More than 23.6 million people, or 7.8% of the population, in the U.S. have diabetes (National Diabetes Information Clearinghouse, 2007). Diabetes mellitus continues to be the leading cause of chronic kidney disease (CKD) in this country; however, the rate has slowed considerably since the mid-1990s. The most recent data show that, in 2007, 108,891 new patients entered the end-stage renal disease (ESRD) program, and 527,283 were under treatment on December 31 of that year. Medicare was providing renal replacement therapy for 47,778 diabetic patients, 44% of the ESRD patient population (U.S. Renal Data Systems, 2007). In 2009 a total of 160,346 people with ESRD due to diabetes were living on chronic dialysis or with a kidney transplant. The percentage of new cases of ESRD caused by diabetes is highest among African-Americans. In 2007 the rate per million population for whites was 128, compared with 151 for Asians, 176 for Latinos, 333 for African-Americans, and 256 for American Indians (U.S. Renal Data Systems, 2009).
What is diabetes mellitus?
Diabetes mellitus is a disease process that prevents proper metabolism of glucose because of insufficient production or inefficient use of the hormone insulin. Insulin is produced by the beta cells of the pancreas. The function of insulin is to regulate blood sugar (blood glucose). Glucose is “food” for the cells of the body, and insulin facilitates the diffusion of glucose from the bloodstream to the cells. If there is a deficiency of insulin, or if the insulin cannot affect transport of glucose into the cells, the cells will “starve.”
What are the two types of diabetes?
Type 1 diabetes, formerly called juvenile diabetes or insulin-dependent diabetes mellitus (IDDM), is caused by the destruction of the beta cells of the pancreas. The pancreatic beta cells are the only cells in the body that produce the hormone insulin, which is needed to regulate blood glucose. This type of diabetes typically strikes children or young adults. The susceptibility to the disease is inherited, but the actual onset of the disease is due to some environmental trigger such as a virus or allergen. The resulting autoimmune response leads to beta cell dysfunction.
Type 2 diabetes, previously known as adult-onset diabetes or non–insulin-dependent diabetes mellitus (NIDDM), accounts for more than 90% of diabetes cases in the United States. This number is increasing because of the growth in the more susceptible minority populations. In this condition, insulin requirements are greater than the supply, or the patient’s cells are insulin resistant and require help using insulin. Dietary control, exercise, and weight loss are important factors in lowering insulin requirements and increasing insulin use. Family history, obesity, hypertension, and smoking are major risk factors for this type of diabetes. African-Americans, Latinos, and Asians are at a particularly higher risk for this type of diabetes.
How is diabetes treated?
Diabetes is best managed with a multidisciplinary approach, in which the physician, nurse, and dietitian plan and implement a comprehensive plan of care. Often these professionals specialize in diabetic care and work with the primary care physician. The diabetologist (physician) determines the severity of the disease and assesses its effects. Other specialists, such as nephrologists and ophthalmologists, are consulted periodically for assessment of organ damage and for treatment. Annual visits to the ophthalmologist are necessary for all diabetic patients. A podiatrist should be consulted early to treat existing foot problems, assess risk of future problems, and recommend appropriate footwear. The medical goal is to arrest tissue and organ damage by normalizing the blood sugar. Among adults with diagnosed diabetes, 13% take both insulin and oral medications while 14% take only insulin. Oral medications alone are taken by 57% of those diagnosed with diabetes, and 16% do not take either insulin or oral hypoglycemics. (National Diabetes Information Clearinghouse, 2007). For the type 1 patient, glycemic control is achieved through diet, exercise, and insulin administration via subcutaneous injection or insulin pump. For the type 2 patient, the treatment varies and can be diet and exercise alone or may include an oral hypoglycemic agent and/or insulin injections. Monitoring of blood glucose values dictates the need for medication or dosage adjustments (Table 16-1). The dietitian creates a meal plan based on the American Diabetes Association guidelines and the individual’s lifestyle preferences. In addition, the dietitian teaches and counsels the patient about the vital role that diet and exercise play in the patient’s long-term outcomes. The nurse coordinates care, educates the patient and family about all aspects of care, and assesses all parameters of the patient’s health, including psychosocial adjustments, response to medication, diet and exercise, foot care, and other follow-up assessments as needed.
