Pathophysiology of Multiple Sclerosis and Chronic Kidney Disease

Multiple sclerosis is a severe inflammatory, neurodegenerative, and demyelination disease in the central nervous system. The disorder has a chronic effect on the white and grey matter of optic nerves, spinal cord, and brain. The condition is a prevalent cause of non-traumatic disabilities among young and middle-aged individuals. The direct related medical expenses of the condition are approximately $10 billion yearly (Hill et al., 2016). The condition is also mainly accompanied by other conditions such as chronic kidney disease 

During the early stages of multiple sclerosis, there exists a central nervous system inflammation that damages the myelin sheath, which surrounds axons and axons themselves. The histologic analysis shows that the foci of chronic demyelination reduce axonal and oligodendrocyte numbers. The inflammation's actual cause is still unclear, but autoimmune response against the central nervous system antigens is suspected. Patients tend to develop lesions, and others will create signs that are compatible with inflammatory demyelination. The patient will develop clinical relapse ever 1 to 2 years (Brownlee et al., 2017). Therefore, it requires proper medication. 

On the other hand, chronic kidney disease has become more widespread globally than was previously estimated. It now affects more than 10% of the adult population, and the majority of them need expensive medical treatment or sometimes renal replacement therapy (Hill et al., 2016). The chronic kidney's pathophysiology is based on renal structure and functional elements, and the elements of renal tissue injuries and repairs. The main reason for renal injury is immunological responses, tissue hypoxia, ischemia, exogamic elements like drugs, and endogenous material such as Para proteins and glucose. Sometimes it is due to genetic defects. These elements lead to reduced renal function, which will interfere with the kidney's capability to preserve fluid and electrolyte homeostasis. 

The similarities in hormonal elements between multiple sclerosis and chronic kidney disease show that the alteration in the central nervous system leads to dramatic responses in patients' kidney tissues. The responses tend to reduce the central nervous system injuries or increase the lesion region (Brownlee et al., 2017). With this in place, there will be severe impairment of the kidney's secretory duties that may result in brain dysfunction in patients. Many studies have shown that sociodemographic indicators, depression, fatigue, smoking, and cognitive impairment contribute to the increased prevalence of the two disorders. 

Health Assessments and Diagnostic Reasoning 

Regarding multiple sclerosis, mainly physical and occupational therapies are utilized. The main effort is to evaluate and resolve impairments. For fatigue, the primary type of assessment includes Modified Fatigue Scale, 25-foot walk, sleep questionnaire, and depression instrument (Brownlee et al., 2017). Diagnosis of chronic kidney disease needs previous basements of eGFR, proteinuria, or albuminuria. If it is impossible, a patient must have many evaluations for three months to ascertain if the condition is chronic. The main goal of assessment is to reduce the progression of renal diseases instead of stopping them. Assessment of age and other chronic conditions will also be beneficial to develop an impact on the treatment. 

Adaptive and Maladaptive Responses 

Regarding adaptive responses of multiple sclerosis, it shows that a peripheral immune response in which it targets the central nervous system drives the conditioning process in the early stages. The immune reaction with the central nervous system dominates progressive stages. The apparent maladaptive response to multiple sclerosis decreases the connectivity in a progressive state and reduces activation in patients with cognitive impairment. Adaptive response to chronic kidney disease results in hyperkalemia, a common feature due to chronic renal insufficiency, usually due to impaired potassium ions homeostasis. When the new level is attained, the plasma potassium ions remain stable (Liu et al., 2018). Regarding maladaptive response, the repair resulting in chronic kidney disease is characterized by continuous parenchyma inflammation due to increased myofibroblasts and accumulation of extracellular matrices. 

Pharmacokinetics and Pharmacodynamics of the Medications 

The main drugs utilized to treat multiple sclerosis and CKD are corticosteroids and plasma exchange. Corticosteroids such as intravenous methylprednisone and oral prednisone are administered to decrease nerve inflammation. The side effects include fluid retention, the rapid increase of glucose level, insomnia, and increased blood pressure (Liu et al., 2018). Plasma exchange is utilized when symptoms are still new, chronic, and has not reacted to steroids. The process includes removing plasma and separating from other blood cells. It is then mixed with albumin and returned to the body. This aspect reduced the rate of clinical relapses. 

Possible Interactions of Medications 

Ensuring patient safety is an essential issue in medical care because iatrogenic injuries have been a vital concern. Medications tend to be a significant source in medical errors, and comorbidities between chronic kidney disease and multiple sclerosis tend to have multiple factors that threaten the safe administration of treatment (Motl et al., 2017). Patients with chronic kidney disease, for instance, suffer from other conditions, and thus there is a need to coordinate the treatment. A drug such as Lemtrada used in treating multiple sclerosis needs blood and urine evaluation before and after about four years of medication. The main aim to watch severe autoimmune conditions between two comorbidities. 

To ensure that medications do not have adverse effects on patients, a patient needs to stay hydrated, eat healthily, take medications before sleep, and warm injectable drugs to body temperature before using it. For patients suffering from fever, chills, and headaches, they can take a small dose of ibuprofen, Advil, and Motrin before and after injection (Motl et al., 2017). All these aspects will help in reducing the adverse effects associated with drug interactions. 

Education 

Educating the patient on such comorbidities is sensitive and needs an ample environment to learn how to handle the conditions well. Relieving the symptoms and signs of two conditions are smooth and manageable. I will advise the patient to get sufficient rest by looking at sleep habits and treating sleep disorders like obstructive sleep apnea. Another thing is on exercise because it improves strengths, balance, coordination, and muscle tone. Swimming or water exercises are the best physical activities because a patient will not be bothered by the heat (Motl et al., 2017). Another way of ensuring that these two diseases are in stable condition is by eating a balanced diet. Vitamin D is a potential benefit because it helps in increasing the immune system. Above all, it is essential to relieving stress because it tends to trigger or worsen signs and symptoms. Way of relieving stress include deep breathing, massage, meditation, yoga, and tai chi. 

References 

Brownlee, W. J., Hardy, T. A., Fazekas, F., & Miller, D. H. (2017). Diagnosis of multiple sclerosis: Progress and challenges.  The Lancet ,  389 (10076), 1336-1346.  https://doi.org/10.1016/s0140-6736(16)30959-x 

Hill, N. R., Fatoba, S. T., Oke, J. L., Hirst, J. A., O’Callaghan, C. A., Lasserson, D. S., & Hobbs, F. D. (2016). Global prevalence of chronic kidney disease – A systematic review and meta-analysis.  PLOS ONE ,  11 (7), e0158765.  https://doi.org/10.1371/journal.pone.0158765 

Liu, B., Tang, T., Lv, L., & Lan, H. (2018). Renal tubule injury: A driving force toward chronic kidney disease.  Kidney International ,  93 (3), 568-579.  https://doi.org/10.1016/j.kint.2017.09.033 

Motl, R. W., Sandroff, B. M., Kwakkel, G., Dalgas, U., Feinstein, A., Heesen, C., Feys, P., & Thompson, A. J. (2017). Exercise in patients with multiple sclerosis.  The Lancet Neurology ,  16 (10), 848-856.  https://doi.org/10.1016/s1474-4422(17)30281-8