End-Stage Kidney Disease
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Institution
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End-Stage Kidney Disease
Abstract
End-Stage Kidney Disease is the last stage of chronic kidney disease, in which the kidneys lose their functionality entirely, making it virtually impossible to survive without a kidney transplant or dialysis. Kidney failure results from several underlying health problems that gradually cause damage to the kidneys, either directly or indirectly. These underlying conditions include diabetes, high blood pressure, urinary tract problems, and even autoimmune problems (Murtagh et al., 2016). In this assignment, we look at End-Stage Kidney Disease by considering the case of Sarah, a 63-year old female patient with a history of diabetes and other health complications such as cirrhosis and gout. In the paper, we will look at the signs and symptoms exhibited by the patient, then link these to her renal disease. Therefore, this paper is a critical analysis of the patient’s health condition, which is the case study.
Introduction
Among the essential organs in the human body are the kidney, liver, and pancreas. The liver is essential in several functions, including metabolism, digestion, detoxification, and in some instances, the storage of vitamins. The liver is a dual blood supply organ, meaning it receives blood from two sources: the portal vein and the hepatic artery (Moore, 2016). The fact that the liver has a connection, either directly or indirectly, with virtually all organs in the body, stresses its importance. The other organ, kidney, is equally important in the human body. The kidney’s primary function is filtering blood to remove metabolic wastes and excess water from the blood. This paper majorly focuses on the kidney and how damage to the kidney affects the functioning of the other organs. Finally, we have the pancreas, which is a composite organ with endocrine as well as exocrine functions (Moore, 2016). The primary function of the pancreas is insulin production, the hormone that regulates blood sugar in the human body.
Question 1
The normal blood calcium levels range between 8.6 (mg/dL) to 10.2 (mg/dL). In the case study, the patient’s calcium level is 7.1 (mg/dL), which is considerably lower than it should be (Moore, 2016). In the human body, the absorption of calcium into the blood is facilitated by Vitamin D (Robinson et al., 2016). However, the patient’s Vitamin D levels are low, which then explains the relatively low calcium levels in her blood. Furthermore, the kidneys are used to convert Vitamin D into calcitriol, the hormone that regulates the absorption rate of calcium into the blood. Since her kidneys are damaged, they cannot convert the available Vitamin D, further affecting the calcium levels adversely (Robinson et al., 2016).
As for sodium, the patient’s levels (126mEq/L) are generally low compared to the average level for a grown-up (136-145 mEq/L) (Moore, 2016). This difference is attributed to the amount of sodium concentration in the body. One of the functions of kidneys is removing excess water from the body (Robinson et al., 2016). Since the patient’s kidneys have lost their functionality, they cannot remove this excess water, which means that more sodium is dissolved, translating to a generally low sodium level in the blood.
Question 2
Anemia is a medical condition that is characterized by inadequate red blood cells, which translates to a general reduction in the amount of oxygen getting to the body tissues. The red blood cells are made in the bone marrow, with the help of a hormone called erythropoietin, produced in the kidneys (Dhondup & Qian, 2017). Therefore, since the patient is suffering from end-stage renal disease, her kidneys are unable to make enough hormone erythropoietin to facilitate the production of enough RBCs in the bone marrow. The result is a general reduction in the number od RBCs in the blood, which translates to less oxygen reaching all the body parts, and thus anemia (Dhondup & Qian, 2017).
Question 3
Hypotension is the medical term used to refer to the general low blood pressure, usually less than 90 mm Hg systolic or 60 mm Hg diastolic (Moore, 2016). Generally, hypotension is caused by loss of blood through bleeding, severe dehydration, the reaction from medication use, and weak heart muscles resulting from heart failure (Dhondup & Qian, 2017). In our case study, the patient’s kidney failure led to the development of hyperkalemia, a medical condition in which the potassium levels in the blood are higher than they should be. The dysfunction that characterizes end-stage kidney disease affects potassium homeostasis, leading to increased potassium levels in the blood by limiting the number of potassium ions excreted (Dhondup & Qian, 2017).
As a way of trying to rectify this condition, her body may attempt to re-establish homeostasis in several ways. The first is establishing a stable state through the maintenance of the internal environment. By doing so, the body will be attempting to attain a balance in body functions; thus, restart homeostasis (Weir & Rolfe, 2010). The other way is through increased renin production, an aspartic protease protein and enzyme secreted by juxtaglomerular cells found in kidneys. The primary function of renin is increasing the blood pressure, therefore restoring the kidneys’ blood pressure. In doing this, the kidneys’ rate of K+ ions excretion is restored (Murtagh et al., 2016).
Question 4
In this case study, the acid-base disorder most likely to develop is metabolic acidosis. Metabolic acidosis is a clinical condition in which conditions originating in the body cells results in a chemical imbalance in the blood, reducing the blood’s pH levels. Like Sarah, patients with chronic kidney diseases are more prone to metabolic acidosis due to the low renal bicarbonate production relative to acid synthesis (Dhondup & Qian, 2017). The patient’s body may compensate for this condition in several ways. The first is through renal compensation, where excessive H+ is removed while ensuring HCO3 is well maintained. This compensation happens in the kidneys. The other way of compensating for this condition is through respiratory practices. These respiratory practices include hyperventilation, where excessive CO2 is released by breathing very fast (Murtagh et al., 2016).