Table 16-1 Medication Monitoring in Diabetes Mellitus

How is blood sugar measured and what is normal?
There are four blood sugar tests used for diagnosing and monitoring diabetes.
• A fasting blood glucose is measured after an eight-hour fast. For a nondiabetic patient, the range is 60 to 115 mg/dL. A value greater than 126 mg/dL on repeated studies may indicate diabetes.
• A random blood glucose greater than or equal to 200 mg/dL is diagnostic if accompanied by classic signs and symptoms.
• The oral glucose tolerance test measures both blood and urine glucose after the patient drinks a 75-g glucose solution. Normal blood values are less than 200 mg/dL after two hours. A value of 200 mg/dL or higher confirms a diagnosis of diabetes. The term impaired glucose tolerance is used if the value is between 140 and 190 mg/dL.
• Nurses teach patients or family members to perform a fingerstick blood sugar for ongoing monitoring and evaluation. It is not used to diagnose diabetes. As implied by the name of the test, blood is obtained from a finger stick, and the amount of glucose is measured by a handheld device called a glucometer.
What is hyperglycemia?
Hyperglycemia means high blood glucose. Signs and symptoms include frequent urination, excessive thirst, nausea and vomiting, weakness, confusion, and dehydration. If hyperglycemia is confirmed by a fingerstick test, the episode is treated with insulin and fluids (if dehydrated).
What is hypoglycemia?
Hypoglycemia means low blood glucose. Signs and symptoms include anxiety, confusion, tachycardia, diaphoresis, and tremors. The blood glucose will usually be less than 70 mg/dL, although some patients become symptomatic at higher values. The treatment is to return the blood glucose value to normal by giving glucose-containing liquids either orally or intravenously.
Both hyperglycemia and hypoglycemia can lead to coma, a life-threatening emergency. Prior to becoming comatose the patient may appear to be very drunk.
Is there a cure for diabetes?
There is no cure for diabetes at this time. Prevention of diabetes is being studied by identifying people at risk and instituting treatments designed to delay or prevent damage to the pancreas in type 1 diabetes or to the insulin receptors on the patient’s cells in type 2 diabetes. A successful pancreas transplant can restore normal insulin production, but, as with any organ transplant, the patient is immunosuppressed and at risk for adverse effects of those medicines.
What is diabetic nephropathy?
Diabetic nephropathy or diabetic kidney disease (DKD) is kidney disease caused by diabetes. It is a complication of the small blood vessels that feed the kidneys brought on by damage to the glomeruli. The pathology glomerulosclerosis is a fibrotic thickening of the glomeruli. It is thought to be caused by hyperfiltration and accumulation of glycosylated, or “caramelized,” proteins. As the disease progresses, the glomeruli lose their ability to filter blood effectively, resulting in the accumulation of waste products, such as urea and creatinine in the body.
Diabetic nephropathy occurs in five stages:
Stage 1. Increased blood flow through the kidney (hyperfiltration) results in enlarged kidneys (renal hypertrophy).
Stage 2. This hyperfiltration of the glomeruli damages the membrane, causing it to leak larger molecules that normally would not pass across. The leak of albumin from the blood into the urine is known as microalbuminuria. As the loss of this and other proteins increase, the clearance of such waste products as urea and creatinine decreases.
Stage 3. Microalbuminuria exceeds 200 mcg/min.
Stage 4. Glomerular filtration rate (GFR) has dropped to 75 mL/min or less, proteinuria is significantly increased, and the patient has become hypertensive. This stage is called advanced clinical nephropathy.
Stage 5. ESRD.
Can diabetic nephropathy and progression to chronic kidney disease be prevented?
Diabetic nephropathy does not occur in all diabetic patients and is more likely in type 1 than in type 2. Studies show that tight glycemic control can significantly reduce the development and rate of progression of diabetic nephropathy. With an intensive regimen of blood glucose monitoring; insulin and/or oral hypoglycemic agent administration; and adherence to a program of diet and exercise, the majority of patients can maintain normal blood glucose levels.
