Urological Patient Case Study Analysis and Management Plan

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SOLUTION
Urological Patient Case Study Analysis and Management Plan
Diagnosis and Classification:
According to the presenting symptoms, the patient suffers from acute kidney injury. The patient’s acute kidney injury is classified as pre-renal acute kidney injury.
Background:
Previously known as acute kidney failure, acute kidney injury is a condition that individuals face characterized by the rapid decline in kidney functioning, especially around the glomerulus of the kidney. Pre-renal acute kidney injury is characterized in individuals by the increase in blood serum creatinine. Creatinine is a waste product of muscle metabolism in the body. The kidneys are known for the excretion of waste materials through urine output. For urine output to occur, the renal artery supplies the kidney, specifically the glomerulus, with blood filled with waste materials (Lawrence et al., 2018). The glomeruli, located in the nephrons of the kidneys, are responsible for four primary functions of the kidneys; the filtration of blood, the re-absorption of substances back into the body through blood, the secretion of other substances from the blood into the nephron tubules (Ogobuiro & Tuma, 2019). The glomeruli effectively create the filtration system for waste products to leave the bloodstream through the afferent arteriole when the renal artery branches in the nephrons (Ogobuiro & Tuma, 2019). Re-absorption and secretion of waste materials into and out of the bloodstream happen, and blood moves back into the body through efferent arterioles, leaving behind filtrate that is excreted as urine. However, that is not usually the case in pre-renal acute kidney injury.
During pre-renal acute kidney injury, there is decreased blood flow into the kidneys. This happens because of a decreased loss of body fluids. Loss of body fluids may be because of diarrhea, vomiting, or hemorrhaging (Tyagi & Aeddula, 2019). Also, pre-renal acute kidney injury can occur when the renal artery is constricted by an embolism or renal artery stenosis. Therefore, the less the blood flows into the kidneys, the less the blood is being filtered; hence, a decrease in glomeruli filtration rate (GFR) (Tyagi & Aeddula, 2019). Resultantly, decreased filtered blood leads to decreased creatinine and urea excreted out of the body (Tyagi & Aeddula, 2019). Consequently, there is an increase in blood serum nitrogen (BUN), known as azotemia, and blood serum creatinine (Tyagi & Aeddula, 2019).
In addition, decreased blood filtration by the glomeruli leads to the activation of the rennin-angiotensin aldosterone system. This system in pre-renal acute kidney injury leads to the adrenal glands’ production of the aldosterone hormone. Aldosterone is responsible for the re0absorption of sodium from the filtrate in the nephron tubules before excretion happens (Ba Aqeel et al., 2017). Consequently, increased sodium re-absorption in the blood leads to increased water retention and re-absorption. Water re-absorption increases the re-absorption of BUN and creatinine, leading to a BUN to creatinine ratio that is greater than 20:1, which is the expected ratio of BUN to creatinine in the blood (Ba Aqeel et al., 2017; Tyagi & Aeddula, 2019). This leads to the development of pre-renal acute kidney injury.

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