Acute Renal Injury and Chronic Kidney Disease

Document Type:Case Study

Subject Area:English

Document 1

In addition to that, there should be honesty, confidentiality, good communication skills, and display of high level of competence. This can be achieved when patients are educated well on their condition, the pathology, and how the patient can participate in achieving their own well-being by ensuring they take their drugs early enough and manage their diet appropriately (Allinson, 2016). Through this means, there will be patient cooperation and proper management of the condition. What is the difference between azotemia and uremia? Kidneys are one of the major vital organs in the body. They perform a number of functions such as waste filtration, urine formation, control of blood pressure, absorption of electrolytes, and maintenance of fluid balance, among many others. Patients having the condition do not have symptoms manifestation in spite of high levels of nitrogen and creatinine in the blood.

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This is a starter sign that will eventually lead to uremia. Ideally, amino acids and proteins metabolism result in nitrogenous by-products that should be removed via urine. When the kidneys are defective, there is no filtration of the by-products thus accumulates in the blood. The normal serum creatinine and BUN are between 0. The proteins will result in increased glomerular filtration and intra-glomerular pressure. As a result, the glomerular structure will be damaged and this will deteriorate the kidney disease. Therefore, implementation of a diet having fewer proteins is crucial. The recommended protein levels in the management of a chronic kidney disorder is between 0. 6 to 0. Ideally, the kidneys are bean-shaped organs that produce erythropoietin. When a person such as Will develops ESKD, some of the kidneys’ functions are lost, and this includes the production of erythropoietin.

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Usually, the production of EPO is significantly decreased, or it’s not produced totally in severely damaged kidneys. Thus, only a few red blood cells will be produced and this leads to anemia. In anemia, there are few red blood cells available for gaseous exchange which leads to oxygen deprivation and thus accumulation of carbon dioxide that causes body fatigue and weakness. Thus, treatment of anemia by supplying erythropoietin is important since it reduces the extent of LVH. Other predisposing factors that can lead to the formation of LVH in CKD persons include disorders of mineral metabolism such as secondary hyperthyroidism, low vitamin D levels, hyperphosphatemia, and hypocalcemia. In addition to that, there could be endothelial dysfunction, hyperhomocysteinemia, oxidative stress, and elevated asymmetric dimethylarginine; this increases atherogenesis and inflammation (Taddei, Nami, Bruno, Quatrini, & Nuti, 2011).

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