+1 (208) 254-6996 [email protected]

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 580


Don't use plagiarized sources. Get Your Custom Essay on
Refer To Question
Just from $13/Page
Order Essay

Special Article

Chronic Kidney Disease and Pain Perception

Theodora Kafkia, RN, MSc, PhD Clinical Lecturer, Department of Nursing, Alexander Technological Educational Institute of Thessaloniki, Greece

Katri Vehvilainen-Julkunen, RN, RMW, PhD Professor, Department of Nursing Sciences, University of Eastern Finland, Kuopio, Finland

Sofia Zyga, RN, MSc, PhD Associate Professor, University of Peloponnese, Faculty of Human Movement and Quality of Life Sciences, Nursing Department, Sparta, Greece

Despina Sapountzi-Krepia, RN, RHV, PhD Professor, Department of Nursing, Frederick University, Nicosia, Cyprus

Correspondence: Theodora Kafkia, A.Nastou 12, 54248, Thessaloniki, Greece


Background: Pain is considered to be a challenge for healthcare professionals. It is a multidimensional phenomenon affecting everyday life and functionality. People with renal problems, acute or chronic, are experiencing various types of pain either due the illness itself, adverse effects or due to clinical interventions. Objectives: The aim of the present study was to present the different theories regarding pain and to familiarize readers with the various types of pain experienced by patients and in particular patients with renal problems. Methods: A comprehensive literature search was undertaken regarding pain, particular in pain experienced by patients on different stages of Kidney Disease and on various types of Renal Replacement Therapies. Results: Several explanatory theories regarding pain have been published by scholars since the mid-1960s. According to researchers brain is dictating how much pain a person feels caused by a harmful stimulus. In other words, if the route from peripheral nerves to the central nervous system is occupied by positive and relaxing thoughts pain could not be experienced, as only one impulse can travel at a time. In renal patients pain can be attributed to the primary kidney disease or comorbidities, such as Diabetes Mellitus and Cardiovascular Disease, and/or dialysis. Conclusion: Renal patient’s high levels of pain could be effectively and individually assessed and managed if healthcare professionals are more familiarized with different types and aetiology of pain, as well as the current ways of treatment. Through curriculum and continuous education, clinicians can choose from a cascade of treatments aiming at maintaining the quality of life of renal population.

Key words: Chronic Kidney Disease, Theories of Pain, Aetiology of Pain


Despite the advances in the medical and health- related sciences over the last century, pain continues to be seen as an “intriguing puzzle” and a challenge for healthcare professionals (Madjar 1998, Greek Nurses Code of Ethics 2001, Ferrell & Coyle 2008, IOM 2011). Pain is a multidimensional phenomenon with physical, psychological as well as social components often determined by personal beliefs and cultural values (Turk & Okifuji 2002, IOM 2011, Vaajoki et al. 2013). It is a subjective bodily response to

physical and psychological stressors imposed to the individual by his/her health status and the clinical environment (Mann & Carr 2008, Wilkstrom et al. 2014). It is associated with problematic interpersonal relationships, psychological distress and depression, activity limitations in work, family and social life and, quite often, excessive use of health care services (Dysvik et al. 2004, Davison 2007a, Heiwe & Bjuke 2009, Hogan & Norby 2010). Pain warns the human body for any health-threatening situations and is considered to be a major defense mechanism of the body. Furthermore, it is

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 581


recognised as an important part of the psychosocial impact of illness and the adoption to the chronic sick role.

Kidney Disease can be manifested either as an acute health problem (Acute Renal Failure, ARF) or as a result of a long procedure of deterioration of renal function (Chronic Kidney Disease, CKD). To the best of our knowledge, in the literature there is limited information on renal patient’s pain perception and management. Thus, the aim of the present paper was to present the different theories regarding pain and to familiarize readers with the various types of pain experienced by patients and in particular patients with renal problems.


McCaffery in the late 1960s was the first to describe pain as “whatever the experiencing person says it is, existing whenever she/he says it does”. This early definition emphasizes in the subjective nature of pain. The patient, not the healthcare professional, is the authority on pain and her/his self-report is the most reliable indicator. A decade later, in 1979, the International Association for the Study of Pain (IASP) stated that “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey & Bugduk 1994). Localisation, type and intensity of pain vary greatly from person to person.

Theories of pain

Several explanatory theories regarding pain have been published by scholars. In 1965, an innovative theory about pain was proposed by Melzack and Wall, which is still updated by further research (Wall & Melzack 1994, McMahon et al. 2013). According to this theory, only one impulse (signal) can travel up the spinal cord to the central nervous system at a time. If positive and relaxing thoughts are occupying the route, then the sensations that activate pain cannot reach the brain to trigger a perception of pain. Another significant theory is the Gate Control Theory, which states that in substantia gelatinosa (dorsal horn of the spinal cord) pain can be modified by the stimulation of non-pain

ascending or descending fibres. Substantia gelatinosa plays the role of a “gate” modulating the afferent signals before they ascend to the cerebral cortex. On the other hand, feelings like anxiety, excitement and anticipation may open the gate, increasing the perception of pain (Wall & Melzack 1994, Jurf & Nirschl 1993, Ackerman & Turkoski 2000, Chang et al. 2015).