Question 5
Antidiuretic Hormone (ADH) is a hormone made in the brain’s hypothalamus, which helps the kidney regulate the amount of water to be conserved in the body (Weir & Rolfe, 2010). In the case study, recent laboratory tests show that the patient’s blood glucose levels are incredibly high, 220mmol/L compared to the normal range of 4.44 – 5.55 mmol/l while her ADH is elevated. Therefore, considering her diabetes mellitus history, the condition may be the root cause of these readings (Weir & Rolfe, 2010).
Question 6
Since the patient was recently diagnosed with end-stage kidney failure, the kidneys are unable to regulate sodium and potassium levels properly, thus the low levels of aldosterone. With low aldosterone levels, blood potassium levels are bound to increase, leading to hyperkalemia. The condition is known to result in low blood pressure, a condition characterized by low renin levels, as observed in the laboratory results (Weir & Rolfe, 2010). Furthermore, the patient’s past smoking habit is credited for cirrhosis development, a condition in which the liver cells degenerate, leading to a lower bile production. Bile is the greenish fluid made in the liver that aids in digestion and absorption of fat-soluble Vitamins (D, K, E, and A). Therefore, the low bile levels explain the increased fat content observed in the patient’s stool (Moore, 2016).
Question 7
Calcium is one of the essential minerals as it helps in strengthening of bones and teeth. Therefore, where an individual does not have enough calcium in the body, like our patient, they are bound to experience hypocalcemia, which is a calcium deficiency and is characterized by decreased bone mass other bone diseases like osteoporosis (Robinson et al., 2016). In the case study, since the patient is experiencing low calcium levels, the body is bound to generate parathyroid hormone. Once released, the parathyroid hormone stimulates the release of calcium from the large calcium stores, which primarily include bones and teeth, into the bloodstream to restore the balance as required (Robinson et al., 2016).
Question 8
The yellowish discoloration of the skin and sclera are indications of complications in the liver. When red blood cells are broken down, they form bilirubin. Increased level of the bilirubin results is the discoloration of the mucous membrane and the skin, turning them yellow, which is a pigment signature of bile (Robinson et al., 2016). Therefore, the yellowish patches and sclera on the patient’s skin, which are signs of jaundice, indicate the extensive damage resulting from cirrhosis. The patient bruises and general weakness observed in the patient could be as a result of the general reduction in red blood cells, and the resulting anemia. Finally, one of the most common signs of kidney failure is swelling of limbs. Therefore, since the patient had edema, it is a further indication of the end-stage renal disease. Furthermore, edema is associated with vitamin E deficiency (Moore, 2016).
Question 9
One of the abnormalities observed in the patient’s stool was a grey colored stool. When such an observation is recorded, it usually means that insufficient bile was produced during digestion (Moore, 2016). When the bile produced is low, it means that the liver is having problems. In this case, the problem will be cirrhosis. Grey colored stool could also be an indication of a blockage in the bile ducts. Additionally, since bile is used in digestion and absorption of fat-soluble vitamins, the low bile levels are associated with the increased fats in the patient’s stool. Finally, discoloration of urine usually suggests the presence of infections in the urinary tract. According to Moore (2016), diabetes patients are prone to UTIs due to poor circulation, which reduces the rate of transporting blood cells to the area to fight off infections. Another reason is that the high blood sugars generally increase the chances of developing UTIs.
Question 10
Glisten, a diabetes medication that is designed to work on beta cells, which are responsible for the secretion of insulin from the pancreas. Glisten causes the closure of sensitive potassium channels. The medication facilitates the entry of glucose into beta cells, leading to polarization. Once polarization has occurred, magnesium and ADP are significantly reduced, allowing for the closure of potassium channels and the subsequent opening of calcium channels. The calcium then facilitates exocytosis, a process that will enable insulin to leave the cell (Moore, 2016).
Conclusion
In conclusion, it is evident that the liver and kidney are interdependent, and they collectively contribute to the general well-fare of the human body. Once there is a dysfunction in one of the organs, it affects not only the general functioning of the body but also the normal functioning of the other organ in one way or another. Finally, as observed in the case study, end-stage renal disease is a life-changing and threatening medical condition. Therefore, individuals should maintain healthy living standards to avoid such medical conditions (Moore, 2016).
References
Dhondup, T., & Qian, Q. (2017). Electrolyte and acid-base disorders in chronic kidney disease and end-stage kidney failure. Blood purification, 43(1-3), 179-188.
Moore, T. (2016). Observations and monitoring. Clinical Skills for Nursing Practice, 161.
Murtagh, F. E., Burns, A., Moranne, O., Morton, R. L., & Naicker, S. (2016). Supportive care: comprehensive conservative care in end-stage kidney disease. Clinical Journal of the American Society of Nephrology, 11(10), 1909-1914.
Robinson, B. M., Akizawa, T., Jager, K. J., Kerr, P. G., Saran, R., & Pisoni, R. L. (2016). Factors affecting outcomes in patients reaching end-stage kidney disease worldwide: differences in access to renal replacement therapy, modality use, and hemodialysis practices. The Lancet, 388(10041), 294-306.
Weir, M. R & Rolfe, M. (2010). End-Stage Kidney Disease. Clinical Journal of American Society of Nephrology. CJASN, 5 (3) 531-548; DOI: https://doi.org/10.2215/CJN.07821109