Delaying Dialysis: Managing Reduced Kidney Function

By Stephen Z. Fadem, MD, FACP

Chronic kidney disease (CKD) is common, affecting approximately 20 million (one out of every nine) people in the United States. In the majority of cases, it is the result of hypertension or diabetes. Nearly three years ago, the National Kidney Foundation (NKF) published a simple classification system and method of estimating kidney function. Thus making it easier to screen, identify and classify high-risk persons. What is not easy, however, is to accept and hear for the first time that you have kidney disease.

This article will identify and discuss three objectives to keep in mind when facing CKD:
1) Delaying the progression of disease.
2) Maintaining the quality of life.
3) Decreasing morbidity.

Delaying the progression of disease

Studies in the last 12 years have shown us that we can delay the onset of renal failure. The top three measures are controlling blood pressure, using a converting enzyme inhibitor or angiotensin receptor blocker medications and strict control of diabetes.

Maintaining the quality of life

Quality of life can be measured and quantified by several tests. The most popular and useful is the Kidney Disease Quality of Life (KDQOL). In essence, it relates to one’s energy level and exercise tolerance and sense of well-being.

Anemia is a major factor in determining quality of life. In anemia, there is a decrease in red blood cells (the little elements containing iron and hemoglobin that carry oxygen to tissues and take carbon dioxide products away). Medications that stimulate this production alleviate anemia and drastically improve quality of life. They also improve severe heart failure. Malnutrition and inflammation are both related to feeling badly, but can also be symptoms of underlying diseases.

In the late stages of kidney disease, the development of malnutrition usually responds to dialysis – the removal of the acids and waste products. Thus, patients at this stage often feel better after initiating dialysis. In addition, quality of life is related to the presence of pain, such as bone and joint pain, coexistence of neuropathy (nerve injury from diabetes and uremia), limit ambulation and preoccupy patients leading to a decrease in the quality of life.

Complications require evaluation and therapy. Heart disease and failure can be aggressively treated, but must first be assessed. In my experience, any kidney patient who has persisting fatigue should be evaluated for underlying coronary artery disease, and should have tests to determine cardiac function. Treating bone and calcium disease associated with kidney disease can be done with vitamin D analog supplements – control of serum phosphorus. Proactive and preventive care are ideal. The chemical abnormalities begin in early stage three kidney disease when the GFR is around 60 cc/min. These laboratory abnormalities persist for months to years before leading to symptoms, and thus ample time to aggressively prevent progression to symptomatic disease. However, what is more compelling is research showing that the same abnormalities that eventually cause bone disease also lead to calcium deposits inside the walls of blood vessels. This is fast becoming recognized as a major contributor to the late morbidity and mortality in kidney patients.

Decreasing morbidity

The major cause of death in CKD is cardiovascular disease. This is related to a combination of hypertension, atherosclerosis and vascular calcification. It is becoming apparent that the earlier we begin to manage these entities, the better chance we have of lowering the risk of a cardiovascular event. Blood pressure is one of the major problems that we must deal with, and it is prudent to start as early as possible in managing this disease. It challenges the health of 65 million Americans, and is a major promoter of kidney disease. Controlling blood pressure is the major means by which patients can decrease morbidity, prolong the life of their kidneys and enjoy a higher quality of life. Thus, it is important to understand something about hypertension.

Blood pressure

The heart is a pump, and beats with pressure. The top number of our blood pressure is a measurement of the direct action of the heart against the blood pressure. It is systolic because the segment of the heart rhythm where blood is squeezed out the heart is systole. The bottom number is the measure of the residual pressure in the blood vessels when the heart is resting between beats – that resting period is called diastole. The normal blood pressure is around 120/80. Interestingly, in primitive cultures where free salt ingestion is not part of the diet, blood pressures are much lower. If the pressure with which the heart beats is greater than 120/80, the blood vessel cells undergo changes that make them thicker. Throughout a period of many years, the thickening worsens, damaging blood vessels that supply organs like the kidney and brain. Thick blood vessels are narrow, and have a high resistance to the flow of blood, forcing the heart to have to pump with an increased pressure to get the same amount of blood to tissues. When the heart works at a higher level for a long period, heart failure may develop. Meanwhile, the higher pressure against the tissue causes damage to the walls of the filters, which may lead to kidney disease.

In May 2004, NKF published Clinical Practice Guidelines for hypertension in CKD patients. The goal to keep blood pressure at 130/80 or lower was based upon clinical trials showing blood pressures at this level were less likely to damage the kidney. Higher blood pressures associated with GFR (the glomerular filtration rate – a means of measuring kidney function and classifying kidney disease) loss around 13 cc/min per year. Patients should reduce their sodium intake to less than 2.4 grams per day. In addition, patients were encouraged to modify their lifestyle. The main stay of therapy is the use of antihypertensive therapy. Preferably, kidney patients should be on either an angiotensin receptor blocker (ARB) or a converting enzyme inhibitor (CEI) medications. In addition to reducing the blood pressure, these types of medicine relax or widen the blood vessels in the kidney. This reduces the pressure that is placed on the kidney filter (glomerulus). Increased pressure on any tissue, especially kidney blood vessels will result in damage over a period of years. In diabetics, there are studies that show that both these types of medication slow deterioration of renal function.

Controlling hypertension will often require several medications. Since hypertension is associated not only with kidney failure, but also with stroke and heart failure, it is important to screen patients at risk for CKD very early – starting with those who have known risk factors.