Furthermore, during tissue damage, cells are breaking down, resulting in the release or production of chemicals-mediators (bradykinin, histamine, serotonin, prostaglandins and cytokines), which react with each other and on nerve endings, sending signals from there to the dorsal horn of the spinal cord and up the cortex of the brain, where the perception of pain takes place (Pham et al. 2009).

Another theory coming from Melzack (1999), proposes that a neural network, “the body-self neuromatrix”, is included in the brain translating painful stimuli. Although genetically determined, it accepts cognitive, emotional, sensory and visual inputs during a persons’ life in order to create the specific pattern of individual’s pain perception (the neurosignature). Neuromatrix Theory is used to explain why some individuals develop chronic pain, while others do not (Melzack & Wall 2003).

In conclusion, all the different theories stress that the brain is dictating how much, if any, pain a person feels from a potentially harmful stimulus. Acute, as well as chronic pain is addressed in the context of Gate Control Theory.

Classification of Pain

Pain can be encountered in many types. The most common types of pain are presented in Figure 1. Acute pain is considered to be the pain of recent onset, usually transient in nature. It is viewed as a “complex, unpleasant, experience with emotional and cognitive, as well as sensory, features that occur in response to tissue trauma” (Chapman & Nakamura 1999). Acute pain is caused by tissue damage and is often associated with some degree of inflammation. Generally, it warns the body of the likelihood or the extent of injury, and it subsides as the healing process moves forward.

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 582


Figure 1. Pain classification.

Chronic pain is defined as “pain that has lasted six months or longer, is ongoing, is due to non- life-threatening causes, has not responded to currently available treatment methods, and may continue for the remainder of the patient’s life” (Merskey & Bogduk 1994). Usually, it persists beyond the course of an acute illness/injury and lasts beyond the healing process. It is associated with a pattern of recurrence over months or years (Thienhaus & Cole 2002, Turk & Okifuji 2001) and excessive use of health care services (Davison 2005).

In addition, chronic pain can be described as a persistent feeling that “disrupts sleep and normal living, ceases to serve as a protective function, and instead degrades health and functional capability” (Chapman & Stillman 1999). Moreover, chronic pain can be caused by injury, malignancy, or other non-life-threatening conditions, such as arthritis or neuropathies, and can be neuropathic and/or nociceptive. It can also be of unknown cause, idiopathic pain.

As presented in the figure 1, another type of pain is Neuropathic pain which has been defined as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory system” (Treede et al. 2008). It can be attributed to autonomic dysfunction or associated with vascular occlusion or nerve involvement either in the central or the peripheral nervous system, and it is characterised as burning or lancinating (Turner et al. 2007, Pham et al. 2009). Alas, this type of pain does not provide a protective benefit, but instead precipitates ongoing suffering.

Direct stimulation of peripheral sensory neurons called nociceptors (A-δ and C), cause Nociceptive pain. A type of pain associated with tissue injury or inflammation, and excited by endogenous chemical substances. Nociceptors receiving input of pain from internal organs are responsible for visceral pain which is deep, dull and of vague localisation, whereas those receiving input from outer body tissues are responsible for somatic pain. Somatic pain according to its origin can be further categorised as superficial (cutaneous) or deep (Kurella et al 2003).

Life-threatening conditions, such as cancer, can produce malignant or cancer pain. This form of pain can be caused either by the disease itself (tumor compressing nerves, blood vessels or organs) and/or by painful diagnostic procedures, such as biopsies, chemotherapy or radiation. For some researchers, however, malignant pain is included in acute or chronic pain (Turk & Okifuji 2001).

Finally, psychogenic pain is caused by emotional, psychological or behavioral factors. Headache, back pain and stomachache can be regarded as psychogenic. A kind of pain which cannot be attributed to any known cause can be characterised as psychogenic. Most of the times, it reflects inability to diagnose a medical situation or it is due to inadequate analgesic management (Melzack & Wall 2008).

Chronic Kidney Disease and pain perception

Patients with renal problems experience pain, acute and chronic, quite often. Irrespective of its

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 583


aetiology, renal pain is a debilitating condition and often leads to avoidable over-investigation, suboptimal management and poor quality of life, as well as morbidity (Binik et al. 1982, Bailie et al. 2004, Cohen et al. 2007, Davison & Jhangri 2010, Davison et al. 2014).

The prevalence of symptoms such as pain, sleep disturbance, fatigue, and abnormal psychosocial status may be similar to that of diabetes and other chronic medical illnesses such as cancer or Human Immunodeficiency Virus (HIV) (Davison & Jhangri 2005, Murtagh et al. 2007a, Murtagh et al. 2007b, Bouattar et al. 2009, Harris et al. 2012, Gamondi et al. 2013, Cohen & Davison 2015, Zyga et al. 2015). Although patients with Chronic Kidney Disease experience severe disease burden, denial is quite often used as a coping strategy to deny the severity of their illness and its symptoms or adverse effects (Shayamsunder et al. 2005, Weisbord et al. 2005, Cohen et al. 2007, Salisbury et al. 2009).

