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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

Abstract

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

Background

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

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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.

Definitions

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.

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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

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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

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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

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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).

Conclusion

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.

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