peritoneal membrane permeability.
For non-diabetic stable dialysis patients daily protein intake recommendations based on NKF- KDOQI data (21) and supported by nitrogen balance studies are 1.2 g/kg/day for HD patients and 1.2, 1.3 g/kg/day for CAPD patients.
Adequate total energy intake is required to maximise the effectiveness of dietary protein utilisation (20).
MINERAL AND VITAMINS Potassium Hyperkalaemia in dialysis patients is a potential cause of sudden death. Recommendations to keep serum potassium levels between 3.5, 6.5 mmol/l pre- dialysis for HD patients and 3.5, 5.5 mmol/l for CAPD patients were published in 2002 (26). Potassium restrictions are usually unnecessary in CAPD patients due to the continuous nature of this form of dialysis. By way of contrast, HD patients accumulate potassium between dialysis sessions.
Phosphate Hyperphosphataemia is very prevalent among patients with ESRD and is a cause of hyperparathyroidism, metastatic calcification (when the serum calcium, phosphate product exceeds 5.5 mmol/l) (27) and has been associated with excess cardiovascular mortality in HD patients (28). The recommended
Table 15.5 Amino acid and protein losses during dialysis
Dialysis Modality Amino acids (g) Proteins/peptides (g)
CAPD/day 2, 3.5 5, 15 HD/session 6, 12 2, 3
DIABETES AND RENAL REPLACEMENT THERAPY 239
dietary intake of phosphorus for HD and PD dialysis patients is approximately 17 mg/kg/day.
The removal of phosphate during dialysis is limited due to the high distribution volume for phosphate and the rapid rebound of serum phosphate following dialysis.
Hyperphosphataemia is common and dietary restriction of dairy products, bony fish and offal meats combined with the use of phosphate buffers remains the best means of minimising hyper- phosphataemia.
Medical and dietary treatment of hyperphosphataemia is aimed at keeping the parathyroid hormone level within two to three times the upper limit of the normal range and the alkaline phosphatase and calcium concentrations within the normal range.
Sodium On starting dialysis sodium intake should be limited to below 100 mmol, equivalent to 6 g salt/day.
When dialysis patients become anuric their fluid and sodium intake needs to be further restricted, to 1 litre fluid/day and 80, 100 mmol sodium/day.
In patients able to maintain a urinary output above l l/day, fluid restriction of 1.5, 2 l/day and more flexible sodium intake may be appropriate.
Residual urinary excretion is maintained for longer in PD than HD patients and hence fluid and sodium intake can initially be more liberal in PD patients.
V|tamins The role of vitamin supplementation in dialysis patients is controversial.
Vitamin status is compromised in dialysis patients due to poor nutritional intake and the cooking methods required for a low-potassium and low- phosphate diet.
Fat-soluble vitamins other than vitamin D are not routinely prescribed due to the risk of vitamin A toxicity.
Vitamin D is prescribed for bone protection and the prevention of hyperparathyroidism.
Among the water- soluble vitamins 10 mg/day of pyridoxine and 60 mg/day of ascorbic acid are recommended as low concentrations can occur in dialysis patients.
In addition folic acid may also be low and there may be a need for supplementation.
L-carnitine is an essential co-factor in fatty acid and energy metabolism and recent work suggests that it might be effective in reducing the erythropoetin requirements for controlling anaemia.
The US Food and Drug Administration department have recently approved its use in the prevention and treatment of carnitine deficiency in HD patients.
Currently, however, there is insufficient evidence to support its routine use in such patients (29).
240 NUTRITIONAL MANAGEMENT OF DIABETES MELLITUS
NUTRITIONAL MANAGEMENT IN DIALYSIS PATIENTS
There are general principles regarding the nutritional management of patients on dialysis with ESRF. These are generally applicable to both diabetic and non-diabetic subjects (30,31) and are briefly covered below.
PREVENTION OF HYPERKALAEMIA
Hyperkalaemia in the HD patient may be due to dietary indiscretions, either as a result of unfamiliar foods of high potassium content or increased portion sizes of known potassium-containing foods.
Patients on haemodialysis are usually advised to limit their potassium intake to less than 1 mmol/kg/day.
Patients therefore need to avoid high-potassium foods, limit the intake of fruit and vegetables and cook using techniques to lower potassium levels.
Patients with residual urinary function can still excrete some urinary potassium and therefore may safely consume more fruit and vegetables provided there is close monitoring.
Hyperkalaemia is less common in CAPD due to continuous potassium removal on dialysis.
In diabetic patients with poor glycaemic control, undergoing dialysis, hyperkalaemia can result from insulin insufficiency.
Improving glycaemic control can reduce serum potassium levels.
Insulin requirements can drop following the commencement of haemodialysis.
In addition to poor glycaemic control, hyperkalaemia is also associated with a number of other non-dietary causes of hyperkalaemia.