Renal patients experience pathological pain due to their disease, but also pain generated by diagnostic and treatment procedures or interventions carried out by renal nurses. Such pain is often seen as a side-effect and not a result of insensitive and uncaring staff. Inflicted pain is often both inevitable and necessary in order to provide an accurate diagnosis and appropriate treatment (Madjar 1998, Aitken et al. 2013) and can be affected by the physical and social environment of the hospital, the stage of Chronic Kidney Disease, the impact of treatment (pre- dialysis or dialysis), and the concerns about rehabilitation and returning to a prior status. Nephrologists and renal nurses play an important role in emotional, social, and spiritual support of their patients (Davison 2007a).

Research on Chronic Kidney Disease suggests that patient’s perceptions of physical symptoms, such as pain, are associated with depression and insomnia, which are more important than objective assessments in determining the health- related quality of life of patients with Chronic Kidney Disease and their families (Lindqvist et al. 2000, Shayamsunder et al. 2005, Weisbord et al. 2005, Gamondi et al. 2013, Minasidou et al. 2016, Kafkia et al. 2017). Chronic Dialysis patients are presenting a number of physical and emotional symptoms, including pain, fatigue, anorexia, nausea, pruritus, shortness of breath, muscle cramps, paresthesias, depression, sexual difficulty and sleep disturbance (Mercadante et

al. 2005, Yamamoto et al. 2009, Harris et al. 2012, Zyga et al. 2015).

Researchers have reported that the severity of pain is often at the same magnitude to pain experienced by cancer and HIV positive patients, alas moderate to severe in intensity in 50-80% of haemodialysis patients (Davison 2003, Gamondi et al. 2013, Wu et al. 2015). Furthermore, joint and bone pain secondary to arthritis or renal osteodystrophy was the main cause of pain in long-term haemodialysis patients (Davison 2003, Gamondi et al. 2013). In the cases of Polycystic Kidney Disease (PKD), flank or abdominal pain, acute or chronic, affects almost 60% of the patients and is accompanying renal infection, cyst haemorrhage, renal stone, traction of the kidney pedicle or compression of surrounding structures (Bajwa et al. 2004, Torres et al. 2007, Tellman et al. 2015). Almost half of the Chronic Kidney Disease population (Atalay et al. 2013, Santoro et al. 2013) report Neuropathic pain compared to 7-8% of the general population (Smith et al. 2007, Bouhassira et al. 2008).

A major problem regarding Chronic Kidney Disease patients’ pain is that it is undertreated. Davison (2005) reports that 74% of patients with pain negatively affecting their work had no analgesic prescribed to them. The same researcher in a previous study (Davison 2003) found that 35% of haemodialysis patients with chronic pain were not prescribed any analgesics and less than 10% were prescribed strong opioids. Furthermore, 74% of Chronic Kidney Disease stages 4-5 patients with moderate to severe pain or pain that interfered with their work were undertreated (Bailie et al. 2004, Bulter et al. 2014, Wu et al. 2015).

Aetiology of Pain in Chronic Kidney Disease Patients

There are numerous causes of pain in Chronic Kidney Disease and their manifestations vary. Pain may result from the primary kidney disease, such as Polycystic Kidney Disease (PKD) or Systemic Lupus Erythematous (SLE), or comorbid situations, such as Diabetes Mellitus (DM), Peripheral Vascular Disease (PVD), and Cardiovascular Disease (CVD). There are, also, several other conditions that produce pain and are associated with renal disease (nephrogenic fibrosing dermopathy, secondary hyperparathyroidism, calcific uremic arteriolopathy), or RRT (abdominal distension from PD, steal syndrome from an arteriovenous

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 584


fistula for HD, needle insertion, and muscle cramps) (Davison 2007a, Salisbury et al. 2009, Bagheri-Nesami et al. 2014, Moss & Davison 2015). Furthermore, painful ischaemic neuropathies can be caused by chronic infections, such as osteomyelitis or discitis; complications from central venous catheters used for dialysis or infected arteriovenous fistulas. Finally, pain between the twelfth thoracic (T12) and the third lumbar (L3) vertebra can be caused either by injury to back muscles or the spine, or by renal problems (Manias & Williams 2007, Heiwe & Bjuke 2009).

Polycystic Kidney Disease (PKD) is the most common renal hereditary disease, which can be found either as autosomal dominant or autosomal recessive PKD, due to a gene mutation or defect. The prevalence of PKD in Europe and USA is ranging from 1/200 to 1/1000 individuals. PKD is characterised by kidney cyst development and growth resulting in progressive enlargement of them. Pain in patients with PKD can either begin with an acute episode and persist as chronic, or develop gradually and become more severe over time. Either type of pain (acute or chronic) is the source of great frustration and distress for PKD patients (Steinman 2000, Bajwa et al. 2004, Rizk & Chapman 2003, Torres et al. 2007, Shetty et al. 2012, Walsh & Sarria 2012, Savige et al. 2015). During cyst formation or enlargement, the surrounding tissues are compressed, the pedicle of the kidney is pulled and renal capsule becomes swollen (Steinman 2000, Cohen et al. 2006, Torres et al. 2011, Shetty et al. 2012). These mechanisms are the source of chronic and localised pain, usually in the anterior abdominal area (Walsh & Sarria 2012). According to the researchers, afferent fibers from the renal capsule, parenchyma, and vasculature go to neuraxis, passing through sympathetic nerves and prevertebral ganglia, and join the lesser and least splanchnic nerves. These nerves then travel cranially along the retrocrural space to the T10- T12 and L1 spinal levels through the respective paravertebral ganglia and rami communicans. Intercostal somatic nerves are nerving part of the renal capsule and nearby musculoskeletal structures, corresponding to T7-T12 dermatomal levels. Large cysts result in bigger pelvic angle and lumbar lordosis causing mechanical low back pain, as the abdomen projects, more strain is forced to lower back muscles and disc disease is established in the lumbosacral area (Steinman 2000, Bajwa et al. 2004, Tozzi et al. 2012).