Progression of diabetic nephropathy can be delayed by the use of an angiotensin-converting enzyme (ACE) inhibitor medication. This class of drugs is usually prescribed to control hypertension but is useful for both purposes in the patient with diabetic nephropathy. It is given in stage 1 to control hyperfiltration. The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (KDOQI) 2007 guidelines recommend screening patients with diabetes annually for DKD. This screening should include measurements of microalbiminuria or urinary albumin-creatinine ratio, measurements of serum creatinine, and estimations of GFR.
When should a diabetic patient who has nephropathy start dialysis?
Initiation of dialysis depends on the individual needs and condition of the patient, but a clear indicator is a low creatinine clearance combined with symptomatic edema. Patients with diabetes suffer symptoms of uremia earlier than their nondiabetic counterparts. For this reason, it is usual to begin dialysis when the creatinine clearance rate is between 10 and 15 mL/min, but it may be started with a clearance of up to 20 mL/min. Hypertension is very difficult to manage in patients with a clearance less than 10 mL/min. Blood pressure control is important in the management of diabetic retinopathy, as well as cardiovascular and peripheral vascular disease.
For a patient with diabetes, is hemodialysis better than peritoneal dialysis?
There are advantages and disadvantages to both modalities of treatment. The healthcare team and the patient must choose the treatment that best suits his or her lifestyle, taking into consideration comorbidities and medical history.
Advantages of in-center hemodialysis include frequent medical surveillance and smaller loss of protein into the dialysate. Disadvantages are a higher risk of vascular access complications, risk of predialysis hyperkalemia, and an increased incidence of hypotension during dialysis.
Peritoneal dialysis may offer better glycemic control, especially if intraperitoneal insulin is used; it also offers better cardiovascular tolerance and potassium control and does not require vascular access. Some patients have difficulties with glycemic control because of the high peritoneal exposure and potential absorption to the intraperitoneal glucose. Contraindications are all of the usual problems of peritoneal dialysis magnified. Examples include more episodes of peritonitis due to reduced immune response to infection, protein loss, and increased intraabdominal pressure complications, such as gastroparesis.
Finally, inability to do peritoneal dialysis because of poor eyesight or poor fine motor control requires the patient to be dialyzed in-center if he or she does not have an assistant at home.
Can a patient with diabetes receive a transplant?
Living related donor transplantation is the treatment of choice for diabetes patients because it offers a higher rate of survival than dialysis. Many younger patients with type 1 diabetes receive combined kidney-pancreas transplants that offer the additional benefit of normal insulin production. However, many patients are not considered transplant candidates because of advanced age and/or atherosclerosis. A thorough evaluation is required and cardiac surgery is often necessary before listing the patient for a deceased donor transplant. A higher percentage of transplanted patients with diabetes undergo limb amputation than do their dialysis counterparts. Infection and peripheral vascular disease are exacerbated by steroids. However, the increased length of survival posttransplant probably accounts for the development of these complications in this patient population.
Why do diabetic patients need more dialysis than those without diabetes?
Diabetes affects every cell, tissue, and organ of the body, as does uremia. Patients with diabetes who also have CKD offer a unique challenge. According to current mortality data, only one in five such patients who begin dialysis will be alive in five years. To have better survival prospects, patients with diabetes need to achieve higher urea clearance rates than other patients. Some sources say they need a Kt/V (delivered dose of dialysis) of 1.4 or greater, but with multisystem organ involvement this may be difficult to achieve. Patients with diabetes and autonomic neuropathy are at risk for underdialysis because of hypotension in the first hour of dialysis. A diseased cardiovascular and autonomic nervous system cannot adequately respond to intravascular volume changes that occur with ultrafiltration. Dialysis blood flow is frequently lowered to treat this hypotension, along with administration of extra saline. Symptomatic hypotension sometimes leads to early termination of treatment, affecting the adequacy of dialysis and leaving the patient with fluid overload, thus further stressing the cardiovascular system. Peripheral vascular disease contributes to vascular access problems with subsequent inadequacy of dialysis. Because of steal syndrome and previous graft failures, many patients with diabetes can only dialyze with catheter access.
Why do some dialysis patients say that they are “no longer diabetic” after they start dialysis?
