|Year : 2018 | Volume
| Issue : 3 | Page : 68-69
Diabetes-metabolic impact on kidneys and nutritional status
Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
|Date of Web Publication||23-Apr-2019|
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Saxena A. Diabetes-metabolic impact on kidneys and nutritional status. J Renal Nutr Metab 2018;4:68-9
Diabetes is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of different organs, especially the eyes, kidneys, nerves, heart, and blood vessels. Several pathogenic processes are involved in the development of diabetes. These range from autoimmune destruction of the β-cells of the pancreas with consequent insulin deficiency to abnormalities that result in resistance to insulin action. Type 2 diabetes is associated with substantially increased risk of all-cause and cardiovascular mortality. Kidney disease is common among people with diabetes and associated with substantially increased mortality risk. This excess risk is associated with kidney disease manifested as albuminuria, impaired glomerular filtration rate (GFR), or both. Studies also show that diabetics with kidney disease predominantly account for the increased mortality observed in Type 2 diabetes. This article focuses on the metabolic impact of diabetes on kidneys and nutritional status.
Among individuals with diabetes but without kidney disease, standardized mortality has been reported to be 11.5% (95% confidence interval [CI], 7.9%–15.2%), representing an absolute risk difference with the reference group of 3.9% (95% CI, 0.1%–7.7%), adjusted for demographics, and 3.4% (95% CI, −0.3%–7.0%) when further adjusted for smoking, blood pressure (BP), and cholesterol. Among individuals with both diabetes and kidney disease, standardized mortality is 31.1% (95% CI, 24.7%–37.5%), representing an absolute risk difference with the reference group of 23.4% (95% CI, 17.0%–29.9%), adjusted for demographics, and 23.4% (95% CI, 17.2%–29.6%) when further adjusted.
The basis of the abnormalities in carbohydrate (CHO), fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of hormone action. Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclear which abnormality, if either alone, is the primary cause of the hyperglycemia.
Symptoms of marked hyperglycemia include polyuria, polydipsia, weight loss, sometimes with polyphagia, and blurred vision. Impairment of growth and susceptibility to certain infections may also accompany chronic hyperglycemia. Acute, life-threatening consequences of uncontrolled diabetes are hyperglycemia with ketoacidosis or the nonketotic hyperosmolar syndrome.
Long-term complications of diabetes include retinopathy with potential loss of vision; nephropathy leading to renal failure; peripheral neuropathy with risk of foot ulcers, amputations, and Charcot joints; and autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms and sexual dysfunction. Patients with diabetes have an increased incidence of atherosclerotic cardiovascular, peripheral arterial, and cerebrovascular disease.
In some individuals with diabetes, adequate glycemic control can be achieved with weight reduction, exercise, and/or oral glucose-lowering agents. These individuals, therefore, do not require insulin. Other individuals who have some residual insulin secretion but requires exogenous insulin for adequate glycemic control can survive without it. Individuals with extensive-cell destruction and therefore no residual insulin secretion require insulin for survival. The severity of the metabolic abnormality can progress, regress, or stay the same. Thus, the degree of hyperglycemia reflects the severity of the underlying metabolic process and its treatment more than the nature of the process itself.
Diabetes is the most common cause (in some populations) of end-stage renal disease (ESRD). The proportion of patients with both diabetes mellitus (DM) and ESRD is increasing, and this increase is described as a real epidemic with an abysmal prognosis. Many factors are involved, in particular, poor glycemic control., A poor nutritional status plays a role in the poor outcome of uremic diabetes patients.
Diabetic nephropathy is defined as any deleterious effect on kidney structure and/or function caused by DM. Stage wise, diabetic nephropathy is first characterized by microalbuminuria (30–300 mg urinary albumin/24 h) which may progress to macroalbuminuria, or overt nephropathy (>300 mg urinary albumin per 24 h), and later, without specific interventions, Without specific interventions –80% of patients with Type 1 diabetes with sustained microalbuminuria, urinary albumin excretion increases at a rate of –10%–20%/year. ESRD develops in 50% of Type 1 diabetic individuals with overt nephropathy within 10 years and in >75% by 20 years. 20%–40% of patients with Type 2 diabetes with microalbuminuria progress to overt diabetic nephropathy (DN), in 20 years ~20% progress to ESRD.