Infected renal cysts can cause diffuse, generalised unilateral or bilateral pain accompanied by fever, unrelieved by position change. This type of pain is similar to pyelonephritis in general population. Raptured cysts, on the other hand, manifested by haematuria, are the cause of acute flank pain which is, usually, localised and finger pointed by patients. It can, also, reflect to anterior abdominal area (Hogan & Norby 2010, Haseebuddin et al. 2012) or even the shoulder if the cysts are larger and compressing the surrounding tissues (Bajwa 2001). In case of ruptured cysts which are on the surface of the kidney, sub-capsular hematoma is caused, resulting in mild and steady pain persisting until it is absorbed (Steinman 2000). Clots within the renal cysts can lead to urinary tract obstruction, like the one caused by kidney stones, and renal colic. The actual renal colic caused by kidney stones (calcium oxalate, calcium phosphate, calcium carbonate or uric acid) can be found in almost 20% of patients with PKD. Anatomic deformity caused by the cysts may contribute to the formation of kidney stones, possibly due to increased urinary stasis (Grampsas et al. 2000). Liver cysts, found in 85% of the individuals in Bae et al (2006) CRISP study are associated with more severe pain and abdominal distension while in standing position.

It is worth mentioning the in the PKD population persisting headache or migraine could be an early sign of cerebral aneurysm, even though its prevalence is between 4%-6% of the total ADPKD group (Bajwa et al. 2001).

Secondary hyperparathyroidism, a serious complication of Chronic Kidney Disease, originates from deregulation of serum calcium, phosphorus and vitamin D, resulting in elevated levels of parathyroid hormone and, furthermore, in abnormal bone metabolism and muscle weakness, skeletal deformities and bone pain, called renal osteodystrophy. Ergocalciferol (vitamin D2), cholecalciferol (vitamin D3), and their metabolites and derivatives are involved in this process. Vitamin D3 is produced after the conversion of skin’s 7-Dehydrocholesterol in the presence of sunlight. As it is not active, it has to be hydroxylated in the liver to produce 25- hydroxyvitamin D3. Then in the normal kidney it is converted into calcitriol (1.25 dihydroxyvitamin D3). The same process happens with vitamin D2, which comes from plants and fungus, producing 1.25

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 585


dihydroxyergocalciferol. Both of them maintain normal calcium homeostasis via the vitamin D receptor to increase intestinal calcium absorption and to modulate mineral mobilization from bone (Palmer et al. 2009). These mineral and hormonal abnormalities start early in Chronic Kidney Disease process, usually in Stage 3, when GFR is <60mL/min/1.73m2. If left untreated, hyperparathyroidism can lead to onset of purpuric plagues, discolored skin and nodules, signs of calciphylaxis, and could evolve in necrotic ulcers, gangrene, and amputation. Painful proximal myopathy can accompany the skin manifestations, resembling dermatomyositis. Biopsy findings show varying degrees of calcification of the media layer of the blood vessel walls of subcutaneous or digital arteries causing ischaemic necrosis of the skin and other organs (Rich et al. 2001, Perlman 2005, Terzibasioglu et al. 2005, Schlosser et al. 2008, Strippoli et al. 2010).

In addition to the pain caused by the disease itself, HD patients are exposed to clinically inflicted pain, such as insertion of Central Venous Catheters (CVC) for HD or cannulation of vascular access (Arteriovenous fistula or graft). Haemodialysis sessions are held, usually, three times a week and involve at least one puncture at the arterial and one at the venous part of the vascular access for every session, a total of at least 320 punctures each year. This repeated puncturing leads to a considerable pain, due to the tearing of the skin, and the punch in the walls of the vessels (Montero et al. 2004, Verhallen et al. 2007, Figueiredo et al. 2008). Due to irritation of the skin’s nerve endings, pain perception mechanism is triggered and pain is experienced.

Another problem common among patients on dialysis, HD or PD, for more than 5 years is Dialysis-related amyloidosis (DRA) (Moss et a 2004). B2-microglobulin deposits in bone, synovium, tendons and peripheral nerves and causing bone cysts, fractures, arthritis, and carpal tunnel syndrome accompanied by pain (Kelly et al. 2007). It is a cause of musculoskeletal pain in 51% of dialysis patients, as described by Davison (2003) and 37% of another HD population studied by Carreon et al. (2008).

