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Chronic Renal Failure - Case Study Paper

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Chronic Kidney Disease 1

Chronic Kidney Disease Alexandria Corcoran NURS 2003 Trent University Victoria Reid-De Jong & Rachel Klompmaker March 24, 2021

Walter has a low urine output (200cc/24hr) (oliguria) and is the result of decreased renal function (11% remaining), which is based on the calculated eGFR (12mL/min/1). As glomerular filtration deteriorates and the kidneys can no longer efficiently filter out waste products from the blood, an accumulation of nitrogenous wastes results. Uremia is the accumulation of urea (a by-product of protein metabolism) and excess fluids, causing integumentary, neurological, and GI symptoms. The accumulation of waste products, metabolic acidosis, and electrolyte imbalances produces symptoms of central nervous system (CNS) depression, such as fatigue, headaches, and difficulty concentrating. Manifestations such as paresthesias in both feet and muscle cramping in legs arise due to peripheral neuropathy. The neuropathy associated with diabetes mellitus exacerbates uremic neuropathy in diabetic patients. This is caused by the nerve fibers and axonal atrophy’s demyelination, thereby reducing nerve conduction to specific areas of the extremities. As CKD progresses, the kidneys’ functional loss causes excess urea to build-up in the blood, which stimulates inflammation and irritation of the mucosa, evidenced by Walter’s nausea and diarrhea (liquid-like stools). As kidney function fails in CKD it can cause pruritus (dry/itchy skin). Pruritus develops from the combination of abnormal calcium-phosphate metabolism, an increase in PTH, DM, build-up of toxins, and sensory neuropathy evoked by renal failure. This can result in calcium-phosphate deposition within the skin, eliciting an itching response. Anemia refers to a lack of RBCs within the blood. The kidneys’ ineptitude to regulate the hormone erythropoietin prevents the bone marrow’s precursors from producing RBCs is due to a reduced functional renal mass manifesting as anemia (Malkina, 2020; Lewis et al., 2019). Excess fluid volume is manifested as weight gain, bilateral pitting edema, and edematous hands and fingers. This results from CKD, kidney malfunction, causing fluid to retain as the person cannot effectively eliminate fluid as evidenced

by his oliguria. The swelling and weight gain can also be the result of albumin, a protein that helps to regulate oncotic pressure. A decrease of protein in the vascular space, can cause fluid to leak from the kidney capillaries into the interstitial tissue. Further, a sign of heart failure is heard by an S3 gallop. Damaged kidneys can produce too much renin, an enzyme that helps regulate blood pressure, increasing the chances of having CHF in conjunction with dyslipidemia. CHF is seen in Walter as evident by the hypopnea and crackles to bases bilaterally caused by hypertrophy of the left ventricle. Hypopnea leads to inadequate gas exchange, resulting in deficient tissue oxygenation (hypoxia). Cardiac cell death leads to HF, and cerebral hypoxia can compromise motor coordination resulting in seizures, coma, and eventually death. Walter’s low 02 (94%) results from an impaired gas exchange in the lungs’ air sacs, as fluid excess causes pulmonary edema and fluid collection in the alveoli. Tachycardia (HR 128BPM) with a bounding pulse and hypertension (BP 178/92 mmHg) is because of an excess production of renin caused by impaired renal function, increased extracellular fluid volume, and sodium retention in turn, requiring a greater threshold for the ventricle to initiate contraction. Tachypnea (RR 30 BPM) causes a decrease in carbonic acid and an increase in H+ ions, which helps compensate for metabolic acidosis. Diagnostics/Laboratory Tests RBC count is low (3 x 1012/L) (male normal 4.7-6 x 1012/L) and is the outcome of the kidney’s inadequate regulation of the hormone erythropoietin, diminishing the production of RBCs. Hemoglobin, a protein molecule found in RBCs, is responsible for excreting CO2 and carrying O2 throughout the body. Considering that the RBC count is low, hematocrit (0/L) and hemoglobin (88g/L) are low. The labs indicate normal sodium levels (141mmol/L) due to kidney insufficiency, it inhibits sodium excretion. Sodium is thus retained along with water,

