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NUR 660 Week 11 Discussion 1 Team A Renal Disorders NUR 660 Week 11 Discussion 1 Team A Renal Disorders NUR 660 Week 11 Discussion 1 Team A Renal Disorders Team A Please use this thread to create your reply posts, as indicated in the forum instructions. To ensure you do not miss any questions, please copy and paste all questions into your discussion post. Team A Renal Disorders Explain why hematuria and proteinuria reflect a glomerular problem rather than a tubular problem in the kidney. Explain the change in filtration if excess glucose is present in the blood entering the kidney. Explain factors that may contribute to elevated blood pressure in a patient with renal disease. Compare acute and chronic renal failure with respect to cause, reversibility, and urinary output at onset. Why is there an increased risk of drug toxicity in the later stages of renal failure? Why is protein intake restricted in patients with kidney disease? Compare the causes and pathophysiology of acute pyelonephritis, APSGN, and nephrotic syndrome. Posting to the Discussion Forum Highlight and copy your assigned question from the list. Select Reply. Select Advanced. Delete the subject line from the subject line field. Type your assigned question number (e.g. “Question # 1”) into the subject line field. Paste your assigned question into the reply text field. Create your response. Select Post when completed.   Explain why hematuria and proteinuria reflect a glomerular problem rather than a tubular problem in the kidney. Hematuria is small, microscopic amounts of blood which are associated with infection, inflammation, or tumors in the urinary tract, large amounts which is gross hematuria point to increased amounts of red blood cells which indicate glomerular permeability or hemorrhage in the tract. Glomerular disease can also leak blood into your urine (National Kidney Foundation, 2017). Proteinuria indicates a leak of albumin or mixed plasma proteins into the filtrate due to inflammation and increased glomerular permeability. If there is a glomerular disease present it can cause glomeruli to leak protein into your urine (National Kidney Foundation, 2017). In glomerulonephritis a type III hypersensitivity reaction activities the complement system to cause an inflammatory process which leads to increased capillary permeability and cell proliferation resulting in increased leakage of proteins and erythrocytes in the filtrate (Huber & VanMeter, 2018). 2. Explain the change in filtration if excess glucose is present in the blood entering the kidney. According to Huber & VanMeter (2018), if glucose is present in excessive amounts in the filtrate there are insufficient carrier molecules in the tubules for the complete reabsorption into the blood in the peritubular capillaries which makes glucose present in the urine. Click here to ORDER an A++ paper from our Verified MASTERS and DOCTORATE WRITERS: NUR 660 Week 11 Discussion 1 Team A Renal Disorders 3. Explain factors that may contribute to elevated blood pressure in a patient with renal disease. Hormones that control reabsorption of fluid and electrolytes are antidiuretic hormone, aldosterone, and atrial natriuretic hormone (VanMeter & Huber, 2018). According to Huber & VanMeter (2018), blood pressure is closely related and elevated in renal disease. When blood flow or blood pressure in the afferent arteriole goes down for any reason, the renin-angiotensin-aldosterone triad is activated. This hormone increases reabsorption of Na + and water to increase blood volume which increases blood pressure. To confirm this serum renin can be tested. 4. Compare acute and chronic renal failure with respect to cause, reversibility, and urinary output at onset. Acute renal failure is reservable if the primary problem is treated and oliguria with increased serum urea will be present. Some causes for acute renal failure include severe shock, burns, nephrotoxins, massive exposure, acute bilateral kidney infection or inflammation. With chronic renal failure it is irreversible, and some early signs are polyuria with dilute urine, anemia, fatigue, hypertension and then oliguria. Some causes of chronic renal failure are nephrosclerosis, DM, long exposure to nephrotoxins, chronic bilateral kidney inflammation or infection, and polycystic disease (Huber & VanMeter, 2018). 5. Why is there an increased risk of drug toxicity in the later stages of renal failure? There is an increased risk of drug toxicity in the later stages of renal failure because some drugs are filtered out by the kidneys and if the kidneys are necrotic and unable to filter then the drug stays in the body increasing in levels not being filtered out. 6. Why is protein intake restricted in patients with kidney disease? In kidney disease the kidneys are limited in their ability to filter out proteins and excrete excess wastes and fluids, therefore protein is restricted along with fluid and electrolytes (VanMeter & Huber, 2018). 7. Compare the causes and pathophysiology of acute pyelonephritis, APSGN, and nephrotic syndrome. Acute pyelonephritis is when an infection extends from the ureter into the kidney and it involves the renal pelvis and medullary tissue, purulent exudate fills the kidney pelvis and calyces, and the medulla is inflamed. Abscesses and necrosis is in the medulla and goes into the cortex of the surface of the capsule. APSGN (Acute poststreptococcal glomerulonephritis) and it follows certain streptococcal infections from upper respiratory infections, middle ear infections or “strep throat.” It is a type III hypersensitivity reaction that lodges in the glomerular capillaries and signals the complement system which leads to increased capillary permeability and cell proliferation. With severe inflammatory response, the congestion and cell proliferation interfere with the filtration in the kidney which leads to decreased GFR and retention of fluids. Nephrotic syndrome is secondary to many renal diseases and systemic disorders such as systemic lupus erythematosus or toxin or drug exposure. The sequence occurs like this: abnormality in glomerular capillaries and increased permeability which allows large amounts of plasma proteins (albumin) to escape into the filtrateà marked hypoalbuminemia with decreased plasma osmotic pressure and generalized edemaà blood pressure remains low and causes include hypovolemia à decreased blood volume increases aldosterone secretion à leading to increased edemaà other components include high cholesterol levels and lipoproteins in urine (possibly related to response of the liver from heavy protein loss) (Huber & VanMeter, 2018).References: National Kidney Foundation. (2017). Understanding glomerular diseases. Retrieved November 08, 2021, from https://www.kidney.org/atoz/content/understanding-glomerular-diseases#:~:text=Protein%20in%20the%20urine%20(proteinuria,build%20up%20in%20your%20body. VanMeter, K. C., & Hubert, R. J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders. Order Now