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REVIEW ARTICLE


Diabetic Nephropathy:Nutritional Challenges

Amit Gupta, Anita Saxena

Department of Nephrology SGPGIMS, Lucknow



D

D

iabetes is a major cause of chronic kidney disease and India among all the SAARC countries has become the diabetes capital of the world. Twenty to forty percent of type 2 diabetes patients having microalbuminuria progress to overt nephropathy i.e., diabetic nephropathy (DN), and

-20 % progress to end stage renal disease (ESRD) making it the leading cause of ESRD in the past two decades. Diabetes is a heterogenous disease which is mainly of two type, Type I diabetes occuring due to autoimmune destruction of insulin secreting cells called 13 cell and, therefore, manifesting at a young age which requires insulin therapy. Type 2 diabetes occurs at late age due to insulin resistance, usually after the age of 40 years and has genetic component as well, but nevertheless, it can also manifest at a younger age in obese individuals. Long term complications of both types of diabetes are same namely macrovacular disease (coronary heart disease), cerebrovascular disease, peripheral arterial disease and microvascular disease retinopathy and nephropathy. Prevalence of diabetes is increasing most rapidly in both developed countries and in developing countries. DN is characterized by albuminuria, which is usually accompanied by hypertension, progressive rise in proteinuria (albuminuria >0.5 g/24 h), and decline in renal function. DN carries a 20- to 40-fold increased risk for cardiovascular (CV) mortality. To delay progression of DN to ESRD following measures are recommended a) good control of blood glucose, b) low-protein diet, c) control of hypertension, d) restriction of dietary salt, phosphorus and potassium in advanced cases and e) control of hyperfiltration, usually through angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blocking (ARB) agents.

Pathophysiology of Diabetic Nephropathy: The exact cause of diabetic nephropathy is unknown, however, it is postulated that hyperglycemia (causing hyperfiltration and renal injury), advanced glycosylation products, and activation of cytokines play key role in causing renal injury. Hyperglycemia increases expression of transforming growth factor-beta (TGF-beta) in the glomeruli and of matrix


proteins specifically stimulated by this cytokine. TGF­ beta and vascular endothelial growth factor (VEGF) may contribute to the cellular hypertrophy, enhanced collagen synthesis, and vascular changes observed in persons with diabetic nephropathy. Hyperglycemia also may activate protein kinase C, which may contribute to renal disease and other vascular complications of diabetes. Familial or perhaps even genetic factors also play a role.

The severity of diabetic glomerulopathy is estimated by the thickness of the peripheral basement membrane and mesangium and matrix expressed as a fraction of appropriate spaces (eg, volume fraction of mesangium/glomerulus, matrix/mesangium, or matrix/glomerulus). The glomeruli and kidneys are typically normal or increased in size initially, thus distinguishing diabetic nephropathy from most other forms of chronic renal insufficiency, wherein renal size is reduced (except renal amyloidosis and polycystic kidney disease).

In addition to the renal hemodynamic alterations, patients with overt diabetic nephropathy generally develop systemic hypertension. Hypertension is an adverse factor in all progressive renal diseases and seems especially so in diabetic nephropathy.The deleterious effects of hypertension are likely directed at the vasculature and microvasculature.

Hence, nutritional management is fundamental for the prevention of DN. The goals of medical nutritional therapy (figure 9.2) which will be dealt in this article are:

1. Maintenance of near normal blood glucose levels (glycemic control) by controlling food intake and exercise

  1. Achieving optimal serum lipids and blood pressure to reduce the risk of cardiovascular disease (CVD)

  2. Management of body weight.

  3. Maintaining biochemical parameters and fluid status

  4. Prevention of long term complications

  5. Prevention of malnutrition and strategies to control diabetic gastroparesis.

Assessment Of Nutritional Status: According to KDOQI guidelines, there is no single valid tool for assessment of nutritional status. Use of combination of tools for proper assessment of nutritional status like serum albumin and prealbumin (though these are negative phase reactant proteins), subjective global assessment (SGA), anthropometry (edema free body weight, body mass index (BMI), skinfolds, mid upper arm circumference (MUAC) as and when required), dietary diaries, and interviews, serum cholesterol and nPNA should be used. Nutritional assessment using biochemical parameters should be done monthly. SGA should be done every six months. Dietary interviews should be conducted on every visit by a dedicated renal dietician.

