Chronic Kidney Disease Stage 5 Case Study

Prediction, Progression, and Outcomes of Chronic Kidney Disease in Older Adults

  1. Sharon Anderson*,
  2. Jeffrey B. Halter,
  3. William R. Hazzard,
  4. Jonathan Himmelfarb§,
  5. Frances McFarland Horne,
  6. George A. Kaysen,
  7. John W. Kusek**,
  8. Susan G. Nayfield††,
  9. Kenneth Schmader‡‡,
  10. Ying Tian††,
  11. John R. Ashworth,
  12. Charles P. Clayton,
  13. Ryan P. Parker,
  14. Erika D. Tarver,
  15. Nancy F. Woolard§§,
  16. Kevin P. High§§ and
  17. for the workshop participants
  1. *Department of Medicine, Oregon Health and Science University, Portland, Oregon; Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan; Department of Medicine, University of Washington and VA Puget Sound Health Care System, Seattle, Washington; §Department of Medicine, Maine Medical Center, Portland, Maine; Association of Specialty Professors, Washington, DC; Department of Internal Medicine, University of California-Davis, Davis, California; **Kidney and Urology Branch, National Institute of Diabetes and Digestive and Kidney Diseases and ††Geriatrics and Clinical Gerontology Branch, National Institute on Aging, Bethesda, Maryland; and ‡‡Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina, and §§Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina
  1. Correspondence:
    Dr. Kevin P. High, Section on Infectious Diseases, Department of Internal Medicine, Wake Forest University School of Medicine, 100 Medical Center Boulevard, Winston-Salem, NC 27157-1042. Phone: 336-716-4584; Fax: 336-716-3825; E-mail: khigh{at}wfubmc.edu

Abstract

Chronic kidney disease is a large and growing problem among aging populations. Although progression of chronic kidney disease to end-stage renal disease (ESRD) is a costly and important clinical event with substantial morbidity, it appears less frequently in aging people compared with cardiovascular mortality. The measurement of kidney function and management of kidney disease in older individuals remain challenging, partly because the pathophysiologic mechanisms underlying age-related decline in kidney function, the interactions between age and other risk factors in renal progression, and the associations of chronic kidney disease with other comorbidities in older people are understudied and poorly understood. The Association of Specialty Professors, the American Society of Nephrology, the American Geriatrics Society, the National Institute on Aging, and the National Institute of Diabetes and Digestive and Kidney Diseases held a workshop, summarized in this article, to review what is known about chronic kidney disease, identify research gaps and resources available to address them, and identify priority areas for future research. Answers to emerging research questions will support the integration of geriatrics and nephrology and thus improve care for older patients at risk for chronic kidney disease.

Chronic kidney disease (CKD), defined by reduced glomerular filtration rate (GFR), proteinuria, or structural kidney disease, is a growing problem among the aging population (Figure 1).1 Although ESRD, defined as kidney failure treated with dialysis or transplantation, is less prevalent than earlier CKD stages, the number of patients who have ESRD and are older than 65 yr almost doubled during 25 yr, and the fastest growing segment of that population during the past decade is older than 75 yr.

Figure 1.

Prevalence of CKD by age group in National Health and Nutrition Examination Survey (NHANES) data 1988 through 1994 and 1999 through 2004. Adapted from Coresh et al.65

Proteinuria, hypertension, diabetes, race, and ethnicity are strong risk factors for progression from CKD to ESRD,2–9 and the higher ESRD incidence among men than among women is most pronounced in older patients. Declines in renal function, measured by creatinine clearance, occur in approximately two thirds of “healthy” older adults over time10 but progresses to ESRD in only 1 to 2% of these patients,1 yet mortality rates are high among older patients with CKD.11 Few studies of older patients with CKD have addressed the mechanisms leading to ESRD or mortality.

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MECHANISMS UNDERLYING CKD IN AGED PEOPLE

The cause of age-related increases in renal fibrosis, which leads to glomerulosclerosis, interstitial fibrosis, tubular atrophy, vascular sclerosis, and loss of renal function, is poorly understood; however, in animal models, collagen seems to accumulate with age in the glomerulus, peritubular capillary, and tubulointerstitium because of increased transcription of the gene encoding type III collagen.12 Preliminary studies in aged rats showed a loss of polycomb-mediated (epigenetic) collagen gene silencing despite a significant decrease in histone modifications associated with repressed genes, suggesting that other polycomb-related abnormalities contribute to age-associated loss of gene regulation.13,14 Calorie restriction, a robust antiaging intervention in animal models, resulted in increases in histone modifications, similar to those seen in aged rats on a regular diet, but restored gene expression and prevention of kidney sclerosis in the calorie-restricted animals suggest the restoration of effective polycomb-mediated silencing. How increases in epigenetic silencing mechanisms are circumvented in these models is not known.

Telomere shortening and increased p16INK4A expression, which are implicated in somatic cellular senescence pathways (Figure 2), are observed in aging human kidneys.15,16 Increased p16INK4A expression is also observed in aging rodents,17 but telomere shortening is not.16 Cellular senescence is associated with several features of the aging kidney15 and accelerates in patients with progressive kidney disease18,19 and transplant nephropathy,18 in biopsies from patients with hypertensive nephropathy,20 and in animal models of experimental hypertension20 and ischemia/reperfusion-induced injury.21,22

Figure 2.

