Week 8 Discussion

Discussion #1

Why does she have bacteria and white blood cell casts in her urine? Include the pathophysiological response of body for your analysis.

In acute pyelonephritis, the upper urinary tract and kidneys are affected and can lead to a life-threatening infection that can cause kidney scarring (Fulop,2018). Pyelonephritis can be contracted due to bacteria traveling up to the upper urinary tract and into the blood stream from the lower urinary tract, usually begins as a UTI, bacteria could be found within the urine due to the infection (Fulop, 2018). The most common bacteria to cause pyelonephritis is Escherichia coli, but other bacteria such as enterococci, staphylococcus aureus, pseudomonas aeruginosa, etc can be the cause of the infection (Fulop, 2018). The infection can lead to inflammation in the urinary tract/kidneys and a medullar spread of white blood cells to stop the infection (McCance & Huether, 2014).

What are the differences when comparing prerenal acute renal injury, intrarenal acute renal injury, and postrenal acute renal injury?

Give examples of each and pathological processes related to each disease process.

Prerenal acute renal failure Involves sudden hypoperfusion in the kidneys that causes decreased filtration/ kidney function due to low filtration pressure and the decrease of blood flow to the kidneys, although there is no damage to the kidney itself, there might be a decrease in urine output (McCance & Huether, 2014). Common causes include loss of blood, dehydration, severe burns, low blood pressure, renal artery clots, and medication that affect the renal blood flow (McCance & Huether, 2014).

Intrarenal acute renal failure involves acute tubular necrosis (McCance & Huether, 2014). Tubular cells are damaged by medications that can be toxic to these cells and lead to several damaged internal structures within the kidneys. This can impair filtration and lead to an irreversible kidney injury (McCance & Huether, 2014).

Post renal acute renal failure involves an increase in intraluminal pressure that can lead to reduced kidney filtering in the glomeruli (McCance & Huether, 2014). Post renal acute renal failure can be cause by obstructions such as clots, engorged prostates, urinary stones, and muscular triggered bladder obstruction (McCance & Huether, 2014).

Discussion #2

1. Why does she have bacteria and white blood cell casts in her urine? Include the pathophysiological response of body for your analysis.

The reason that Ms. Cornwall has bacteria and white blood cell in her urine is because the bacteria have the ability to attach itself to the uroepithelium. The strains of bacteria (E. coli) are called type-1 pili. These organisms have mucosal receptors allowing them to bind to the cells and resisting flushing during micturition. The uropatic cells uropatic strains of E. coli have fimbrae that are pyelonephritis type which cam bind to uroepithelial p-blood antigen and go up to the urinary tract causing a UTI (McCance & Huether, 2014).

E. coli is a bacteria associated with pyelonephritis. It can split urea into ammonia making alkaline urine. A urine’s high PH makes a person susceptible to kidney stones. Pyelonephritis is infection of the urinary tracts. It can be caused by obstruction and urine travelling from the bladder to the ureters. These uropathic organisms find their way up through the ureters, but they can also spread from the blood stream. The medulla becomes infiltrated with WBC’s causing kidney swelling and inflammation with purulent urine (McCance & Huether, 2014).

2.  What are the differences when comparing prerenal acute renal injury, intrarenal acute renal injury, and postrenal acute renal injury? Give examples of each and pathological processes related to each disease process.

Prerenal acute renal injury- The kidneys become hypoperfused with blood over a period of hours. BUN and plasma creatinine levels become elevated as a result. Autoregulatory mechanisms tries to compensate to maintain the glomerular filtration rate. Causes of prerenal acute renal injury include vomiting, diarrhea, heart failure and sepsis. Kidney function is returned to baseline after volume depletion is fixed (McCance & Huether, 2014).

Intrarenal acute renal injury- It can be caused by acute tubular necrosis, glomerulopathies, vascular damage and acute pyelonephritis. The most common type of acute renal injury is acute tubular necrosis. Caused by ischemia and nephrotoxicity. It does not improve with fluid replenishment and blood flow to the kidneys. Temporary renal replacement therapy may be required, but it can resolve over time (Rahman, Shad, & Smith, 2012).Postischemic ATN involves hypoperfusion leading to ischemia and reduced levels of ATP that generates toxin oxygen-free radicals with loss of antioxidant protection. The contributing factor to cellular injury is activation of inflammatory cells and complement and release of inflammatory cytokines.

Postrenal acute kidney injury- This type of kidney injury is rare. It usually occurs with urinary obstruction. There is a decrease in GFR with an increase in intraluminal pressure above the site of obstruction. Anuria and flank pain followed by polyruria are seen in patients with postrenal acute kidney injury (McCance & Huether, 2014).