Last by not least, diabetic peripheral neuropathy, affecting large and small fibres, is another cause of pain in Chronic Kidney Disease patients and is correlated with duration of Diabetes Mellitus

(DM), degree of glycaemic control and level of uraemia (Edwards et al. 2008). Sensory deficits overshadow motor nerve dysfunction and appear first in the distal portions of the extremities and progress proximally in a “stocking-glove” distribution (Pop-Busui et al. 2010).


Renal patients experience high levels of pain due to nature of their disease or painful interventions, such as vascular access cannulation, insertion of peritoneal dialysis catheter or examinations. In order to effectively and individually assess and manage pain healthcare professionals need to be familiar with different types and aetiology of pain, as well as the current ways of treatment. Through curriculum and continuous education clinicians can choose from a cascade of treatments aiming at maintaining the quality of life of renal population.


Ackerman CJ, Turkoski B. (2000) Using guided imagery to reduce pain and anxiety. Journal of Healthcare Nurse 18: 524-530.

Aitken E, McLellan A, Glen S, Serpell M, Mactier R, Clancy M. (2013) Pain resulting from arteriovenous fistulae: prevalence and impact. Clinical Nephrology 80: 328-333.

Atalay H, Solak Y, Biyik Z, Gaipov A, Guney F, Turk S. (2013) Cross-over, open-label trial of the effects of gabapentin versus pregabalin on painful peripheral neuropathy and health-related quality of life in haemodialysis patients. Clinical drug Investigation 33: 401-408.

Bouattar T, Madani N, Hamzaqui H, Alhamany Z. (2009) Severe ethylene glycol intoxication by skin absorption. Nephrol Ther 53: 205-209. (in French).

Bae KT, Zhu F, Chapman AB, Torres VE, Grantham JJ, Guay-Woodford LM, Baumgarten DA, King BF, Wetzel LH, Kenney PJ, Brummer ME, Bennett WM, Klahr S, Meyers CM, Zhang X, Thompson PA, Miller JP for the Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP). (2006) Magnetic resonance imaging evaluation of hepatic cysts in early autosomal-dominant polycystic kidney disease: the Consortium of Radiologic Imaging Studies of Polycystic Kidney Disease cohort. Clin J Am Soc Nephrol 1(1): 64-69.

Bagheri-Nesami M, Espahbodi F, Nikkhah A, Shorofi SA, Charati JY. (2014) The effects of lavender aromatotherapy on pain following needle insertion into a fistula in haemodialysis patients. Complementary Therapy Clinical Practice 20: 1-4.

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 586


Bouhassira D, Lanteri-Minet M, Attal N, Laurent B, Touboul C. (2008) Prevalence of chronic pain with neuropathic characteristics in the general population. Pain 136: 380-387.

Bailie G, Mason N, Bragg-Gresham J, Gillespie B, Young E. (2004) Analgesic prescription patterns among haemodialysis patients in the DOPPS: Potential for underprescription. Kidney International 65: 2419-2425.

Bajwa ZH, Gupta S, Warfield CA, Steinman TI. (2001) Pain management in polycystic kidney disease. Kidney International 60: 1631-1644.

Bajwa ZH, Sial KA, Malik AB, Steinman TI. (2004) Pain patterns in patients with Polycystic Kidney Disease. Kidney International 66: 1561-1569.

Binik YM, Baker AG, Kalogeropoulos D, Devins GM, Guttmann RD, Hollomby DJ, Barre PE, Hutchison T, Prud’Homme M, McMullen L. (1982) Pain, control over treatment, and compliance in dialysis and transplant patients. Kidney International 21: 840-848.

Butler A, Kshirsagar A, Brookhart M. 2014. Opioid use in the US haemodialysis population. American Journal of Kidney Disease 63: 171- 173.

Carreon M, Fried LF, Palevsky PM, Kimmel PL, Arnold RM, Weisbord SD. (2008) Clinical correlates and treatment of bone/joint pain and difficulty with sexual arousal in patients on maintenance haemodialysis. Hemodialysis International 12: 268-274.

Chang KL, Fillingim R, Hurley RW, Schmidt S. (2015) Chronic pain management: nonpharmacological therapies for chronic pain. Family Physician Essentials 432: 21-26.

Chapman CR & Nakamura Y. (1999) A passion of the soul: an introduction to pain for consciousness researchers. Consciousness & Cognition 8: 391-422.

Cohen LM, Moss AH, Weisbord SD, Germain MJ. (2006) Renal palliative care. Journal of palliative medicine 9: 9772-992.

Cohen SD & Davison SN. (2015) Pain and Chronic Kidney Disease in Chronic Kidney Disease. In Kimmel PL & Rosenberg ME (eds). Elsevier, USA, 854-860.

Cohen SD, Patel SS, Khetpal P, Peterson RA, Kimmel PL. (2007) Pain, sleep disturbance and Quality of Life in patients with Chronic Kidney Disease. Clinical Journal of American Society of Nephrology 2: 919-925.

Davison SN, Jhangri GS. (2005) The impact of chronic pain on depression, sleep, and the desire to withdraw from dialysis in heamodialysis patients. Journal of Pain and Symptom Management 30: 465-473.