Senescence-associated changes in gene expression.145 Cellular senescence is marked by increased expression of cell-cycle inhibitors and extracellular matrix proteins and by decreased expression of proteins involved in cell-cycle progression. Redrawn from ref. 145 (Melk A: Senescence of renal cells: Molecular basis and clinical implications. Nephrol Dial Transplant 18(12): 2474–2478, 2003), by permission of Oxford University Press.

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GENES AND CKD

Efforts are under way to identify genes associated with CKD and diabetic nephropathy and to establish biomarkers of risk for CKD and likelihood of benefit from intensive treatment; however, replication of potential CKD candidate genes is inconsistent because of phenotype specificity, varying genotyping technologies, and challenges with study design. How genetic variation will predict CKD risk, how patients will respond to their individual risk assessment, and how genetic risk contribution differs across ancestral groups are not clear. Gene–gene and gene–environment interactions are also poorly understood. Several candidate age-associated genes have been identified, including genes involved in regulating metabolism and enhancing tissue integrity. Global age-associated changes in gene expression also have been observed for the kidney.23 Selection pressure,24 epigenetic mechanisms, and changes in telomere biology and the proliferative capacity of renal stem or progenitor cells25–27 also might modulate dysfunction in the aging kidney.28

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ACUTE KIDNEY INJURY AND CKD PROGRESSION

The incidence of acute kidney injury (AKI) is increasing,29 particularly among older patients.30 Patients with CKD are more likely to experience AKI,31 and AKI is a risk factor for progression to ESRD. In the rat ischemia/reperfusion model, AKI is characterized by a temporary but substantial decrease in GFR, compromised urine-concentrating ability, proteinuria and interstitial fibrosis, and impaired sodium processing.32 Injured kidneys in this model also show a dramatic increase in hypoxia and renal fibrosis.33,34 Glomerular capillary density and interstitial peritubular vascular density decrease with age in the absence of other insults and are exacerbated by acute injury,35,36 and the ability to repair and regenerate tissue after injury declines with age.37 Thus, progression of CKD might not be a smooth, continuous course so much as a stepwise function marked by repeated episodes of AKI.

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MEASURING AND CLASSIFYING CKD

Although measured GFR is considered the best overall measurement of kidney function, it is often not practical in clinical or epidemiologic settings. Thus, there are few studies of measured GFR in older adults, and they have small sample sizes.38 GFR declines with age in the general population,38 but the rate of decline varies widely among individuals, and it is not clear whether declining GFR is part of “normal aging.” The annual rate of GFR decline was only 0.8 to 1.4 ml/min per 1.73 m2 in one community-based cohort of adults who were older than 65 yr and did not have diabetes,39 and one third of “healthy” older patients in another study showed no appreciable declines in kidney function during 10 yr.10

GFR is usually estimated (eGFR) from serum levels of endogenous filtration markers, most commonly creatinine and recently cystatin C40,41; however, factors other than filtration, including generation, tubular secretion or reabsorption, and extrarenal elimination, affect these markers.42 Estimating equations, which incorporate some of these non-GFR determinants, yield more accurate estimates of kidney function than do serum marker levels alone; however, current creatinine-based estimating equations have been reported to be less accurate in patients without kidney disease, and muscle wasting and inflammation might interfere with the accuracy of creatinine or cystatin C–based estimating equations in older people with frailty or comorbid illnesses. Improved measures of kidney function in older patients are needed to estimate better the prevalence of CKD and AKI, to manage and diagnose comorbidities appropriately, and to dose medications properly.

A new creatinine-based estimating equation,41 developed in a pooled sample in which the mean age was 52 yr, reduces bias by 50% and offers small but consistent improvement in precision and accuracy, compared with the most commonly used equation. In addition, accuracy of creatinine-based equations does not differ significantly from that of cystatin C–based equations in populations studied thus far, but equations based on the combination of the two markers might provide the best accuracy.41 Non-GFR determinants affecting each marker, such as low muscle mass and possibly obesity, might lead to systematic over or underestimation of GFR in specific individuals.

The term “preclinical kidney disease”43 has been proposed to describe patients with a creatinine-based eGFR >60 ml/min per 1.73 m2 and a cystatin C level >1.0 mg/L (equivalent to an eGFR of approximately 75 ml/min per 1.73 m2). On the basis of these criteria, 39% of the Cardiovascular Health Study sample, in which the mean age is 75 yr and patients do not meet the GFR-based criteria for CKD, have preclinical kidney disease. The incidences of death and CKD, defined on the basis of creatinine-based eGFR, is higher among these patients than it is among patients with eGFR >60 ml/min per 1.73 m2 and low cystatin C (Figure 3).

Figure 3.

Effects of preclinical kidney disease.43 Incidence for progression to CKD and for all-cause mortality is higher among patients with preclinical kidney disease, defined as GFR >60 ml/min per 1.73 m2 and cystatin C >1.0 mg/L, than it is among patients with normal kidney function. Redrawn from ref. 43.