Kidney failure due to diabetes has the paradoxic outcome of making the insulin that is available last longer because it cannot be broken down and excreted as efficiently. Patients with uremia frequently eat a lot less, and therefore need less insulin. Patients with type 1 diabetes will always need some insulin injected unless they have a successful pancreas transplant. Type 2 patients, however, frequently no longer need additional insulin or oral medications. If they lose weight, their own insulin will be better used. Oral hypoglycemics, especially the long-acting ones, can cause severe hypoglycemia in the hemodialysis patient. These drugs are excreted by healthy kidneys and are not dialyzable.
How does hemodialysis affect the patient with diabetes?
The chemical composition of the dialysate is designed to be compatible with normal blood values. It has been determined that a dextrose level of 200 mg/dL is optimal for all patients. For those with diabetes, this level prevents hypoglycemia and improves hyperglycemia.
Should the diabetic patient with retinopathy get standard-dose heparin?
No. Definitive evidence has been presented to show that heparinization during dialysis puts the diabetic patient at increased risk for progression of retinopathy. However, heparin requirements should be carefully monitored and dosages adjusted accordingly.
Are insulin and oral hypoglycemic agents dialyzable?
Insulin is the most common hypoglycemic agent for patients with diabetes who are on hemodialysis. Insulin and most oral hypoglycemic agents are not dialyzable. Exceptions are metformin (Glucophage) and chlorpropamide (Diabinese). These drugs are contraindicated for use in the ESRD patient.
How is hypoglycemia managed during hemodialysis?
Hypoglycemia must be verified with a glucometer. The signs and symptoms of hypoglycemia can be confused with hypotension. Changes in the patient’s schedule to accommodate dialysis treatment may interfere with eating routines and medication administration, placing the patient at risk for a hypoglycemic episode. Some patients require a snack or some apple juice. However, blood volume diverted to the gut for digestion may increase a patient’s risk for hypotension. Profound hypoglycemia may require a physician’s order for an intravenous dextrose infusion.
How is hyperglycemia managed during hemodialysis?
If hyperglycemia is verified with a glucometer, the physician may order some regular insulin. Hyperglycemia can be a sign of infection, and the patient must be assessed and treated if an infection is present. Heparin doses may need to be increased if unusual incidences of clotting occur associated with hyperglycemia.
Are diabetic patients more difficult to keep healthy than nondiabetic hemodialysis patients?
Statistics show a higher mortality rate for patients with diabetes who are on dialysis. Cardiovascular disease is the leading cause of death, followed by sepsis and voluntary withdrawal from dialysis. The progression of atherosclerosis is accelerated in diabetic patients on hemodialysis, making them more prone to cardiovascular complications, such as hypertension, angina, gangrene, and myocardial infarction. Hyperglycemia coupled with uremia delays wound healing and compromises immunity. Gastrointestinal neuropathy resulting in constipation as well as sudden, uncontrollable diarrhea can be a source of great distress to the patient with diabetes. Gastroparesis may cause regurgitation and aspiration.
What is gastroparesis?
Gastroparesis occurs as a consequence of autonomic neuropathy. Delay of gastric emptying is evidenced by difficulty swallowing, heartburn, nausea and vomiting, abdominal pain, and erratic blood glucose values. Treatment includes small low-fat, low-fiber meals; the use of drugs, such as metoclopramide (Reglan) and cisapride (Propulsid), to improve gastric motility; and improved glycemic control.
Do individuals with diabetes have more vascular access problems than nondiabetic patients?
Along with atherosclerotic peripheral vascular disease, calcification of the vascular tree further limits the quantity and quality of blood vessels normally used to create a vascular access. Diabetic patients on dialysis do not experience more episodes of sepsis with their vascular access, but do require more hospitalization and have a poor prognosis. These patients do have a higher rate of graft thrombosis.
How should diabetic patients modify their diets when they are on hemodialysis?
Patients with diabetes already know about diet modification necessitated by errors of glucose metabolism. Now they must further modify their diets to accommodate renal failure and hemodialysis. Some patients hear about restrictions in the renal diet and feel there is nothing left to eat. Not so! Although they must make new adjustments to avoid the dangers of hyperkalemia and bone disease, it is imperative that they eat well to meet the demands of hemodialysis, which increases the risk for malnutrition. Hemodialysis removes nutrients by depleting amino acids at the rate of 1 to 2 g/h during treatment. Blood loss in the dialyzer and lines also contributes to protein loss. Dietary protein replacement should be at a minimum of 1.2 g/kg/day. A caloric intake of 35 kcal/kg is required to prevent the body from burning protein stores for energy. Generally, protein should make up about 20% of the diet, with the rest being 30% fat (preferably monounsaturated) and 50% carbohydrate. Diets should be tailored to patient preferences and customs. The dietary goal is to make eating pleasurable while meeting nutritional needs. Highly refined carbohydrates such as candy, cake, and pie can be incorporated into the diabetic renal diet as long as they are factored into the overall dietary plan. High-calorie, low-nutrient foods must be limited, but are not forbidden. The goal is to maintain good glycemic control. Fluid control may be a challenge, as hyperglycemia may increase thirst.