One of the mainstays of managing CKD, is to try to reduce proteinuria. Remember, the filters in the kidney are designed to hold back proteins and red blood cells, while letting waste products pass through. Studies with angiotensin converting enzyme inhibitors (ACE inhibitors or CEIs, such as lisinopril) and the angiotensin receptor blockades (ARBs, such as losartan) show these classes of medication are effective in reducing the amount of protein that leaks across the filter. This preserves renal function. It may be necessary to use these medications in larger doses to lower protein losses. Proteinuria is associated with worsening renal function because proteins harm the glomerular filter as they leak across it. While these classes seem to work independent of controlling blood pressure – that is they work directly on the kidney filter blood vessels – the study Modification of Diet in Renal Disease (MDRD), demonstrated that lowered blood pressure to less than a systolic of 130 and a diastolic of less than 75 in patients with reduced kidney function and proteinuria would help slow the decline in kidney function.


CKD is common in the later stages of diabetes, especially if the disease is not aggressively managed early. Type 1 diabetics generally have progressive kidney disease that manifests concurrently with microalbuminuria – small traces of protein leaking into the urine. While one-third of type 2 diabetics have proteinuria when their disease is diagnosed, it coexists with cardiovascular disease, hypertension and obesity. A major study, conducted more than 10 years ago, show the value of reducing blood sugar level and normalizing the HgbA1C – a measure of diabetes management. The second important step in controlling kidney disease in diabetes is to keep the blood pressure under control – again 130/80 is the recommendation. Tight glucose and blood pressure control reduces cardiovascular events, according to a large study published in the United Kingdom around seven years ago. Diabetes is associated with a two to four fold risk in cardiovascular mortality, and lifestyle changes that include increasing activity and reducing the smoking of cigarettes are necessary. The third step in controlling diabetes is to use an ACE or ARB. Screening for small traces of albumin in the urine is easy, and very useful in predicting who will develop kidney disease. These patients, especially, should be treated with ACEs or ARBs – or perhaps both, together, as some research is now suggesting. The fourth step in controlling diabetes is to control weight. One-half of people in the U.S. have criteria for obesity, based upon the calculation of the body mass index. It is recommended that patients with CKD work with a dietitian so that their diet will also help reduce cardiovascular risks. The diet may need to be tailored to the patient’s food preferences and underlying diagnoses.

Heart Failure

Heart failure is associated with the later stages of CKD. It is related to many factors, but most heavily linked to hypertension. Anemia is also associated with heart failure. Left ventricular hypertrophy (LVH) is the consequence of the heart having to work harder than usual to make blood circulate through vessels that are now thickened from hypertension. Any muscle that works harder requires more oxygen, and the requirement for this increase in oxygen is one of many signals that stimulate the formation of new blood vessels. In kidney disease, it is shown that muscles thicken, but the new blood vessels do not form fast enough. Thus, it is not surprising that around five years ago, a study was published showing risk of sudden death from LVH was associated with wall thickness, confirming what has been observed for years in clinical practice. Large clinical trials tried to resolve this problem and showed that death or the development and persistence of LVH could be significantly reduced by lowering blood pressure with an ACE inhibitor.

Bone disease

To add insult to injury, the tendency of late stage kidney patients to accumulate phosphorus causes changes in the blood vessel wall – leading to vascular calcification. This is independent of the forces that cause hypertensive vascular disease and compounded. It is being extensively studied now, but it is very important that kidney patients follow the guidelines for bone disease.

Lipids and inflammation

It is difficult to imagine a link between delicious but fattening food – usually associated with pleasurable events with inflammation – usually associated with pain and swelling. But, both inflammation and hyperlipidemia have a common dark side. All cells in the body will either change their shape, grow, die or release little hormones known as cytokines, when exposed to stress factors. One of those stress factors is the appropriately named oxygen radical. These radical oxidizing agents too often come from eating quantities of foods that our bodies have not yet adapted. When changes occur in the blood vessel walls, they cannot make enough of the nitrogen-containing substance nitric oxide to stay dilated. This begins the story of atherosclerosis. Damaged blood vessels recruit inflammatory cells to repair themselves. These cells see that excess fat (LDL cholesterol) has been oxidized and is foreign to the body and try to devour it. Engorged with oxidized fat, these cells die and stimulate the cascade of events that lead to plaque formation or atherosclerosis. Thus, the therapy for atherosclerosis is not only to reduce LDL (bad) cholesterol and those fat-containing foods that metabolize to LDL cholesterol, but also to reduce inflammation. It appears that statin medications (atorvastatin or simvastatin) appear to do both and long term clinical studies are underway to determine how to better-reduce inflammation and cholesterol in kidney patients. These studies are not being done in patients without abnormally high cholesterol. In the later stages of kidney disease, metabolism is altered and the serum measurement of cholesterol is lower than expected. Yet, the presence of atherosclerosis in the renal population cannot be denied. There is now a question of what cholesterol level should be for the general population, and additionally, what the balance between the good HDL and bad LDL cholesterol should be. Our diet is higher in lipids than that of pre-agricultural ancestors, and we will never exercise as ancestors did before the domestication of animals for transportation. Studies of primitive populations who do not share our diet and who ambulate as a means of transportation show that their LDL cholesterols were comparatively lower and HDL cholesterol levels higher than those following the traditional western diet.


The management of reduced kidney function creates a series of challenges that have to be handled in a systematic and orderly fashion. Chronic disease patients should keep these three goals in mind; delay the progression of disease, maintain the quality of life and decrease morbidity/mortality. In CKD, the major steps revolve around the control of blood pressure, reduction of cardiac risk factors, controlling underlying diseases, such as diabetes, and accompanying diseases, such as hypertension.

Stephen Z. Fadem, MD, FACP serves as a member of the AAKP Medical Advisory Board and a Vice President of the AAKP Board of Directors. Dr. Fadem is a practicing nephrologist in Houston.

This article originally appeared in the November 2004 issue of aakpRENALIFE, Vol. 20, No. 3.