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CKD, CARDIOVASCULAR DISEASE, AND ALL-CAUSE MORTALITY

Age-associated macrovascular changes include increased arterial diameter, wall thickness, and stiffness; changes in gene expression related to vascular elasticity and hypertension; increased migration of smooth muscle cells from the media to the epithelial space; and increased endothelial dysfunction.44–47 Similar changes have been observed in kidney disease45,48 and attributed to increased production of reactive oxygen species, decreased production of telomerase reverse transcriptase, and, ultimately, increased levels of C-reactive protein and oxidized LDL cholesterol.49 Impaired vasodilation has also been associated with proteinuria.50

Both aging and ESRD are independently associated with exponential increases in mortality from cardiovascular disease (CVD),51 but they exert an additive effect on mortality risk. The high rate of CVD is also a large factor in the high mortality rates seen among older patients with CKD.11 Among patients undergoing cardiac surgery, mortality risk increases even with a 0.2-mg/dl increase in serum creatinine,52 and patients with serum creatinine levels between 1.2 and 2.1 mg/dl before cardiovascular surgery are at increased risk for AKI requiring dialysis.53

The GFR threshold predictive of cardiovascular events and all-cause mortality has not been established. Several studies have shown increased risk with moderate chronic renal insufficiency or preclinical kidney disease in both older and younger patients.43,54–58 Other studies have observed that increasing age attenuates the association of eGFR with mortality.59–61 Consequently, the threshold eGFR at which mortality or cardiovascular risk increases might differ across the age spectrum, although risk for mortality is consistently increased at eGFR <45 ml/min per 1.73 m2 in all age groups. Furthermore, the association between creatinine-based GFR62 and mortality differs slightly from that seen with cystatin C–based GFR (Figure 3).

Standard risk factors for CVD do not fully explain the increased risk for CVD seen in patients with CKD.63 Urinary albumin concentration, which is a strong risk factor for progression to ESRD64 and increases in prevalence with age,65 is an independent risk factor for CVD.66,67 GFR and albuminuria are poorly correlated, but they exert an additive effect on CVD outcomes,67–70 even in patients aged ≥70 yr.68 Microalbuminuria, defined as 30 to 300 mg/g albumin in the urine, has been associated with left ventricular abnormalities,71 increased inflammatory markers,72 insulin resistance,73 endothelial dysfunction,50,74 and abnormalities in fibrinolytic and coagulation pathways. Antihypertensive drugs used to reduce microalbuminuria might be associated with a lower risk for incident cardiovascular events.75,76

Vascular calcification and hyperphosphatemia are also independent risk factors for CVD in patients with CKD,77–80 as demonstrated by mechanistic data in animal81 and cell culture models.82 CKD bone mineral disorder is characterized by phosphorus, calcium, vitamin D, and pH values associated with abnormal bone turnover and vascular calcification. Higher phosphorus levels, even within the “normal reference range,” also might be associated with all-cause mortality in the general population.83,84 The osteoblastic transcription factor osterix might participate in the causative pathway involving phosphorus, vascular calcification, and CVD.82

Oxidized LDL correlates with increased mortality risk in dialysis patients85 and might play a role in endothelial injury.86 Vascular dropout occurs in patients with hypertension and even more so in patients with CKD,87 and endothelin production increases in animal models of CKD.88 Treatment with an endothelin inhibitor prevents podocyte injury, proteinuria, and glomerulosclerosis in animal models.88,89

Initiation of maintenance dialysis for ESRD is associated with significant improvement in BP and left ventricular mass,90 but common approaches toward management of CVD, including statins91 or reductions in calcification and phosphorus metabolism,92 may not be as successful in patients with CKD or ESRD. Although anemia is a risk factor for CVD in patients with CKD,93,94 data from recent randomized trials of erythropoietin treatment suggested that targeting specific hemoglobin levels might not be appropriate for treatment or prevention.95

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CKD, COMORBID CONDITIONS, AND AGING

Frailty is more prevalent among older patients with CKD than it is among those with normal kidney function.96 Although a large proportion of dialysis patients are frail even at younger ages, frailty is common among older dialysis patients.97 The natural history of frailty in patients with CKD and the factors that increase risk are not known, which has stymied the identification and evaluation of interventions to address frailty in patients with CKD.

Physical activity decreases with age, particularly among patients on dialysis,98 and mortality risk during 1 yr is higher among sedentary than among nonsedentary dialysis patients.99 In older patients, physical performance–based measures predict falls, hospitalizations, length of hospital stay, discharge to a nursing home, or mortality.100 The significance of these measures for CKD or ESRD is not known. Low physical functioning, measured by objective laboratory tests or self-reported measures, predicts survival in ESRD.101–103 Sarcopenia is a significant problem in CKD and may contribute to low functioning and frailty. Although muscle size is comparable between healthy control subjects and dialysis patients, the proportion of contractile tissue in dialysis patients is only two thirds that in control subjects.104

Exercise training improves exercise capacity and physical performance–based measures,105 as well as CVD-related factors,106–110 protein uptake into skeletal muscles,111 dialysis efficiency,112 and quality of life.113 Cardiovascular training improves peak oxygen uptake and muscle strength in patients with CKD,114 and resistance training increases muscle fiber size, improves muscle strength, and reduces inflammation.115 Thus, nephrology practice should include assessments of physical function and interventions to address low function in patients with CKD.

Although age-related criteria for defining anemia in older people are debated, anemia is highly prevalent among older people and associated with depression and impaired physical and cognitive function.116 The prevalence of anemia is much higher117,118 among patients with a GFR <30. The aging process may have an inflammatory component, and some clinical markers of inflammation-associated anemia overlap with those of iron deficiency. The role of inflammation in CKD-associated anemia in older people is poorly understood.

