Pathophysiology of Chronic Kidney Disease
Week 5 Discussion Board- V3 Assignment
Pathophysiology of Chronic Kidney Disease: According to Banasik (2018), end-stage renal disease is the final outcome of chronic kidney disease. It is the deterioration of the kidneys and renal function. The decline in renal function is irreversible. According to the National Kidney Foundation (2014), some of the biggest risk factors for kidney disease include; family history of kidney disease, age 60 or older, diabetes, and hypertension. There are several steps to prevent kidney disease. Some of the most common preventative tips would be to stop smoking, lose weight if overweight, limit alcohol intake, lower sodium intake, and exercise (National Kidney Foundation, 2014). Obesity is a common problem in our society. Being overweight or obese may lead to developing hypertension, diabetes, stroke, arthritis, and kidney disease (National Kidney Foundation, 2014). Hypertension and diabetes are two important risk factors for developing kidney disease. This is important to teach patients because they may not necessarily understand how being overweight can contribute to decreased kidney function. Educating patients to go to their annual physicals and monitor their blood pressure will help promote a healthy lifestyle. For patients who are diagnosed with chronic kidney disease, there are several tips that promote kidney health. These include; monitor blood pressure often, manage blood sugars, reduce salt intake, avoid NSAIDs, moderate protein consumption, and getting an annual flu shot (National Kidney Foundation, 2014).
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Pathophysiology of Chronic Kidney Disease References
Banasik, J. L. (2018). Pathophysiology, 6th Edition. [VitalSource]. Retrieved from https://vsaccess.vitalsource.com/#/books/9780323354813
Prevention. (2014, November 3). In National Kidney Foundation. Retrieved from https://www.kidney.org/prevention
Pathophysiology of Chronic Kidney Disease
Per Banasik, ESRD is a common outcome of chronic glomerulonephritis necessitating dialysis or kidney transplantation. Three major risk factors include diabetes, high blood pressure, a family history of kidney failure and age sixty or older.
In the website, some of the most common preventative tips include; quit smoking, alcohol and your kidneys, lose weight if your overweight or obese, lower salt in your diet, understanding food labels and Exercise.
Reading the nutrition facts label is the most missed preventative tips. Food labels have percent daily values listed for a set of a group of nutrients. The reading label will help the patient to look at the list of ingredients to avoid. Pt can ask for help at their dietician to look labels to meet their needs best and ask for the recommendation to better help them in taking care of their body. Not only it will help us preventing kidney failure, and it will also teach us to be mindful of the food with eating.
Banasik, J. L. (2018). Pathophysiology, 6th Edition. [VitalSource]. Retrieved from https://vsaccess.vitalsource.com/#/books/9780323354813
Nutrition Facts Label. (2014, November 3). In the National Kidney Foundation. Retrieved from https://www.kidney.org/atoz/content/foodlabel
Pathophysiology of Chronic Kidney Disease
Post-infectious acute glomerulonephritis usually follows skin and throat infections. “The infectious organism stimulates the production of antibodies that bind to microbial antigens, initiating formation of antibody–antigen complexes. Antibody deposition leading to inflammation is the key pathologic event. Proliferation of mesangial cells is initiated after immune complex deposition, resulting in characteristic proliferative lesions. Complement is activated within the glomerulus, resulting in release of chemotaxic factors and attracting macrophages, neutrophils, and T-helper cells. Lysosomal enzymes are released and attack glomerular walls. The changes in the structure of the glomerular membranes result in a decrease in the surface area available for filtration and allow substances that were previously restricted to enter the glomerular space.” (Banasik, 2018, p588)
Nephrosis occurs when the injured kidney releases excess protein in the urine due to glomerulonephritis. This inflammation leads to a change in the normal cells of the glomerulus to that of mesangial cells. This change in the wall of the glomerulus allows for proteins to be excreted injuring the kidney leading to nephrosis.
JH’s potassium level is elevated at 5.4 bicarbonate, hematocrit, sodium and arterial carbon dioxide are decreased. BUN, creatinine, and albumin levels are also elevated, protein is positive in the urine which points to the patient progressing to renal failure.
JH’s decreased urine output, increased lethargy, and hyperventilation are physical findings that point to renal impairment. The degree of renal impairment can be determined through creatinine clearance, GFR, CBC and CMP, and Urinalysis.
Should JH’s condition progress from nephrosis to uremia, his therapy would likely include dietary restrictions such as low-protein diet, reduced fluid intake to reduce fluid overload, and sodium and potassium restrictions.
Pathophysiology of Chronic Kidney Disease
Banasik, J. (2018). Pathophysiology, 6th Edition. [VitalSource]. Retrieved from https://vsaccess.vitalsource.com/#/books/9780323354813/
Pathophysiology of Chronic Kidney Disease
Acute glomerulonephritis encompasses a constellation of inflammatory glomerulopathies that are characterized by the abrupt onset of varying degrees of hematuria, proteinuria, oliguria, azotemia, edema, and hypertension (Banasik, 2018). Pneumococcal infection leads to glomerulonephritis through the inflammation process that occurs, resulting in pneumococcal infection injuring the glomerular capillary and basement membrane. Mesangial cells take the place of normal glomerulus cells that become similar in structure to proliferative lesions. JH appears to be progressing into renal failure based on his abnormal lab findings. Lab values suggests association with renal failure: a compensated metabolic acidosis, elevated BUN and creatinine, abnormally high potassium level, and a low hematocrit level. Low sodium and low albumin levels are indicative of nephrosis. To aid in determining JH’s degree of renal impairment, I would look at the estimated glomerular filtration rate via creatinine clearance, urinalysis for protein, and serum calcium levels. JH’s physical findings would include edema as a resultant of fluid retention from decreased urine output and pruritus. Due to low percentage of hematocrit levels, I would also suspect lethargy. Low bicarb levels suggest metabolic acidosis, this would result in the body trying to compensate by hyperventilating. If JH’s condition was to progress from nephrosis to uremia, JH’s therapy would change from a no fluid restriction to a fluid restricted diet. High urine output usually exists in nephrosis and patients are encouraged a high protein intake. A low protein diet would be recommended if JH’s condition turns into uremia. JH’s intake would also benefit from a low salt and a low potassium diet.
Pathophysiology of Chronic Kidney Disease
Banasik, J. (2018). Pathophysiology, 6th Edition. [VitalSource]. Retrieved from https://vsaccess.vitalsource.com/#/books/9780323354813/