An important marker of good diabetes therapy is that blood glucose is maintained below the renal threshold (250 mg/dL), so that it is not passed into the urine. Insulin resistance and glucose intolerance are characteristic features in patients with kidney disease. Target HbAl C should be ::;;7,0

% . However in CKD, the values may be falsely elevated or decreased.Amount and type of carbohydrate (CHO) in food influences blood glucose levels. Energy requirements vary according to age, sex and activity levels. Energy requirements should be calculated depending upon whether the goal is weight loss, maintenance or weight gain. Fiber intake can reduce blood sugars in diabetic patients. ADA recommends fiber intake of 14g/1000 kcal which can be increased up to 35g. Soluble & Insoluble fiber decrease gastrointestinal transit time which improves insulin sensitivity by slowing carbohydrate absorption. Animal studies have shown lower urinary albumin excretion when a soy protein diet or a low casein diet is fed, suggesting a delay in the progression of diabetic nephropathy. Several small studies in humans with diabetic nephropathy have shown that a prescribed protein restricted diet of 0.6 g/ kg day (subjects actually only achieved a restriction of 0.8 g/kg/day) retards the rate of fall of GFR modestly. Protein requirements for dialysis dependent diabetic patients is increased to 1.2g/kg/d due to dialysis induced hypercatabolism and protein losses. On the other hand, dietary phosphorus restriction (800-lOOOmg/day) is often necessary to control hyperphosphatemia in dialysis patients. Calcium intake should be restricted to <2000 mg/d including supplementation. Ideally it should not exceed 1200mg if patient is being treated for vitamin D deficiency. Energy intake should be 50-60 percent of total dietary energy intake. It should not exceed 30 kcal/kg/d.

Dietary sodium intake of less than 2.4 g/ d (one teaspoon salt) is recommended in adults with CKD and hypertension. Studies have shown fall in blood pressure by 2-3 mmHG when sodium intake is lowered from 4.0 g to 2.0 g per day. High BP or a predisposition to high BP is an important factor that contributes towards onset and progression of nephropathy in diabetes. It is, therefore, important to achieve good control of BP. High BP may also lead to other micro-

and macrovascular complications. target blood pressure should be < 130/80 mm Hg. Maintaining systolic blood pressure less than 130 mm Hg is more effective in slowing progression of DKD.

In diabetic patients LDL cholesterol should be < 100 mg/ dl and those with cardiovascular disease should maintain

<70 mg/dl.

Obesity And Diabetic Nephropathy: Obesity is one of the factors causing DM and metabolic syndrome. These disorders increase the severity of chronic renal disease. Good glycemic control, regular exercise, weight reduction diet and other changes in life style are recommended for overweight and obese patients. Glycosuria causes loss of calories in the urine due to poor glycemic control which often results in weight loss, but once glycemic control improves, retention of glucose calories formerly lost during urination can account for weight gain. Study on patients with type 1 diabetes has shown that, 70% of this weight gain is attributed to the transition of changing poorly controlled patients to a more­ intensified treatment regimen. Minimizing insulin dose is one strategy to limit weight gain. Restrict energy intake to 20-25 kcal/kg/d.

Studies have shown that elevated levels of homocysteine are independently associated with the prevalence of peripheral neuropathy. either by direct cytotoxic effects on nerve function, or by small vessel occlusions caused by endothelial damage. To control homocysteine levels folic acid, B12 ,and pyridoxal 5 '- phosphate should be prescribed. In diabetic patients with normal renal function calories from dietary protein should not exceed 15% to 20% of total kilocalories. (ADA). Patients with diabetic nephropathy can take 2 or more servings of fish/week, minimum intake of fiber should be 14 g/1,000 kcal, and saturated fat should be less than 7% of total calories.

