Chronic kidney disease (CKD) is defined as kidney damage or impaired renal function that persists for 3 or more months (National Kidney Foundation [NKF], 2002). The severity of the disease is staged based on the level of kidney function as measured by the glomerular filtration rate (GFR) (Table 13-1). In the United States, it is estimated that 80,000 people are diagnosed with CKD annually, 20 million people are living with this disease, and an additional 20 million people are at increased risk (Coresh, Astor, Greene et al., 2003; NKF, 2006; United States Renal Data System [USRDS], 2005). The incidence and prevalence of CKD in the United States have been rising steadily, likely due to the increased prevalence of obesity and type 2 diabetes and an increasingly elderly population.

The most advanced stage of CKD is end-stage renal disease (ESRD). Patients with ESRD require dialysis or transplantation to survive (Zandi-Nejad & Brenner, 2005). In 2003, about 450,000 patients in the United States had ESRD, of whom 325,000 were being treated with dialysis and the remaining 128,000 received a kidney transplant (USRDS, 2005). There were 82,588 deaths attributed to ESRD in 2003, and about 13.5% of these patients were receiving care from a hospice at the time of their deaths (USRDS, 2005).

Risk factors for CKD include diabetes, hypertension, and family history of kidney disease. In addition, African Americans, Hispanics, Pacific Islanders, Native Americans, and people over the age of 65 are at increased risk (NKF, 2006). Cardiac disease is the single greatest cause of mortality in the ESRD population (USRDS, 2005). Older patients with ESRD and CHF have an annual mortality rate of about 60% and an expected survival of less than 6 months. This emphasizes the importance of palliative care and end-of-life planning for this group of patients (Germain & Cohen, 2001).

Patients with chronic renal failure have a high symptom burden. A study by Wiesbord, Fried, Arnold et al. (2005) showed that the median number of symptoms for patients with ESRD receiving chronic hemodialysis was nine, with the severity of each averaging 3 on a scale of 1 to 5. Dry skin, fatigue, itching, and bone and/or joint pain were reported by at least 50% of patients. The overall symptom burden and severity were each correlated directly with impaired quality of life and depression.

Increasing evidence accrued in the past decades indicates that the adverse outcomes of chronic kidney disease, such as kidney failure, cardiovascular disease, and premature death, can be prevented or delayed through early detection and initiation of interventions to slow progression. Methods to slow the progression of CKD include optimal control of hypertension, optimal management of diabetes and hyperlipidemia, avoidance of nephrotoxins, cessation of smoking, and the use of medications that block the production of or effect of angiotensin II (Shaver, 2004).

The two main causes of chronic kidney disease are diabetes (43%) and hypertension (26%). Other conditions that affect the kidneys are glomerulonephritis, inherited diseases (e.g., polycystic kidney disease), interstitial nephritis and/or pyelonephritis, and secondary glomerulonephritis (e.g., lupus nephritis) (Shaver, 2004). Obstructions due to kidney stones, tumors, or an enlarged prostate gland in men also can lead to kidney damage.

Each human kidney contains about 1 million nephrons, consisting of the renal corpuscle (glomerulus) and renal tubules, that function to maintain homeostatic functions of the body (Kumar, 2004) (Table 13-2). Insult to the kidney causes acute inflammation of glomeruli leading to a cascade of proteinuria, glomerular sclerosis, interstitial fibrosis, and, eventually, permanent nephron damage. In response to a reduction in renal function, the remaining nephrons adapt with hyperfiltration. For this reason, patients can lose up to 75% of GFR with no pronounced symptoms (Shaver, 2004). The hyperfiltration causes glomerular capillary hypertension, which leads to glomerular sclerosis and nephron death. The glomerular capillary hypertension is maintained by the renin-angiotensin-aldosterone system (Zandi-Nejad & Brenner, 2005). The kidneys lose their ability to concentrate urine adequately, putting patients at risk for dehydration. As the GFR further declines, the body is unable to rid itself of excess water, salt, and other waste products, and serum urea nitrogen and creatinine levels increase (Molzahn, 2005a). The process of nephron death, hyperfiltration, and additional nephron death means that CKD tends to be progressive. This progression, however, may be slowed with optimal management.