Davison SN, Jhangri GS. (2010) Impact of pain and symptom burden on the Health-Related Quality of Life of haemodialysis patients. Journal of pain and symptom management 39: 477-485.

Davison SN, Koncicki H, Brennan F. (2014) Pain in Chronic Kidney Disease: a scoping revew. Seminars in Dialysis 27: 188-2014.

Davison SN. (2003) Pain in hemodialysis patients: prevalence, cause severity, and management. American Journal of Kidney Diseases 42: 1239- 1247.

Davison SN. (2005) Chronic Pain in End-Stage Renal Disease. Advances in Chronic Kidney Disease 12: 326-334.

Davison SN. (2007a) Chronic kidney disease. Psychosocial impact of chronic pain. Geriatrics 62: 17-23.

Dysvik E, Lindstrom TC, Eikeland OJ, Natvig GK. (2004) Health-related quality of life and pain beliefs among people suffering from chronic pain. Pain management nursing 5: 66-74.

Edwards JL, Vincent AM, Cheng HT, Feldman EL. (2008) Diabetic neuropathy: Mechanisms to management. Pharmacological Therapy 120: 1- 34.

Ferrell B, Coyle N. (2008) The nature of suffering and the goals of nursing. Oxford University Press, Cary, NC, USA.

Figueiredo AE, Viegas A, Monteiro M, Poli-de- Figueiredo CE. (2008) Research into pain perception with arteriovenous fistula (AVF) cannulation. Journal of Renal Care 34: 169-172.

Gamondi C, Galli N, Schonholzer C, Marone C, Zwahlen H, Gabutti L, Bianchi G, Ferrier C, Cereghetti C, Giannini O. (2013) Frequency and severity of pain and symptom distress among patients with chronic kidney disease receiving dialysis. Swiss Medical Weekly 143: w13750.

Grampsas SA, Chandhoke PS, Fan J, Glass MA, Townsend R, Johnson AM, Gabow P. (2000) Anatomic and metabolic risk factors for nephrolithiasis in patients with autosomal dominant polycystic kidney disease. American Journal of Kidney Diseases 36: 53-57.

Greek Nurses Code of Ethics, Greek Government Newspaper No 167/2001, part 2 & 18.

Harris TJ, Nazir R, Khetpal P, Peterson RA, Chava P, Patel SS, Kimmel PL. (2012) Pain, sleep disturbance and survival in haemodialysis patients. Nehpr Dial and Transpl 27: 758-765.

Haseebuddin M, Tanagho YS, Millar M, Roytman T, Chen C, Clayman RV, Miller B, Desai A, Benway B, Bhayani S, Figenshau RS. (2012) Long-term impact of laparoscopic cyst decorticataion on renal function hypertension and pain control in patients with Autosomal Dominant Polycystic Kidney Disease. Journal of Urology 188: 1239-1244.

Heiwe S, Bjuke M. (2009) “An Evil Heritage”: interview study of pain and Autosomal Dominant Polycystic Kidney Disease. Pain Management Nursing 10: 134-141.

Hogan MC, Norby SM. (2010) Evaluation and management of pain in Autosomal Dominant

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 587


Polycystic Kidney Disease. Advances in Chronic Kidney Disease 17: e1-e16.

Institute of Medicine (IOM). (2011) Relieving pain in America: A blueprint of transforming prevention, care, education and research. The National Academies Press. Washington, DC, USA.

Jurf JB, Nirschl A. (1993) Acute postoperative pain management: a comprehensive review and update. Critical Care Nursing Quarterly 16: 8- 25.

Kafkia T, Vehvilainen-Julkunen K, Sapountzi- Krepia D. (2017) Renal patients’ quality of life as it is affected by pain. International Journal of Caring Sciences 10(2): 1108- 1113.

Kelly A, Apostle K, Sanders D, Bailey H. (2007) Musculoskeletal pain in dialysis-related amyloidosis. Canadian Journal of Surgery 50: 305-306.

Kurella M, Bennett W, Chertow G. (2003) Analgesia in patients with ESRD: a review of the available evidence. American Journal of Kidney Diseases 42: 217-228.

Lindqvist R, Carlsson M, Sjoden PO. (2000) Coping strategies and health-related quality of life among spouses of continuous ambulatory peritoneal dialysis, haemodialysis, and transplant patients. Journal of Advanced Nursing 31: 1398- 1408.

Madjar I. (1998) Giving comfort and inflicting pain. Qual Institute Press. Edmonton, Alberta, Canada.

Manias E, Williams A. (2007) Communication between patients with chronic kidney disease and nurses about managing pain in the acute hospital setting. Journal of Chronic Illness and Healthcare in association with Journal of Clinical Nursing 16: 358-367.

McCaffery M. 1968. Nursing practice theories related to cognition, bodily pain and man environmental interactions. UCLA Students Store. Los Angeles, CA, USA.

McMahon S, Koltzenburg M, Tracey I, Turk DC. (2013) Wall & Melzack’s textbook of pain. Elsevier Health Science. Philadelphia, USA.

Melzack R, Wall PD. (2008) The Challenge of pain. Penguin Books Ltd. London, UK.