CKD is associated with an increased risk for cognitive decline and dementia.119–121 Accumulating data120,122 suggest that the prevalence of cognitive impairment begins to increase early in CKD, as GFR drops <60 ml/min per 1.73 m2. Other CKD markers, including increased cystatin C and microalbuminuria, have also been linked with an increased risk for cognitive impairment.123,124 Thirty percent of dialysis patients overall and up to 70% of dialysis patients aged ≥55 yr have moderate to severe impairment.125,126 Cerebrovascular disease, both clinical (e.g., stroke) and subclinical, might play a large role in the development of cognitive impairment among patients with CKD and ESRD.119,127 Other factors that might contribute to cognitive impairment include anemia128; accumulation of uremic toxins; and, in patients with ESRD, a dialysis delirium–like syndrome that, over time, might have deleterious effects on cognition.129

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GOALS FOR CLINICAL MANAGEMENT IN OLDER PATIENTS WITH CKD

Among older patients with CKD, mortality and cardiovascular events are more common than progression to ESRD.56,130–132 Studies suggest that hypertension therapy that preserves cardiac muscle might not prevent ESRD or a 50% decline in GFR.56,130,131,133 Thus, care for patients with CKD should focus more on reducing CVD risk than on progression to ESRD. Furthermore, functional outcomes, such as cognition and physical functioning, might be more meaningful outcomes in older patients with CKD. More study is needed to determine how CKD affects independent function, and interventions should be developed and assessed in terms of maintaining active life expectancy. Such approaches might facilitate intervention in older patients before disability develops.

The appropriate treatment of older patients with CKD is not clear. Among patients who had CKD and were not referred to a nephrologist, increasing age attenuated the association of serum creatinine with mortality risk, but in a multivariable analysis, reduced eGFR independently predicted death, whereas age did not.134 Other work demonstrated that early referral to nephrology care reduced adverse CKD outcomes.135–138 The effects of multidisciplinary care are also debated. Two studies correlated multidisciplinary care with modest improvements in survival,39,139 but another study showed no differences in kidney function or mortality between patients who received multidisciplinary, intensive care and those who did not.140

The benefits of long-term dialysis in older patients are controversial. Although one study suggested that dialysis improves survival in patients aged ≥65 yr,141 mortality rates are exceedingly high among very old patients who initiate dialysis.141 In one small observational study of patients who were aged ≥75 yr and had stage 5 CKD, those who initiated dialysis survived longer than those who did not; however, among the subgroup with a high number of comorbidities, survival was similar among those treated conservatively and those who initiated dialysis.142

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AREAS OF FUTURE RESEARCH

Potential research questions in the areas of CKD biology, measurement and prognosis, CVD, other comorbidities, and management are listed in Table 1.

The manifestations and prognosis of CKD differ between older and younger adults. Additional studies are needed to delineate age-related differences in the mechanisms and pathways that contribute to progression of CKD and adverse cardiovascular and metabolic events. Randomized clinical trials are also needed to explore novel therapeutic approaches to reduce CVD and mortality in older patients with CKD. More study is needed to determine not only whether aging and CKD mechanisms differ but also how they interact.

Measurement of GFR in representative populations without significant illnesses is needed to determine “normal” GFR and allow development of more accurate estimating equations for older people. Improved methods to estimate GFR in the frail and in sick older patients will likely require new filtration markers or combinations of markers, particularly those not affected by muscle or disease. In addition, more study is needed to determine the length of time needed to see decreases in the numbers of glomerular and functional tubular cells.

Additional information on CKD complications would facilitate greater understanding of the overall impact of CKD on the patient. Markers other than GFR, such as AKI markers, are needed to assess patients’ risk and to measure kidney damage more directly. Although proteinuria already has been identified as an important risk factor, other risk factors might include microalbuminuria, erythropoietin/anemia ratios, advanced glycation end products and their receptors, vitamin D metabolism, and serum phosphate. The identification of new measures that are clearly in the causal pathway for CKD and ESRD would be useful, as would studies including the long-term follow-up needed to distinguish true kidney disease from normal GFR declines in older people.

How age influences vascular biology and cardiovascular risk factors and how these changes contribute to CKD-associated increases in risk for CVD are not clear. The connection between CKD and other comorbidities, such as frailty and cognitive impairment, and how age influences these connections should be explored further. Further study is also needed to determine how age affects interventions to prevent or reduce these comorbidities in patients with CKD.

Geriatricians, internists, general family practitioners, and nephrologists should work together to optimize care for older patients with CKD and ESRD. Recent epidemiologic evidence correlated serum polyunsaturated fatty acid levels, which have a strong anti-inflammatory effect,143 with slower rates of decline in creatinine clearance in an aging population (Figure 4).144 How target BP and other surrogate markers can be used to preserve patients’ ability and independence, as opposed to preventing progression to ESRD, should be studied further. More study is also needed to determine how to identify patients most likely to benefit from dialysis, reduce the number of inappropriate dialysis starts, and aid patients and family members in decision-making regarding dialysis. More clinical trials are needed, particularly those that include physical and cognitive function as outcomes.

Figure 4.

Polyunsaturated fatty acids (PUFAs) and creatinine clearance. Higher PUFA serum levels have been associated with shallower declines in creatinine clearance in an aging population.144 n-3 PUFAs seem to have the greatest effect (Table 2). Redrawn from ref. 144.

Table 1.

Questions for future research

Table 2.

Relationship between change in creatinine clearance during 3 yr and total PUFAs at baseline144a

  • Copyright © 2009 by the American Society of Nephrology

REFERENCES

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  14. Breiling A, Sessa L, Orlando V: Biology of polycomb and trithorax group proteins. In: International Review of Cytology: A Survey of Cell Biology, edited by Kwang W, San Diego, Academic Press, 2007 , pp 83– 136

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Dialysis and Fatigue: Implications for Nurses – A Case Study Analysis

Ann Horigan, MSN, RN, CNE, Doctoral Candidate, Judith Rocchiccioli, PhD, RN, Professor of Nursing, and Donna Trimm, DNS, RN, Assistant Professor of Nursing

Medsurg Nurs. Author manuscript; available in PMC 2012 Aug 8.