CKD is a common microvascular complication of diabetes. Microangiopathy affecting the afferent and efferent arterioles of the nephron causes glomerulosclerosis. This leads to scarring of the glomerulus, tubules, and interstitium of the kidney and an increase in intraglomerular pressure. Microalbuminuria occurring about 10 to 15 years after the diagnosis of diabetes (preclinical diabetic nephropathy) is an early marker of developing diabetic nephropathy. With progression of the disease, more and more protein is excreted in the urine and renal insufficiency ensues (Barnett & Braunstein, 2004; Molzahn, 2005b).

A sustained systemic high blood pressure leads to nephrosclerosis. There is a direct correlation between the duration and degree of hypertension and the severity of renal damage. Kidney disease can also lead to hypertension. For example, hypertension may result from the kidney’s decreasing ability to excrete salt and water when glomeruli are damaged (Molzahn, 2005b). Thus, a vicious cycle occurs as the renal damage causes hypertension and hypertension worsens renal damage.

Many people have no symptoms of declining renal function until their kidney disease is advanced, that is, stage 4 or 5. Uremia affects every organ system and is likely due to multiple factors, including retained molecules, deficiencies of important hormones, and metabolic factors (Shaver, 2004). Table 13-3 shows the major manifestations of uremia.

History includes identification of those patients at high risk for CKD, including patients with any family history of CKD and those with diabetes, hypertension, recurrent urinary tract infections, urinary obstruction, or a systemic illness that affects the kidneys (Snyder & Pendergraph, 2005). The history should also include the onset of any of these high-risk diseases, the treatments used to manage the disease over time, and the effectiveness of these treatments.

Patients with a diagnosis of renal disease may present in various ways. In addition to the signs and symptoms of uremia as presented in Table 13-3, physical findings that might suggest the presence of renal disease include the following:

Several diagnostic tests may be required to identify the cause of CKD and to monitor the progression of the disease over time. The following may provide valuable information (Veterans Hospital Administration/Department of Defense [VHA/DoD], 2001):

The following laboratory data may be helpful to identify complications in stages 3 and 4 CKD (Snyder & Pendergraph, 2005):

When CKD is diagnosed, it is important for the patient and family to understand the illness and its management, taking into account the nature of the disease in the context of patient and family values and wishes. Aggressive management of CKD involves using interventions to slow or arrest disease progression. As mentioned earlier, these interventions include optimal control of hypertension, optimal management of diabetes and hyperlipidemia, avoidance of nephrotoxins, cessation of smoking, and the use of medications that block the production of or effect of angiotensin II. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers lower blood pressure and demonstrate a nephroprotective effect beyond that of their ability to lower blood pressure (Shaver, 2004). Restricting dietary protein may slow CKD progression, but protein malnutrition must be avoided.

Renal impairment affects medication selection and dose. Nephrotoxic drugs should be avoided, and medications eliminated via the urine may require dose reduction. Table 13-4 lists dosage modifications for selected medications when used in patients with renal failure.

Patients with ESRD require kidney replacement therapy to survive, either some form of dialysis (home peritoneal dialysis, home hemodialysis, in-center hemodialysis) or a renal transplantation. Hemodialysis is associated with significant symptom burden, leading some patients, especially the elderly and those with multiple comorbid medical conditions, to decline dialysis. Those who decide to forgo dialysis should be referred to a hospice program and receive maximal palliative care (Moss, 2001).

Offering the patient a trial of dialysis for 3 to 6 months may be an acceptable choice for those with a limited prognosis (Cohen, Germain, & Poppel, 2003).

Over time, some patients who are on dialysis may elect to stop treatment. Often, this decision is due to (1) failure to thrive despite aggressive intervention, (2) poor quality of life as defined by the patient, or (3) worsening of comorbid complications (amputations, calciphylaxis, stroke, CHF), terminal illness (malignancies, AIDS, etc), or acute catastrophic illness. Death after dialysis withdrawal usually occurs quickly. Studies of patients who withdrew from dialysis showed that the time to death after stopping dialysis was less than 30 days, with a median of 8 to 10 days (Cohen, McCue, Germain et al., 1995; Neely & Roxe, 2000). The presumed immediate cause of death in most of these patients was uremia, which is often described as a painless and peaceful death. However, patients who stop dialysis are at high risk for delirium and accumulation of toxic metabolites of certain medications; these symptoms should be anticipated and appropriately managed. Box 13-1 provides a helpful checklist to use when patients elect to withhold or withdraw from dialysis.