Pain management in patients with chronic kidney disease
Pain is one of the most common complaints in clinical practice because it is a symptom for a myriad of physical and mental problems. Indeed, chronic non-malignant pain has been reported to affect 11–24% of the general population [1–3]. Among dialysis patients, Murtagh et al. had documented a mean pain prevalence of 47%, with a range of 8–82% [4]. Similar data for pre-end-stage renal disease (pre-ESRD) or chronic kidney disease (CKD) stage 1–4 patients, however, are lacking. Nonetheless, in a recent small study involving 130 CKD patients at a tertiary referral medical centre in Los Angeles, California, the prevalence of pain, whether acute or chronic, was reported to be over 70% [5]. The sources of pain were musculoskeletal (62%) followed by other organ systems including gastrointestinal (13%), genitourinary (10%), haematological/oncological (10%), central and peripheral nervous system (9%), cardiovascular (7%) and others (10%) [5].
The high prevalence of pain in the CKD population is particularly concerning because pain has been shown to adversely affect quality of life [6]. In a cross-sectional analysis in the Renal Research Institute-CKD study, the presence of physical pain in patients with CKD stages 3–5 was found to be associated with lower quality of life scores (QOL) (as measured by the Medical Outcomes Study Short Form-36 (SF-36)) compared to that of the general population. Where a higher numerical value for QOL indicates better quality of life, the mean QOL scores were 67.4 ± 27.1, 59.0 ± 29.2 and 75.2 ± 23.7, for CKD, dialysis and general population, respectively, P < 0.0001 for both dialysis and general population when compared with CKD patients [6]. In dialysis patients, poor QOL scores were associated with hospitalization and death [7,8]. Whether CKD patients suffer the same fate is unknown.
Because pain is a common problem that has been shown to have a negative impact on quality of life, and both pain and its treatment can lead to various morbidities, more notably in the CKD population, prompt recognition and proper management of pain in this population are critical.
We herein review the pathophysiology, clinical manifestations and general management guidelines for pain with special considerations for pre-ESRD patients to optimize pain control while minimizing both renal and non-renal complications.
The significance of pain
The spectrum of acute-to-chronic pain is believed to encompass important biological roles. The evolutionary development of the sensation for acute pain is thought to be protective and well adaptive for organisms against potential injurious events or actions. The evolutionary preservation of mechanisms to allow for the persistence of pain beyond the healing phase or various chronic pain syndromes, however, is presumed to be a maladaptive diseased state [9].
Acute pain
Acute pain sensation results from the direct stimulation of sensory neurons found throughout the body, known as nociceptors. Nociceptors receiving input from outer body tissues are responsible for somatic pain, while those receiving input from internal organs are responsible for visceral pain. Nociceptors can be stimulated by mechanical, thermal, chemical and inflammatory stimuli. Substances released from tissue injury including vasoactive peptides (i.e. calcitonin gene-related protein, substance P, neurokinin A) and mediators such as prostaglandin E2, serotonin, bradykinin and epinephrine can sensitize peripheral nociceptors [10,11]. Action potentials generated from the stimulation of nociceptors are conducted in the peripheral nervous system along the sensory neuron axon via peripheral nerves to the dorsal root ganglion and spinal cord dorsal root, where central terminals of the neurons can synapse with dorsal horn neurons and allow for transmission to the brain. Nociceptors have two different types of axons, the rapidly conducting thinly myelinated Aδ fibre and the more slowly conducting unmyelinated C fibre axons. The clinical relevance of these two different axon types is reflected in the two phases of acute pain. The pain sensed in the first phase, i.e. an initial extremely sharp pain, is associated with the fast-conducting Aδ fibres while the pain sensed in the second phase, typically a more prolonged and less intense feeling of pain following the injury, is mediated by the slowly conducting C fibre axons. The pain signal may be modulated at various points in both segmental and descending pathways by neurochemical mediators including endogenous opioids and monoamines including serotonin and epinephrine. The mechanisms whereby CNS-active drugs such as opioids, antidepressants and anticonvulsants alleviate pain rely on their interaction with specific pain modulating receptors (i.e. μ, κ, δ opioid receptors) and neurochemicals (reviewed in 9, 11–13).
Chronic pain
Pain lasting longer than 3 months or beyond the duration required for complete tissue healing is typically classified as chronic pain. Chronic pain may arise from prolonged tissue injury with persistent activation of nociceptors, a lesion or disease affecting the somatosensory system known as neuropathic pain, or other indistinct mechanisms [14]. In the event where tissue damage has occurred, acute infiltration of inflammatory cells and associated surrounding inflammatory reactions become the noxious stimuli to stimulate nociceptors, an effect that gives rise to inflammatory pain. It is believed that inflammatory pain serves to minimize movement or further stress to the damaged area until complete healing has occurred [9,12,13,15].
Neuropathic pain has been defined by the International Association for the Study of Pain as pain that arises as a direct consequence of a lesion or disease affecting the somatosensory system [14]. Neuropathic pain is thought to involve peripheral or central sensitization, or both. Peripheral sensitization is a process where regenerated C-fibres of damaged axons develop pathological spontaneous activity and amplified excitability and sensitivity to various mechanical, chemical and thermal stimuli. Central sensitization refers to the increase in general excitability of spinal cord dorsal horn neurons as a result of peripheral nerve injury. The hyperexcitability of spinal cord neurons has been attributed to increased neuronal background activity, enhanced activity in response to noxious stimuli and expanded neuronal receptive fields. Other mechanisms of neuropathic pain include the spontaneous firing of higher order neurons in the presence of injured or disrupted peripheral sensory pathways, a process known as deafferentation (e.g. phantom limb pain, diabetic neuropathy, post-herpetic neuralgia); loss of inhibitory interneuronal activity; development of abnormal electrical communications across adjacent demyelinated axons, a process known as ‘ephaptic cross-talk’; or release of neuroexcitatory substances by non-neural glial cells [9,12,13,16]. In sympathetic pain associated with the complex regional pain syndrome (also known as reflex sympathetic dystrophy), where a painful stimulus can trigger autonomic activity at the same dermatomal level of the spinal cord, ephaptic cross-talk between sensory and sympathetic fibres is thought to play a role [9,12,13,17].
While the pathophysiology of various neuropathic pain conditions can be explained, the mechanisms of many other pain syndromes remain to be elucidated. Many pain conditions have neuropathic features but lack any known injury or dysfunction of the nervous system to be considered as neuropathic pain. These conditions have been classified as non-neuropathic pain syndromes and include myofascial headaches, fibromyalgia, chronic back and neck pain among others [9,12,13].
Clinical manifestations of pain
Most often, acute pain is described as sharp, aching or throbbing. While acute somatic pain may be easily described and localized, the same may not necessarily apply to acute visceral pain. Acute pain typically resolves within days to weeks. In contrast, chronic pain is usually not manifested with an easily identifiable aetiology or duration. In general, the overall pattern of pain quality and spatial characteristics under chronic pain conditions differs considerably between neuropathic and non-neuropathic pain. In a recent study, Dworkin et al. documented that patients with peripheral neuropathic pain reported significantly more intense hot, cold, sensitive, itchy and surface pain and significantly less intense dull and deep pain than patients with non-neuropathic pain [18]. Common symptoms for neuropathic and non-neuropathic pain syndromes are summarized.
Source: https://academic.oup.com/ckj/article/doi/10.1093/ndtplus/sfp001/697087/Pain-management-in-patients-with-chronic-kidney
Wednesday, May 27, 2026
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