Prevalence of malnutrition is high in patients with diabetic nephropathy, 63% are malnourished, 48% are mild-to-moderately malnourished, and 15% are severely malnourished. To maintain nutritional status of, the medical nutritional therapy aims at maintenance of near-normal blood glucose levels through behavioral modification and lifestyle changes by balancing food intake and exercise, achieving optimal serum lipids and BP to reduce the risk of cardiovascular disease (CVD), maintain ideal body weight (body mass index >18 <24.9) with tight regulation of energy intake, bring down proteinuria to <1 g/day, prevention of long-term complications, and prevent malnutrition from setting in.
Patients with decreased kidney function (CKD stages 3–5) have increased risks for hypoglycemia for two reasons: decreased clearance of insulin and some of the oral agents used to treat diabetes and impaired (decreased) kidney gluconeogenesis due to reduced kidney mass. Various interventions which can help increase insulin sensitivity are weight loss, exercise, reduced protein intake, anti-inflammatory agents, Vitamin D, insulin sensitizers, better dialysis, antioxidant, and treatment of metabolic acidosis. The component of diet has greatest impact on management. The most important issue is how much in amount (in grams) and the type of CHO and when to consume it as CHO influences blood glucose levels. Those who use CHO counting method for meal planning should read food labels and measure portion sizes for CHO foods and counting grams of CHO. For the final insulin dose, exercise and blood glucose levels should be taken into account. To fine tune, Glycemic Control Glycemic Index concept can be used. Below 60 years of age should be prescribed 35 kcal/kg/day patients and 30 kcal/kg/day to those who are 60 years of age. DCCT recommends 25 kcal/kg/day for people with diabetes which can be increased to 35 kcal/kg/day if required and 50%–60% calories from carbohydrates. Protein requirement is usually 0.8 g/kg/day in the early stages of diabetic nephropathy. As GFR decreases, protein intake should be reduced to 0.6 g/kg/day with restrictions on raw salad and selected vegetables for fear of hyperkalemia.
Brenner 20 years ago identified glomerular hyperfiltration as key mediator of progressive kidney damage caused by a variety of initiating injuries, including DM. Elevation in single-nephron GFR in response to a reduction in functional nephron number depends on increase in glomerular pressure, plasma flow, adaptive reductions in preglomerular and postglomerular arteriolar resistances. Progressive kidney disease is characterized by glomerular hyperfiltration and albuminuria. For controlling hypertension and edema, salt restriction to between 1.5 and 2 g/day is recommended. Vegetarian diet (as in the DASH trials) have a beneficial effect on BP by reducing postprandial hyperfiltration.
Abnormalities of lipoprotein metabolism are often found in people with diabetes, therefore, fat restriction to the tune of 500 ml/month should be advised with preference to MUFA (olive oil) and PUFA (peanut oil, soybean oil, rice bran oil, or mustard oil). Combination of oil recommended is 15–20 ml of oil, 1–2 tsp mustard oil + groundnut, or soyabean +1 tsp desi ghee (liquid at room temperature)/soyabean butter/margarine. Use of low-fat or nonfat milk products is recommended. Foods containing trans-fatty acids such as commercially baked goods (cakes, pastries and biscuits, french fries, doughnuts) should be avoided.
Soy products (in at least one meal/d) 25 g/day would bring down proteinuria. Plant stenols are helpful in lowering LDL cholesterol (margarine). American Heart Association (AHA) recommends total fat should be 25%–35% of total calories, saturated fat should be <7%, and transfats should be <1%.
The AHA recommends – healthy, balanced diet that is rich in fruits and vegetables, whole grains, and fat-free or low-fat dairy products for preventing hyperhomocystenemia. However, kidney involvement in diabetes does not allow unlimited use of fruits and vegetables, therefore, folic acid should be prescribed after B12 levels are testing. The AHA and the KDOQI™ CPGs for CVD in dialysis patients recommends including 1 serving of cold-water fish (salmon, mackerel, herring, and albacore tuna) in the diet 3 times per week. High fiber diet reduces hyperglycemia hyperinsulinemia and lipemia. Within constraints of renal diet, ADA recommends 14 g/1000 kcal/d of fiber (same as that for general population) which can be increased to 20–35 g/day. For beneficial effect on serum lipids, soluble fiber (cereals such as oat bran) may be prescribed which may reduce postprandial hyperglycemia.
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