Published in final edited form as:

Medsurg Nurs. 2012 May-Jun; 21(3): 158–175.

PMCID: PMC3414425

NIHMSID: NIHMS383261

See other articles in PMC that cite the published article.

Abstract

Fatigue is one of the most common symptoms experienced by patients receiving dialysis. When patients with chronic kidney disease (CKD) and end-stage renal disease are admitted to acute care settings, they require management of their often profound fatigue. CKD, renal pathology, and renal fatigue are examined in relation to a case study.

Caring for patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) challenges all health care providers. While a great deal of the maintenance care for patients with ESRD occurs at hemodialysis centers in the community, admission of affected patients to the hospital requires nurses to demonstrate knowledge of renal disease and renal pathology, and expertise in the identification and management of the debilitating fatigue that often impacts patients’ quality of life. Research suggests fatigue is one of the most common symptoms experienced by patients receiving dialysis (Jablonski, 2007; Weisbord et al., 2005). Prevalence of fatigue ranges from 60% to 97% (Murtaugh, Addington-Hall, & Higginson, 2007; Weisbord et al., 2005). Assessment and management of fatigue thus are important in improving clinical outcomes and quality of life for patients receiving dialysis.

Several factors may be associated with fatigue in patients receiving dialysis. These include depression (Leinau, Murphy, Bradley, & Fried, 2009; Liu, 2006), female sex (Liu, 2006; O’Sullivan & McCarthy, 2007), and anemia (Williams, Crane, & Kring, 2007). While the cause of renal fatigue remains unclear, it is clearly problematic. An understanding of how patients receiving dialysis describe and experience fatigue, the similarities and differences in fatigue experienced by patients receiving hemodialysis and peritoneal dialysis, and knowledge of the cultural differences in the experience of fatigue are critical in order to assess it accurately and intervene appropriately. Chronic kidney disease, renal pathology, and renal fatigue are discussed and related to the case of Mary R.

Overview of Renal Pathology and Renal Disease

Incidence and Prevalence of End-Stage Renal Disease

End-stage renal disease, the last stage of chronic kidney disease, is a common chronic illness that is increasing in incidence and prevalence. The incidence of ESRD in 2006 was 360 per million, an increase of 2.1% since 2005. Patients receiving dialysis now live longer, with the mortality rate decreased by 10%. Additionally, the rate of kidney transplantation has not kept pace with the incidence of ESRD, and increasing numbers of patients with failed transplants are returning to hemodialysis. In 2006, the number of new patients receiving dialysis or transplant in the United States exceeded 100,000; over 350,000 patients were receiving dialysis (National Institute of Diabetes and Digestive and Kidney Disease [NIDD KD], 2008). As the number of affected patients continues to grow and medical advances allow patients to lead longer lives, symptom management becomes an important part of care for patients receiving dialysis.

Overview of Chronic Kidney Disease

The current National Kidney Foundation (NKF) guidelines define chronic kidney disease as irreversible kidney damage or decreased kidney function for at least 3 months (Castner, 2010; Murphy, Jenkins, Chamney, McCann, & Sedgewick, 2008; NKF, 2002), which ultimately affects all kidney functions. The nephrons, the functional unit in the kidneys, lose their ability to filter wastes and extra fluid, creating fluid and electrolyte imbalances. Loss of kidney function occurs slowly, with the kidneys initially adapting well to the underlying causes of kidney damage (Castner, 2010). Symptoms of kidney failure, such as alterations in salt and fluid balance, protein-urea, and anemia, do not appear until renal function decreases significantly (Molzahn & Butera, 2006).

The severity of kidney disease is determined by the individual’s glomerular filtration rate (GFR), which is the best measure of the overall health and function of the kidneys (Kinzner & Hain, 2007). The glomerulus is a collection of capillaries in the nephron, and the glomerular membranes act as the filtering mechanism for wastes and fluid. The rate at which the glomerulus filters wastes and fluid is an indication of its health. A GFR of 90 mL/minute per 1.73 m2 or higher is considered normal. A decreasing GFR signifies increasing kidney damage. A GFR less than 60 mL/minute per 1.73 m2 indicates a loss of approximately half the kidney’s normal function in an adult. As the GFR continues to decrease in kidney failure, occurrence of complications related to kidney disease, such as anemia, bone disease, and malnutrition, increases (Castner, 2010; NKF, 2002).

Five stages of chronic kidney disease have been identified (NKF, 2002) (see Table 1). A healthy kidney is able to differentiate between protein and wastes when filtering the blood. A damaged kidney is unable to do this, and thus protein is excreted inappropriately along with the wastes in the urine. The early stages of CKD are characterized by protein-urea and decreasing GFR. Many complications, such as anemia and bone disease, become evident as CKD progresses (NKF, 2011). During the later stages of CKD, continued management of complications as well as preparation for renal replacement therapy (dialysis or transplantation) are important. When the kidneys have failed completely and irreversibly, renal replacement therapy is necessary to sustain life. At this point, most patients experience symptoms of uremia (NKF, 2002), including decreased appetite, malnutrition, drowsiness, shortness of breath, and palpitations (Murtaugh et al., 2007).