Melzack R. (1999) From the gate to the neuromatrix. Pain 82: S121-S126.

Melzack R, Wall P. (2003) Handbook of Pain Management: A Clinical Companion to Textbook of Pain. Churchill Livingstone. Edinburgh, UK.

Mercadante S, Ferrantelli A, Tortorici C, LoCascio A, LoCicero M, Cutaia I, Parrino I, Casuccio A. (2005) Incidence of chronic pain in patients with end-stage renal disease on dialysis. Journal of Pain and Symptom Management 30: 302-304.

Minasidou E, Spanoudi K, Kafkia T. (2016) Spirituality/reliosity and health-related quality of life in chronic patients and patients with life-

threatening diseases. Hellenic Journal of Nursing Science 9(1): 30-37.

Merskey H, Bogduk N for the Task Force on Taxonomy of the International Association for the Study of Pain. (2012) Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed (revised). IASP Press Seattle, WA, USA.

Montero RC, Arellano FR, Contreras Abad MD, Martinez Gomez A, Fuentes Galan MI. (2004) Pain degree and skin damage during arterio- venous fistula puncture. EDTNA/ERCA Journal 30: 208-212.

Moss AH, Davison SN. (2015) How the ESRD quality incentive program could potentially improve quality of life for patients on dialysis. Clinical Journal of American Society of Nephrology 10: 888-893.

Moss AH, Holley JL, Davison SN, Dart RA, Germain MJ, Cohen L, Swartz RD. (2004) Core Curriculum in nephrology: Pain management in renal patients. American Journal of Kidney Diseases 43: 172-185.

Murtagh FE, Addington-Hall J, Higginson IJ. (2007b) The prevalence of symptoms in end stage renal disease: a systematic review. Advances in chronic kidney disease 14: 82-99.

Murtagh FE, Addington-Hall JM, Edmonds PM, Donohoe P, Carey I, Jenkins K, Higginson IJ. (2007a) Symptoms in advanced renal disease: a cross-sectional survey without dialysis. Journal of Palliative Medicine 10: 1266-1276.

Palmer SC, McGregor DO, Craig JC, Elder G, Macaskill P, Strippoli GFM. (2009) Vitamin D compounds for people with Chronic Kidney Disease requiring dialysis. Cochrane Database of Systematic Reviews 4, Art.No.: CD005633. Pub2.

Perlman RL, Finkelstein FO, Liu L, Roys E, Kiser M, Eisele G, Burrows-Hudson S, Messara JM, Levin N, Rajoqopalan S, Port FK, Wolfe RA, Saran R. (2005) Quality of life in Chronic Kidney Disease (CKD): a cross-sectional analysis in the Renal Research Institute-CKD study. American Journal of Kidney Diseases 45: 658-666.

Pham PC, Toscano E, Pham PM, Pham PA, Pham SV, Pham PT. (2009) Pain management in patients with chronic kidney disease. Nephrology, Dialysis and Transplantation 2: 111-118.

Pop-Busui R, Roberts L, Pennathur S, Kretzler M, Brosius FC, Felman EL. (2010) The management of Diabetic Neuropathy in CKD. American Journal of Kidney Diseases 55: 365-385.

Rich D. (2001). If communication were easy, everyone would do it. Healthplan 42(3): 46-50.

Rizk D, Chapman A. (2003). Cystic and inherited kidney diseases. Am J Kidney Dis 42(6): 1305- 1317.

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 588


Salisbury EM, Game DS, Al-Shakarchi I, Chan M, Fishman L, Tookman L, Brown EA. (2009) Changing practice to improve pain control for renal patients. Postgraduate Medical Journal 85: 30-33.

Santoro D, Satta E, Messina S, Costantino G, Savica V, Bellinghieri G. (2013) Pain in end-stage renal disease: a frequent and neglected clinical problem. Clinical Nephrology 79: 2-11.

Savige J, Tunnicliffe DJ, Rangan GK. (2015) KHA- CARI: Autosomal Dominant Kidney Disease Guideline: management of chronic pain. Seminars in Nephrology 35: 607-611.

Schlosser K, Schmitt CP, Bartholomaeus JE, Suchan KL, Buchler MW, Rothmund M, Weber T. (2008) Parathyroidectomy for renal hyperparathyroidism in children and adolescents. World Journal of Surgery 32: 801-806.

Shayamsunder AK, Patel SS, Jain V, Peterson RA, Kimmel PL. (2005) Psychosocial factors in patients with chronic kidney disease. Seminars on Dialysis 18: 109-118.

Shetty SV, Roberts T, Schlaich M. (2012) Percutaneous transluminar renal denervation: A potential treatment for polycystic kidney disease- related pain? Journal of Cardiology 162: e58 – e59.

Smith BH, Torrance N, Bennett MI, Lee AJ. (2007) Health and quality of life associated with chronic pain of predominantly neuropathic origin in the community. Clinical Journal of Pain 23: 143- 149.

Steinman TI. (2000) Pain management in polycystic kidney disease. American Journal of Kidney Diseases 35: 770-772.

Strippoli GFM, Tong A, Palmer SC, Elder GJ, Craig JC. (2010) Calcimimetics for secondary hyperparathyroidism in chronic kidney disease patients. Cochrane Database of Systematic Reviews 4. Art.No. CD006254.