2020). Total cholesterol levels were done and indicated elevated levels (7/L). A component of metabolic dysregulation is insulin resistance. Hyperinsulinemia puts people with CKD at risk for other health problems, including dyslipidemia, hypertension, and proteinuria (Whaley-Connell & Sowers, 2018). Dyslipidemia contributes to elevated LDLs and a lowered HDL lipoprotein profile. This is due to metabolic dysregulation of lipids, referring to a decrease in enzyme lipoprotein lipase, which is responsible for the breakdown of lipoproteins. Elevated LDLs are related to the development of atherosclerosis increasing chances of CHF. Elevated PTH levels (9/L) are due to a decrease in calcium concentration. The parathyroid glands will secrete PTH in response to elevate the calcium levels. One way to achieve this is to release calcium from the bone through bone demineralization, thereby constantly breaking bone down (renal osteodystrophy). It can also inhibit erythropoiesis, shortening RBC survival, causing bone marrow hematopoietic cells. Glucose levels are also high (14/L) (hyperglycemia) which is caused by uncontrolled blood glucose levels (diabetic neuropathy). Uncontrolled blood glucose levels can damage the blood vessels of the kidneys. The combination of damage and oliguria prevents him from eliminating and filtering wastes. In turn, his insulin cannot store or excrete his glucose, thus a high level. Urea levels are high (37mmol/L) due to the kidneys’ ineptness to effectively filter waste from the blood. Creatinine levels are also elevated (623umol/L). They are caused by the kidneys’ inability to excrete wastes due to malfunction, resulting in a low GFR, and when the GFR is low, creatinine levels increase. Treatment Plan For Walter’s excess fluid volume, treatment should involve administering a diuretic (as prescribed by the physician) to decrease his excess fluid volume. This would reduce the risk of cardiovascular complications worsening (heart failure) and help resolve respiratory

complications (pulmonary edema) secondary to renal failure. Since Walter will be starting hemodialysis, it might be of benefit that he be given a referral for a nutritionist. Nutritionists can provide education on managing dietary restrictions, as he should be put on nutritional constraints for sodium, potassium, protein, phosphate, and strict fluid intake to fix electrolyte imbalances and get his hypertension under control. This is crucial as it will decrease fluid overload. Monitoring input and output is essential for the nurse to help monitor progression or worsening of fluid excess and reduce dehydration risk. If other medications are to be administered to treat any other underlying conditions, administer as directed and provide teaching for Walter on his medications. A 12-lead ECG should be done as Walter is exhibiting heart failure symptoms. He should be monitored for dysrhythmias related to his electrolyte imbalances (hyperkalemia, hypophosphatemia, and hypocalcemia) and CKD. Continue to monitor his vital signs during his visit (HR, BP, RR, etc.). He may need to be admitted to the hospital if his symptoms worsen—review lab data for changes in electrolyte and fluid status. Lastly, patient education of his upcoming hemodialysis treatment is essential. He needs to fully comprehend the significance and role of RRT in maintaining fluid stability. Doing all this will help reduce Walter’s edema, return his vital signs to baseline, have his weight return to normal, and with the aid of dialysis, the fluid within the lungs should be removed. For Walter’s psychosocial nursing diagnosis, social isolation treatment should concentrate on education, support, and mental well-being. It is crucial to assess the patient’s perception and feelings regarding his situation. The patient’s viewpoint acts as a starting point for implementing a plan of care. Walter may benefit from a referral to a mental health specialist or resources easily accessible and suitable to his needs. It is important that he is emotionally supported before, during, and after treatment (hemodialysis) as well as throughout the entire

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Malkina, A. (2020). Chronic Kidney Disease. Merck Manual Professional Version.

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O’Brien, F. (2020). Diabetic Neuropathy. Merck Manual Professional Version.

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Distinct Role Separate from That of Diabetes or Obesity. Cardiorenal Med, 8, 41-

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Chronic Renal Failure - Case Study Paper

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Course : Nursing Therapeutics (NURS-2003H-A)