Pregnancy And Diabetic Nephropathy: New Joint National Committee (JNC) B's recommendations for target blood pressure for treatment of the elderly is raised to :2:150 mm Hg systolic or :2:90 mm Hg diastolic, and for patients with chronic kidney disease and with diabetes to :2:140 mm Hg systolic or :2:90 mm Hg diastolic but have no mention about special conditions as chronic kidney disease in pregnancy.

Since, atpresent there are no studies onpregnant diabetics in CKD Stage 5 therefore management of hyperglycemia, high blood pressure, and dyslipidemia may be extrapolated from the recommendations for women with earlier stages of CKD. Diabetes and CKD together may adversely affect the health of both the mother and her offspring. HbAlC should be as close to normal as possible (< 1% above upper limit of normal).

Pregnancy and Diabetic nephropathy: It is recommended to liberalize dietary protein intake to 1.0-1. 2g /kg preconception weight/ day.Energy intake should be 35 kcal/ kg/d sufficient enough for protein sparing effect. Insulin should be used to control hyperglycemia. Some patients may

require oral nutritional supplements (ONS) to fulfill protein and energy requirement. While prescribing ONS, care should be taken to choose ONS with low glycemic load and it should not be hyperosmolar. Target BP should be <130/80 mm Hg because of CKD. Hypotension should be avoided.

Summary: Hyperglycemia plays an important role in the development of DN. Positive family history and poor glycemic control greatly increases the risk for development of DN. It is advisable for patients with diabetic nephropathy to ensure the following: maintain good glycemic control Diabetics should eat at fixed times and eat several small meals a day because blood sugar level are at peak one to two hours after eating meal, after which levels fall. Snacks in between meals should be preferred. Meals should be well-balanced containing the right mix of starches, fruits and vegetables, proteins, and fats. Carbohydrate quantity at each meal and snack should be constant to regulate blood sugar levels. Maintaining food dairies is helpful. Use of measuring cups or a scale to ensure proportion size should be encouraged. Coordination of meals and medications to avoid hyperglycemia and hypoglycemia is important. Too little food in comparison to medications for diabetes may result in dangerously low blood glucose levels (hypoglycemia). On the contrary, too large portions of meal taken at a time can cause blood glucose levels to rise (hyperglycemia). Diet prescription for a patient with diabetic nephropathy is given in Table 1.


Body weight 82 kg, Height 165 cm

Hb 10.5 g/dL Creatinine 2.3 mg%,

Na: 136, K: 4.2, Ca: 8.2, P: 5.5

Proteinuria: +3

Energy

25k cal/kg/d (weight reduction)

Protein

0.6-0.7g/kg/d + 3g for Proteinuria (If renal function was normal Protein 0.8g/kg/d)

Visible Fat:

15-20g/d

Dietary Fiber

20 g/

Serum Na

< 2.4 g/d

Serum K

lmEq ideal body weight. K 60-65 mEq

Serum P

<800 mg/d

Serum Calcium

1500 mg

Cholesterol

<150 m, g/d (no egg Yolk, cream)

Phosphate binders are a must to be taken with meals.

Folic acid and iron supplements are a must

Body weight 82 kg, Height 165 cm

Hb 10.5 g/dL Creatinine 2.3 mg%,

Na: 136, K: 4.2, Ca: 8.2, P: 5.5

Proteinuria: +3

Energy

25k cal/kg/d (weight reduction)

Protein

0.6-0.7g/kg/d + 3g for Proteinuria (If renal function was normal Protein 0.8g/kg/d)

Visible Fat:

15-20g/d

Dietary Fiber

20 g/

Serum Na

< 2.4 g/d

Serum K

lmEq ideal body weight. K 60-65 mEq

Serum P

<800 mg/d

Serum Calcium

1500 mg

Cholesterol

<150 m, g/d (no egg Yolk, cream)

Phosphate binders are a must to be taken with meals.

Folic acid and iron supplements are a must

Table 1 :Diet Prescription: For a Patient with Diabetic Nephropathy


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