Difference Between Azotemia and Uremia Paper Example

Introduction

Azotemia and Uremia are types of kidney conditions. Suganya, Priya, Samuel, and Rajagopalan (2016 p.131) indicate that azotemia is a medical condition that occurs when extremely high levels of nitrogen compounds such as urea, uric acid, and creatinine accumulate in the blood. Uremia is what occurs when azotemia remains uncontrolled. Azotemia is related to the dysfunctional and insufficient ability of the kidney to filter blood. Also, depending on the causative origin, azotemia has three classifications, which include pre-renal, post-renal, and renal. The characteristics of all forms of azotemia are a low amount of glomerular filtration rate of the kidney, a rise in blood urea nitrogen, and concentration of serum creatinine (Suganya, Priya, Samuel, and Rajagopalan, 2016 p.131). In clinical diagnosis, doctors determine the type of azotemia by examining the ratio of blood urea nitrogen and serum creatinine. Renal azotemia, also known as acute renal failure leads to uremia because, at that stage, the renal parenchymal is already damaged. Post-renal azotemia causes a blockage in the flow of urine, uterus, and the urethra. Pre-renal failure occurs when high ratios of blood urea (Suganya, Priya, Samuel, and Rajagopalan, 2016 p.132). Brown and Shah (2014 p.76) affirm that laboratory results cannot show the presence of uremia in a patient. Instead, uremia is a clinical syndrome that is attributed to renal failure. The manifestations of Uremia are nausea, confusion, seizures, malaise, pruritus, bleeding, fluid overload, and pericarditis.

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The reason Will's Physician warned him about his Diet

The physician warned will about his protein diet because, in a case of renal sufficiency, the kidney is unable to secrete waste products of protein metabolism. Suganya, Priya, Samuel, and Rajagopalan (2016 p.132) articulate that in gaestrinogen bleeding, the blood urea levels increase significantly because the blood, which mainly contains protein hemoglobin is broken into amino acids. After metabolism of the protein, the end product is urea because the protein meal is present in the blood in form of urea. As discussed above, high concentrations of urea, a nitrogenous waste, results in azotemia, which if left uncontrolled, will eventually, lead to uremia. Pre-renal causes are identified by high ratios of urea and creatinine (Suganya, Priya, Samuel, and Rajagopalan, 2016 p.132). Diets, which are rich in protein cause the increased ratios of urea in the blood. WANTABE (2016 p.1) indicates that a diet that has minimal protein results in the preservation of the kidney function, improves hyperphosphatemia and hyperkalemia, minimizes the excretion of urinary protein, reduces kidney complications, improves renal failure symptoms, and prolongs hemodialysis. A low-protein diet has always been used in Japan to control renal failure. The low protein diet is necessary for patients who have chronic kidney disease that is leading to kidney failure. In an observation of a 52-year old man who had chronic kidney disease under a strict low protein diet, his blood urea nitrogen and creatinine decreased considerably (WANTABE, 2016 p.1). The clinical dose for patients with chronic kidney disease is 0.5 g/kg b.wt. In the 52-year man's case, his protein intake was limited to 0.75 g/kg. The man managed to control his renal function for over 10 years with the low protein diet. Notably, if the kidneys are not working well, because of a pre-existing condition like hypertension just as Will's case, urea builds up in the blood stream. In essence, a low-protein diet reduces the workload of the kidneys thus making them remain healthy to carry out their functions.

The Reason Will is Anemic

Will is anemic because, during a renal failure, the production of red blood cells becomes minimized. Kimmel and Rosenberg (2014, p.266) articulate that anemia is common in patients who have chronic kidney disease and have lower levels of creatinine. Anemia in patients with kidney disease is hyper-proliferative in nature. The count of circulating reticulocyte is minimal and an examination of the bone marrow does not depict an increase in the progenitor cells as usually seen in anemic patients who do not have chronic kidney disease. Furthermore, the dominant factor associated with the production of red blood cells in the bone marrow is the regulatory hormone called erythropoietin that allows the circulation of red blood cells in the body. More so, in patients with chronic kidney disease, the basis of the anemia is the deficiency of erythropoietin. When the amount of red blood cells and hemoglobin is reduced in the blood, the levels of oxygen in the body reduce as well thus result in anemic symptoms. Besides that, Will is anemic because of anorexia. His loss of appetite makes him lack proper feeding, which is necessary for the formation of red blood cells. Mamou, Sider, Bouscary, Moro, and Blanchet-Collet (2016 p.1) articulate that anemia is a hematological complication of anorexia nervosa. Anemia in anorexia nervosa patients is often misdiagnosed as iron deficiency but it is mostly the patient's feeding habits. Will's lack of appetite makes him unable to eat the required nutrition necessary to equalize the number of blood cells in his body. Anemia with anorexia patients is categorized in etiology groups such as hemolysis, blood deprivation, bone marrow malfunction, and loss of hemoglobin or inflammation. All in all, clinicians should be keen in their diagnosis to ensure that they find out the right type of anemia that a patient has.

