Title: Diabetic Nephropathy and Diet

Key words: insulin dependent diabetes mellitus (IDDM), renal failure, dietary regimes, micronutrients, blood urea nitrogen, nutritionist

Date: July 2000

Category: 13. Specific Conditions

Type: Article

Author: Dr van rhijn

 

 

Diabetic Nephropathy and Diet

 

 

 

Introduction

The nutritional and therapeutic aims for insulin dependent diabetes mellitus (IDDM) are

These complications are proportional to the degree and duration of hyperglycaemia5. Patient education6, empowerment, nutritional self-management7,8, individualised & prudent glycaemic goals9,10,11 with self-monitoring and ongoing professional support from a multi-disciplinary team are fundamental12, as nephropathy and uremia may prove to be a nutritional challenge at end stage renal failure.

General Dietary Advice in Diabetes

The diet should provide appropriate energy, protein and a maximum of nutrients to meet established standards for normal growth & development and prevent further deterioration in nephropathy. Current management guidelines provide variable, individually13,14 tailor made dietary regimes to reduce daily glucose fluctuations, post-prandial hyperglycaemia and total plasma low-density lipoprotein (LDL) cholesterol and phospholipids15.

General advice is to eat more frequent, multi-composition16 smaller meals, increase physical activity and weight loss to lower plasma glucose, fasting & postprandial insulin concentrations, triglyceride and very low-density lipoproteins levels, to improve insulin sensitivity.

Average daily energy needs is based on estimating basal metabolic rate (BMR), relating to gender and body weight, calculated from age related tables17, expressed in MJ/day or kJ/hour, and multiplied by the physical activity level (PAL). Dietary carbohydrate content provides 40 – 50% of total calories, for higher amounts fail to achieve glycaemic control and promote hypertriglyceridaemia, dyslipidaemia and insulin resistance. Foods with a smaller glycaemic index18 (cereals, pulses, vegetables, fruit) are preferred, in order to achieve good glycaemic control19. Their pectins and hemicellulose (NPS) fractions restrict hydrolysis of their starches and slow glucose absorption20, to improve glycaemic control21, plasma glucose levels22, glycosylated haemoglobin, LDL cholesterol and triacylglycerol levels23.

Recommended intake for protein is set at 10 – 20% of total energy requirements, sufficient enough to ensure normal growth, development and maintenance of body functions, This intake should be increased in pregnancy, childhood or for high levels of physical activity.

 

Fats should contribute 30 - 40% to the total calorie intake, 10% from saturated fat 24, with a ratio of polyunsaturated to monounsaturated fatty acids (PUFA:MUFA) of 2:3. Saturated dietary fat bypasses the body’s insulin control mechanisms and is deposited in adipose tissue by non-insulin sensitive enzyme (lipoprotein lipase), leading to dyslipidaemia. PUFA's & MUFA's are beneficial in reducing plasma triglyceride levels25, increasing HDL cholesterol and improving glycaemic control 26, but may aggravate hyperglycaemia and increase LDL cholesterol if taken in excess (4-6 g/day).

MUFA's enhance insulin sensitivity, glycaemic control 27, reduce LDL susceptibility to lipid peroxidation 28, LDL uptake by macrophages and have beneficial effects on platelet and factor VII activity. Diabetics require higher PUFA amounts as a D -6-desaturase enzyme defect, limits linoleic acid (LA, C18:2 w -6) 29 conversion to gamma linolenic acid (GLA, C18:3 w -6) 30,31 and subsequent dihomogammalinolenic acid (DGLA, C20:3 w -6) and arachidonic acid (AA, C20:4 w -6).

These reduced precursors of prostaglandins and constituents of phospholipids membranes, lead to microvascular abnormalities, reduced blood flow, insulin secretion & sensitivity and hyperglycaemia. AA promotes insulin secretion, DGLA potentiates insulin effects on lipogenesis in adipocytes and GLA reduces calcium excretion, triglycerides and cholesterol. Supplementation directly with GLA (480 mg/day) avoids this limiting step, and improves the microcirculation32 patients with Type I diabetes.

Several trace elements are essential for normal glucose homeostasis. Chromium forms an organic complex potentiating the action of insulin33, by optimising the membrane insulin receptors34. Deficiency may lead to impaired glucose tolerance35, insulin resistance36, hyperglycaemia37, hypercholesterolaemia38,39 and hypertriglycerides40, all corrected by Cr supplementation (500-1000 m gr/day)41.