TABLE 1

Stages of Chronic Kidney Disease

Common Causes of Chronic Kidney Disease

One of the most common causes of CKD is diabetes. Other causes include hypertension and glomerulonephritis (NIDDKD, 2010). When a patient has diabetes, the glomerulus is damaged. The exact mechanism of damage is unknown, but the most likely cause is denaturization of proteins caused by high blood glucose. This leads to a thickening of the membranes of the capillaries in the glomerulus that eventually results in scarring and stenosis of the capillaries (Bakris, 2011; Redmond & McClelland, 2006). The stenosis of glomerular capillaries causes an inability to filter wastes properly, and contributes to fluid and electrolyte imbalances in the body.

Another common cause of CKD is untreated hypertension (NIDDKD, 2010). Normal regulatory processes in the kidney are compromised when the systemic blood pressure remains elevated over a long period of time, as in untreated or inadequately treated hypertension. First, untreated systemic hypertension causes damage to the systemic blood vessels by causing them to thicken and strengthen to withstand the increased pressure. These vessels become permanently narrowed due to thickening. The arteries that feed the kidneys respond to high systemic pressures by constricting, thus decreasing the amount of blood circulating through the kidneys. The kidneys in turn interpret this as a deficit in blood flow. In response, renin and aldosterone secretion are stimulated, leading to sodium and water retention in order to increase blood volume. This response only perpetuates the systemic hypertension (Hill, 2008). Over time, as the kidneys lack appropriate perfusion due to arterial constriction, nephron damage results and efficient filtration of water and wastes is lost.

Glomerulonephritis is another common cause of kidney failure (NIDDKD, 2010). Cellular, immunologic, and inflammatory factors that damage the glomerulus (capillaries in the nephron) often are triggered by changes in tissue or infections (Redmond & McClelland, 2006). Glomerulonephritis can range from mild to severe, and damage to the glomeruli differs from person to person. Nephrons are destroyed in a predictable pattern that begins with cellular infiltration and exudative reactions. Damage then progresses to macrophage infiltration with differing levels of parenchymal cell proliferation. These changes eventually lead to sclerotic structural changes in the nephron, damaging it and resulting in an inability to function properly (McCance & Huether, 2010).

Complications of Chronic Kidney Disease

As kidney function declines, multiple body systems are affected detrimentally by the accumulation of toxins in the blood (uremia) (Alper, Shenava, & Young, 2010). These symptoms usually begin to appear in stage 3 kidney disease and worsen as kidney function declines to ESRD. The kidneys lose the ability to excrete electrolytes, causing serum electrolyte imbalances. As serum phosphate increases, the additional phosphate binds with calcium and a decrease results in serum calcium levels. The body responds by pulling calcium from the bone to maintain appropriate serum calcium (McCarley & Arjomand, 2008). Bone demineralization, pain, and spontaneous fractures thus can occur as kidney disease progresses (NIDDKD, 2009a).

Serum potassium continues to rise, even to critical levels, as CKD continues. Hyperkalemia can result in muscle weakness, increased neuromuscular irritability manifested as tingling in the fingers and lips, restlessness, stomach cramping, and diarrhea. At critically high levels, potassium can cause changes in the EKG complex, often in the form of bradyarythmias. Conduction is slowed through the heart muscle, resulting in prolonged PR intervals and a widening QRS complex, often resulting in ventricular fibrillation or cardiac arrest (Putcha & Allon, 2007).

Erythropoietin secretion is controlled by the kidneys and is compromised as kidney failure progresses. Red blood cell production in the bone marrow then decreases, resulting in anemia. Additionally, the red cells that are produced have a shortened life span due to the build-up of toxins in the blood (Alper et al., 2010).

Another complication of CKD is impaired creatinine and urea clearance (Broscious & Castagnola, 2006). Creatinine is released constantly from the muscle. As the GFR decreases, the serum creatinine values increase. High serum creatinine is an indicator of kidney dysfunction (NIDDKD, 2009b). Urea, the end product of protein metabolism, also increases as the kidneys fail. Retention of urea can cause loss of appetite, nausea, vomiting, and pancreatitis (McCance & Huether, 2010).

Dialysis in Chronic Kidney Disease

Complications of CKD worsen as renal failure progresses. Eventually, hemodialysis (HD) or peritoneal dialysis (PD) must be initiated to replace kidney function in most patients. Approximately 100,000 new patients began receiving HD in the United States in 2006; over 325,000 patients received hemodialysis treatments that year. These numbers accounted for approximately 92% of the total dialysis population. Patients on PD accounted for 6.2% of new dialysis cases, and 8.2% of the total dialysis cases (NIDDKD, 2008).

The debate continues over which treatment modality is more effective and has better outcomes. No conclusive evidence indicates one form of dialysis is better than the other (Lee, Sun, & Wu, 2009). Many factors must be considered when choosing a dialysis modality, including physician recommendation, patient preference, and availability of the treatment (Shahab, Khanna, & Nolph, 2006). Dialysis modality selection often is based on the patient’s clinical and social status (Shahab et al., 2006). In general, patients who are younger and adherent to therapy; have some residual renal function, cardiovascular disease, and family or social support; and are independent in self-care are more likely to be recommended for peritoneal dialysis. Peritoneal dialysis is contraindicated in patients who have ostomies, or a ventro-peritoneal shunt. Older adults, obese persons, and individuals without social support also are less likely to be recommended for peritoneal dialysis (Shahab et al., 2006).