If diabetic patients on dialysis no longer need medication for blood sugar control, should their blood sugar still be checked?
Daily blood sugar checks are important to confirm good glycemic control. More frequent checks are made if the patient is not feeling well. An elevated blood sugar may indicate the presence of infection.
What is glycosylated hemoglobin?
A glycosylated hemoglobin value is the measurement of glucose bound to the hemoglobin of the red blood cells. Elevated blood sugar levels cause the hemoglobin to become saturated with glucose in the form of glycohemoglobin. Glycohemoglobin is present for the 120-day life span of the red blood cell. An average of the measurement of the glycolated part of the hemoglobin is called hemoglobin A1. It can be measured as subunits designated as hemoglobin A1a, hemoglobin A1b, and hemoglobin A1c. In most laboratories only hemoglobin A1c is measured because it is the most prevalent form. Other laboratories measure the total glycohemoglobin as A1. Glycohemoglobin A1 values are 2% to 4% higher than hemoglobin A1c values, so it is imperative to know which standard of measurement is being used by the laboratories serving the hemodialysis facility. This test is a good indicator of compliance with the prescribed diet and medication regimen because it measures long-term glycemic control. However, studies have not been done to demonstrate that hemoglobin A1c values are a reliable measurement for evaluating diabetic patients with uremia. Estimated Average Glucose (eAG) is a new term recommended by the American Diabetes Association. While A1c is reported as a percent, the eAG is reported in the same units (mg/dl or mmol/l) used by the patient’s daily self monitoring device. This value is more meaningful to the patient and may facilitate improved patient glycemic control. The values and interpretations for both tests in the general population are presented in Table 16-2.
Table 16-2 Values for Hemoglobin A1c and Glycosylated Hemoglobin
|
Values for hemoglobin A1c |
Values for estimated Average Glucose (eAG) |
||
|
eAG (mg/dl) |
eAG (mmol/l) |
||
|
6% |
126 |
7.0 |
|
|
6.5% |
140 |
7.8 |
|
|
7% |
154 |
8.6 |
|
|
7.5% |
169 |
9.4 |
|
|
8% |
183 |
10.1 |
|
|
8.5% |
197 |
10.9 |
|
|
9.0% |
212 |
11.8 |
|
|
9.5% |
226 |
12.6 |
|
|
10% |
240 |
13.4 |
|
Examples of how A1c is related to an average blood sugar level.
Patient Education – A1c test. Mosby’s Nursing Consult. 2010 RelayHealth.
American Diabetes Association, Living with Diabetes – Estimated Average Glucose (eAG). http://www.diabetes.org/living-with-diabetes/treatment-and-care/blood-glucose-control/estimated-average-glucose.html. Accessed November 13, 2010.
What assessments of diabetic patients on dialysis are critically important?
Although diabetic patients make up only 7.8% of the U.S. population, 60% of all lower limb amputations are performed on this population (National Diabetes Information Clearinghouse, 2007). Frequent and careful assessment of the feet and legs of diabetic patients on dialysis should be done to identify potential problems of skin breakdown or infection. Early detection and prompt treatment may prevent serious complications.
Can diabetic foot problems be prevented?
Absolutely! Regular foot inspections should be done by the nephrology nurse with referrals to the podiatrist for attention to potential problem areas, such as toenails, corns, bunions, and so on. Patients should never cut their own corns or calluses and should be warned never to use heating pads, hot water bottles, or unsupervised hot water soaks. Patients and caregivers must be educated on the basics of good foot hygiene. Prosthetic footwear to protect insensitive feet from trauma is a necessity. Medicare now reimburses for prescribed shoes.