Will's Left Ventricular Dysfunction

Based on Will's story, the left ventricular dysfunction is a concern for his physician because hypertension increases pressure on that side making an individual has a high demand for oxygen. Lovic, Narayan, Pittaras, Faselis, Doumas, and Kokkinos (2017, p.1) articulate that in hypertensive patients, cardiac adaptations are present, which exert pressure on the left side of the heart, which eventually results in left ventricular hypertrophy. Will's doctor is concerned about his condition because an overload in the left ventricular section of the heart can result in serious complications. Some of those complications include heart failure, myocardial infarction, arrhythmias, sudden cardiac death, and stroke (Lovic et al, 2017, p.1). In hypertension, the heart responds to the elevated hemodynamic load that has both structural and functional changes. Some of the structural changes include hypertrophy of myocytes and an increase in connective tissue that results in mass in the left ventricular (Lovic et al, 2017, p.1). Due to the heavy mass, the left ventricular section can in wall thickness and systolic dimensions. Regarding functional changes, in a patient with hypertension, the workload makes it impossible to normalize the pressure exerted on the left ventricular walls, which results in an increase in left ventricular cavity and contractility, which will eventually cause heart failure. Besides that, another concern for the doctor would be due to polyuria. Furthermore, Lullo, Gorini, Russo, Santoboni, and Ronco (2015, p.1) affirm that systolic hypertension is linked to left ventricular hypertrophy in patients with chronic disease, which suggests that the fluid overload, often recognized as polyuria, increases arterial stiffness in the left ventricular. More to the point, Will's physician is concern about left ventricular dysfunction because of his patient's anemic state. Cho, Mun, Kwon, Shin (2014 p.1) affirm that in anemic patients, low hemoglobin levels are evident in the chambers of the heart. Besides, anemic patients have an increased left ventricular mass and a higher left ventricular filling pressure. The pressure occurs because anemia minimizes the tissue oxygen delivery, which eventually results in cardiovascular response. Particularly, patients who have chronic anemia have structural changes in their heart such as impairment because the heart has a hemoglobin deficiency. Overall, patients who have anemia have an increased cardiac mass, which mostly affect the left ventricular section of the heart.

References

Brown, T.A., & Shah, S.J. (2014). USMLE Step 1 Secrets3: USMLE Step 1 Secrets. San Diego, CA: Elsevier.

Cho, I., Mun, Y.C., Kwon, K.H., and Shin. G.J. (2014). Effect of anemia correction on left ventricular structure and filling pressure in anemic patients without overt heart disease. The Korean Journal of Internal Medicine, 29(4):445-453.

Kimmel, P.L., & Rosenberg, M.E. (2014). Chronic Renal Disease. San Diego, CA: Elsevier.

Lullo, D., Gorini, A., Russo, D., Santoboni, A., and Ronco, C. (2015). Left Ventricular Hypertrophy in Chronic Kidney Disease Patients: From Pathophysiology to Treatment. Cardiorenal Med, vol. 5, no. 4.

Lovic, D., Narayan, P., Pittaras, A., Faselis, C., Doumas, M., and Kokkinos, P. (2017). Left ventricular hypertrophy in athletes and hypertensive patients. The Journal of Clinical Hypertension, vol. 19, Issue 4.

Mamou, G., Sider, A., Bouscary, D., Moro, M.R., and Blanchet-Collet, C. (2016). Anemia in Anorexia Nervosa: The Best Way to Deal with it-An Overview of Literature. Journal of Human Nutrition and Food Science, vol.4, no.1.

Suganya, P., Priya, S., Samuel, R., & Rajagopalan, B. (2016). A Study to Evaluate the Role of Bun/Creatinine Ratio as a Discriminator Factor in Azotemia. Int. J. Pharm. Sci. Rev. Res., 40(1), Article No. 26, Pages: 131-134.

WATANABE, S. (2017). Low-protein diet for the prevention of renal failure. Proceedings of the Japan Academy. Series B, Physical and Biological Sciences, 93(1), 1-9. http://doi.org/10.2183/pjab.93.001