Fatigue in ESRD

The need to identify and assess fatigue in patients receiving dialysis is vital to patient health and quality outcomes. Fatigue frequently is unrecognized and therefore under-treated (Jhamb, Weisbord, Steel, & Unruh, 2008). Physical exercise, epoetin use, and L-carnitine infusion have all been used successfully to alleviate fatigue in patients receiving hemodialysis. Physical exercise also can help with the physiological and functional deterioration that can result from aging, illness, and sedentary lifestyle (Gordon, Doyle, & Johansen, 2011; Kosmadakis et al., 2010), all of which can contribute to dialysis-related fatigue.

Trials have shown physical exercise is safe for patients on dialysis, but exercise is not offered or recommended routinely for patients receiving dialysis. While physical exercise may be safe and help alleviate fatigue, few patients participate in these programs when offered, and many often drop out after beginning (Kosmadakis et al., 2010). Additionally, exercise may not be appropriate for a select group of patients receiving dialysis. Patients with functional limitations, poor cardiac health, or bone disease, and persons who are hemodynamically unstable during dialysis should not be considered for participation in exercise programs (Bayliss, 2006).

Epoetin is used regularly to combat anemia, a common cause of dialysis-related fatigue. Some patients do not respond well to epoetin therapy (Bamgbola, 2011) as demonstrated by no increase in their hemoglobin and hematocrit levels. Unfortunately, increasing doses of epoetin to help reduce anemia in these patients has proven detrimental, as it increases their risk for cardiovascular and cerebrovascular events (Drueke et al., 2006; Singh et al., 2006). Therefore, epoetin use may not be successful in alleviating fatigue in all patients receiving hemodialysis.

Another intervention to lessen the effects of fatigue is the use of L-carnitine, which is important for appropriate muscle function. Patients receiving hemodialysis are deficient in L-carnitine, and supplementation has proven effective in ameliorating dialysis-related fatigue, particularly in patients who are unresponsive to epoetin therapy (Lynch et al., 2008). The Centers for Medicare and Medicaid Services (CMS) only reimburses for L-carnitine used for epoetin-resistant anemia and intradialytic hypotension. Continued use of the drug is not covered if there has been no improvement in anemia or hypotension 6 months after treatment initiation (CMS, 2011).

Interventions that have been successful in alleviating fatigue may not be appropriate or safe for all patients. A significant need exists for the management of fatigue in order to reduce its impact on the lives of patients receiving hemodialysis. Nurses are in a strategic position to assess dialysis-related fatigue and help patients develop strategies to manage its effects. The following case study describes a patient admitted to the medical-surgical unit for management of hyperglycemia. The assigned nurse meets the patient for the first time immediately after her dialysis session. Patient symptoms, assessment of fatigue, evaluation of patient medications and lab results, and nursing interventions are discussed.

Case Study

Mrs. R. is a 33-year-old African-American female with type 1 diabetes, cataracts, and ESRD who has received hemodialysis for 2 years. She was admitted in the morning for hyperglycemia and management of medications, and was taken to dialysis prior to her arrival on the medical-surgical unit. After arrival to her room, she is lethargic, replies to repeated questions slowly, and slurs words at times. She demonstrates delayed response to commands with appropriate one-word answers. When asked how she feels, she responds, “I’m so tired. Please just leave me alone.” Dialysis removed 5 kg of fluid. Vital signs include oral temperature 98.3° F, blood pressure 88/40 mm Hg, pulse 96 beats per minute, respirations 12 breaths per minute, and oxygen saturation 97% on room air. See Table 2 for the patient’s routine medications, and Table 3 for current laboratory results. The patient’s height is 5′5″ and weight 145 lbs. Mrs. R.’s history includes childhood non-adherence to diabetic diet and medications, which contributed to her current health status. She lives with her mother, receives disability payments and is unemployed, and has a 9-year-old daughter. She is unable to drive due to poor vision.

Nursing Management

Fatigue Assessment

Mrs. R. presents as a typical patient with ESRD. Her fatigue is the result of both physiological and psychological influences as well as dialysis treatment inadequacy. When questioned further about her fatigue, the patient explains, “It’s ok; I’m always like this after dialysis.” Emergency interventions are not needed, but assessment of the fatigue should be completed. A simple visual analogue scale could be used to establish Mrs. R.’s baseline perception of fatigue; the scale includes a 100 mm line anchored at the left end with No Tiredness and at the right end with Complete Exhaustion. This type of measurement is a reliable assessment of fatigue in patients receiving dialysis (Brunier & Graydon, 1996; Williams et al., 2007), and can be performed quickly in the clinical setting.

Evaluate How Fatigue Impacts Patient’s Daily Living

Because fatigue can be extremely debilitating, assessing its effects on Mrs. R. is important in helping her improve her quality of life. Assessment can include asking the patient to describe her daily routine or keep a journal for review with the nurse at the dialysis unit at a later date. Mrs. R. explains that she sleeps for 4–6 hours after dialysis because she is completely exhausted. She is unable to work due to her extreme dialysis-related fatigue, and therefore receives disability payments. She lives with her mother to save rent money and receive help from her mother in caring for her 9-year-old daughter. Reviewing a time or event when fatigue was at its greatest intensity may help with planning interventions to minimize fatigue. Mrs. R. states that at times, particularly on dialysis days, she is unable to fix her daughter meals or help with her homework. The nurse can help Mrs. R. identify her support systems and collaborate with her to identify ways she can incorporate these support systems into her life. For instance, could Mrs. R.’s mother help her granddaughter with homework after school and cook evening meals? If Mrs. R. is able, making meals on her non-dialysis days and refrigerating or freezing them will help her mother and make food available when she is unable to prepare it.