Tellman MW, Bahler CD, Shumate AM, Bacallao RL, Sundaram CP. (2015) Management of pain in Autosomal Dominant Polycystic Kidney Disease and anatomy of renal innervation. The Journal of Urology 193: 1470-1478.

Terzibasioglu AM, Akarirmak U, Saridogan M, Tuzun S. (2005) Correlation of back pain, compression fracture and quadriceps muscle strength with bone mineral density in renal insufficiency patients. Europa Medicophysica 41: 303-308.

Thienhaus O, Cole BE. (2002) Classification of pain. In Weiner RS (ed). Pain management: a practical guide for clinicians (6th ed). American Academy of Pain Management. CRC Press. LLC. Boca Raton, FL, USA, 27-36.

Torres VE, Harris PC, Pirson Y. (2007) Autosomal Dominant Polycystic Kidney Disease. Lancet 369: 1287-1301.

Torres VE, Meijer E, Bae KT, Chapman AB, Devuyst O, Gansevoort RT, Grantham JJ, Higashihara E, Perrone RD, Krasa HB, Ouyang JJ, Czerwiec FS. (2011) Rationale and design of the TEMPO (Tolvaptan Efficacy and Safety in Management of Autosomal Dominant Polycystic Kidney Disease and its Outcomes) 3– 4 Study. American Journal of Kidney Disease 57: 692- 699.

Tozzi P, Bongiorno D, Vitturini C. (2012) Low back pain and kidney mobility: local osteopathic fascial manipulation decreases pain perception and improves renal mobility. Journal of bodywork & movement therapies 16: 381-391.

Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW, Hansson P, Hughes R, Nurmikko T, Serra J. (2008) Neuropathic pain: redefinition and a grading system for clinical and research purposes. Neurology 70: 1630-1635.

Turk DC, Okifuji A. (2001) Pain terms and taxonomies of pain. In Loeser JD, Butler SH, Chapman CR, Turk DC (eds). Bonica’s Management of Pain. 3rd ed. Lippincott Williams & Wilkins. Baltimore, USA, 17-25.

Turk DC, Okifuji A. (2002) Psychological factors in chronic pain: evolution and revolution. Journal of Consulting and Clinical Psychology 70: 678- 690.

Turner JS, Cheung EM, Jaya G, Quinn DI. (2007) Pain management, supportive and palliative care in patients with renal cell carcinoma. British Journal of Urology 99: 1305-1312.

Vaajoki A, Pietila A-M, Kankkunen P, Vehvilainen- Julkunen K. (2013) Music intervention study in abdominal surgery patients: Challenges of an intervention study in clinical practice. Int Journal of Nurs Practice 19: 206–213.

Verhallen AM, Kooistra MP, Jaarsveld BC. (2007) Cannulating in haemodialysis: rope ladder or buttonhole technique? Nephrology, Dialysis and Transplantation 22: 2601-2604.

Wall PD, Melzack R. (1994) Textbook of Pain. 3rd ed. Churchill Livingstone. Edinburgh, UK.

Walsh N, Sarria JE. (2012) Management of chronic pain in a patient with Autosomal Dominant Polycystic Kidney Disease by sequential celiac plexus blockade, radiofrequency ablation and spinal cord stimulation. American Journal of Kidney Diseases 59: 858-81.

Weisbord SD, Fried LF, Arnold RM, Fine MJ, Levenson DJ, Peterson RA, Switzer GE. (2005) Prevalence, severity and importance of physical and emotional symptoms in chronic heamodialysis patients. Journal of American Society of Nephrology 16: 2487-2494.

Wilkstrom L, Eriksson K, Arestedt K, Fridlund B, Brostrom A. (2014) Healthcare professionals’ perceptions of the use of pain scales in

International Journal of Caring Sciences January-April 2018 Volume 11 | Issue 1| Page 589


postoperative pain assessments. Applied Nursing Research 27: 53-58.

Wu J, Ginsberg J, Zhan M, Diamantidis CJ, Chen J, Woods C, Fink JC. (2015) Chronic pain and analgesic use in CKD: implications for patient safety. Clinical Journal of American Society of Nephrology 10: 435-442.

Yamamoto Y, Hayashino Y, Akiba T, Akizawa T, Asano Y, Saito A, Kurokawa K, Fukuhara S for J-DOPPS Research Group. (2009) Depressive symptoms predict the subsequent risk of bodily

pain in dialysis patients: Japan Dialysis Outcomes and Practice Patterns Study (DOPPS). Pain Medicine 10: 883-889.

Zyga S, Alikari V, Sachlas A, Fradelos E, Stathoulis J, Panoutsopoulos G, Georgopoulou M, Theophilou P, Lavdaniti M. (2015) Assessment of fatigue in End-Stage Renal Disease patients undergoing haemodialysis: prevalence and associated factors. Medical Archives 69: 376- 380.

Copyright of International Journal of Caring Sciences is the property of International Journal of Caring Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder’s express written permission. However, users may print, download, or email articles for individual use.

Order your essay today and save 10% with the discount code ESSAYHELP