Hypomagnesaemia (partly due to renal tubular defect42) has been associated with insulin insensitivity43, poor glycaemic control44, retinopathy, hypertension, insufficient protein synthesis45, unhealthy LDL/HDL ratio46 and abnormal platelet function, which may be improved by oral supplementation47,48.

Manganese and vanadium49 improve glucose control. Copper50,51 & zinc52 are involved with improving glucose tolerance. In contrast, zinc deficiency increases the prevalence of diabetes53,54. Supplementation is cheap and safe and may aid glucose homeostasis and ameliorate long-term complications.

Nutritional Problems in Renal Failure

Patients with renal failure experience associated nutritional problems such as appetite & weight loss, lipid and carbohydrate intolerance, catabolism of protein (urea) and muscle (creatinine), osteodystrophy (Vitamin D/calcium/phosphorus axis disturbance), erythropoietin production failure, iron deficiency and impaired immunity. The diminished glomerular filtration leads to retention of sodium (oedema and osmotic diuresis), potassium, phosphate, sulphate and organic acids (metabolic acidosis), aluminium and uremia. Uraemia is a metabolic symptom complex comprising these insults to water and electrolyte balance along with azotemia or nitrogen retention (urea & creatinine). Intense antihypertensive treatment improves survival in diabetic nephropathy55, and self-monitoring is a good prognostic indicator of its progression56.

Dietary Advice in Chronic Renal Failure

It is crucial to provide sufficient protein to prevent further breakdown but without risking an increase urea level. A general guide is 0.5-0.8 g/kg/day of protein57, with further restrictions if the creatinine clearance falls below 40 ml/min with high blood urea nitrogen (BUN). Maintain patients in positive nitrogen balance on 35 - 40 g protein/day by supplementing with a high proportion of nitrogen-free analogues of essential amino acids (branched-chained), but considering proteinurea.

Adequate kilocalories (2000-2500 kcal/day) in the form of carbohydrates (300-400 g) and limited fats (75-90g) are essential to supply energy and spare protein for tissue-protein synthesis. It is essential to monitor fluid and electrolyte balances and correct imbalances and acidosis carefully if required.

Secondary hyperparathyroidism and Vit D deficiency may contribute to osteodystrophy and calcium carbonate supplements may buffer metabolic acidosis, but urinary calcium oxalate calculi may result. Multivitamin supplementation is useful in patients with restricted protein intake. Glucose levels and triglycerides should be monitored and strictly controlled by limiting sweets and fats to control triglyceride and HDL levels. Proper glycemic control58,59 remains essential to reduce microalbuminuria and improve lipid levels. Instigate a renal diet on detecting proteinuria.

 

Dietary Advice in End Stage Renal Failure

End stage renal failure is associated with stress hormone-induced negative nitrogen balance, an impaired ability to make non-essential amino acids, and severe catabolism, requiring an increase in calorie intake. Dietary protein must be restricted if the BUN is elevated (urea < 5mmol/L/day) in the presence of oliguria. Sufficient carbohydrates (kilocalories) should be provided to reduce protein catabolism and prevent starvation ketosis.

Fluids, sodium60 and potassium should be restricted according to the degree of oliguria but dialysis may be required with progressive deterioration (urea > 8mmol/L/day). Maintaining an individually nutritionally tailored balance of the above mentioned parameters remains the same, but now planned with more liberal nutrient allowances, depending on dialysis type. Adequate dialysis improves lipid & carbohydrate intolerance and the generous daily allowance of high biologic value protein (1g/kg lbw from eggs, meat, fish but not milk [high electrolytes]) will adequately replace amino acid loss during dialysis.

Ample amounts of simple carbohydrates provide adequate kilocalories (40 kcal/kg lbw). Total fluid intake limit should be limited to 500 ml/day plus an amount equal to urinary output. Monitor electrolytes (Na, K, Mg, Ca [daily] & Cu, Fe, Zn, Se [monthly]) and restrict dietary intake accordingly, especially aluminium (retention from dialysis fluids). Provide water-soluble vitamins but be careful of accumulating fat-soluble vitamins.

Conclusion

Diet is the cornerstone of diabetes management and the nutritionist has become an indispensable member of the renal care team to supervise therapeutic nutrition. This will involve a variety of nutrient adjustments according to individual need, to delay progression of renal failure in diabetes61, 62.

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