Evaluating Laboratory Results and Medications

Irregularities in laboratory results and medication side effects may contribute to Mrs. R.’s fatigue. Evaluation of the patient’s laboratory results reveals serum sodium, calcium, phosphorus, and magnesium are all within normal range albeit slightly low. Her slight hypokalemia could be related to the stress of dialysis. Dialysis can return many electrolyte values to normal ranges, but also may remove insulin. Her serum glucose is elevated, which can lead to cell dehydration due to osmotic pressure in the extracellular fluid. She may need regular insulin for glucose correction. The presence of insulin affects protein (amino acids), glucose, potassium, magnesium, and phosphate uptake by the cells. Without insulin, the cells do not have the adequate glucose and amino acids to function, and weakness and/or fatigue can result. Mrs. R.’s protein and albumin values are already low, which also can cause edema. This in turn can lead to swelling and weight gain, causing tightly fitting clothes and shoes that can affect movement and increase feelings of fatigue. Dialysis removed 5 kg of fluid, which most likely included toxic levels of electrolytes, a small amount of blood, and other waste products. Mrs. R.’s hemoglobin and hematocrit are low, often typical for a patient in ESRD. With low protein and albumin, she also may lack elements to produce red blood cells. The kidney’s ability to make erythropoietin, which stimulates red blood cell production, is compromised and could contribute to Mrs. R.’s fatigue. Epoetin has been prescribed to supplement her kidneys’ failing ability to produce erythropoietin. Supplemental iron and vitamin B12 also may be given. By increasing hemoglobin, patients may experience less lethargy.

Mrs. R. also takes alprazolam (Xanax®) twice a day as needed for restless leg syndrome. This drug also may be contributing to daytime sleepiness and fatigue. The nurse should encourage Mrs. R. to investigate medications other than benzodiazapines for restless leg syndrome with her care provider to alleviate some of the fatigue. Mrs. R. also takes the anti-depressant venlafaxine (Effexor®). Depression has been associated with dialysis-related fatigue in several studies (Kim & Son, 2005; Leinau et al., 2009; Liu, 2006; McCann & Boore, 2000), and it is important that depression is identified and treated. Treating depression could help lessen fatigue levels in patients receiving dialysis. In Mrs. R.’s case, the nurse should ask if she believes her current medication is treating her depression effectively. If depression is under-treated, her fatigue may persist.

Teaching the Patient

After examining the patient’s laboratory results and medications, the nurse should teach the patient the importance of diet, exercise, and healthy sleep routines to decrease symptoms of fatigue. Diet is critically important for patients receiving dialysis. Mrs. R.’s diet should be low in potassium, sodium, and phosphate, and her fluid intake restricted. She needs adequate calories as well as moderate intake of complete protein, low fat, vitamins A and C, and carotinoids. Over time, patients affected with ESRD tend to become malnourished, so aggressively restricting their protein intake may be more detrimental to their health (Arora & Verrell, 2009). Because Mrs. R. also has diabetes, she needs high-complex, fiber-rich carbohydrates with low glycemic index and load necessary for calorie intake (Taillefer, 2008). Collaborating with a registered dietitian and designing menus for Mrs. R. may decrease the burden of planning meals.

Exercise is another essential component of patient teaching. Mrs. R. has none of the previously mentioned complications that would prevent her from participating in exercise. Collaborating with her in planning simple exercises is a must. Suggesting an exercise routine during the dialysis appointment can encourage adherence as well as socialization with others. Thirty minutes of low-intensity exercise, such as modified yoga, should be the goal (Yurtkuran, Alp, Yurtkuran, & Dilek, 2007). Some exercise plans include 30 minutes of cycling with devices adapted to the patient’s bed during dialysis (Quzouni, Kouidi, Sioulis, Grekas, & Deligiannis, 2009). Exercise can lead to significant improvements in the patient’s physical abilities, as well as decreased perception of pain, fatigue, depression, and insomnia.

Sleep disorders, such as apnea and restless leg syndrome, are common among patients receiving dialysis. In addition to management with medication, the patient may need to make behavioral changes, such as staying awake during dialysis and eliminating caffeine, nicotine, and alcohol intake. Some units provide overnight dialysis, which might be helpful. Sleep studies should be performed for sleep apnea and restless leg syndrome with the appropriate interventions of continuous positive airway pressure usage or medications (Unruh, 2008).

Evaluating this patient’s sleep and her participation in routine exercise can improve feelings of depression as well. Her loss of self, a change of status in her family, the inability to care for her daughter, her physical losses, and a loss of a social network can contribute to depression. The nurse should help the patient identify support people and local support groups, listing ways she has coped with crisis in the past. The nurse also can help her establish goals to give her a sense of hope. She may need a professional therapist, guidance in time management, and a social worker to find resources for caring for herself and daughter.

Conclusion

Fatigue is a real problem for patients receiving dialysis. While the specific cause of fatigue remains unknown, multiple conditions are associated with its occurrence. Nursing assessment of fatigue is important in the care of patients receiving dialysis in order to improve their quality of life. Nurses are in an excellent position to review patients’ medications and laboratory results, and collaborate with patients to determine how to use their support systems and individual strengths to help alleviate the effects of fatigue.

Acknowledgments

This project was supported by a grant from the National Center for Research Resources, Duke CTSA, NIH, grant number 1TL1RR024126. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH.

Contributor Information

Ann Horigan, Duke University School of Nursing, Harrisonburg, VA.

Judith Rocchiccioli, James Madison University, Harrisonburg, VA.

Donna Trimm, James Madison University, Harrisonburg, VA.

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