HEALT1112 Assessment Task 1 Analysis: Kidney Function Assignment Sample

Kidney Adaptations and Mechanisms During Blood Pressure Decline

Overview

This assignment will focus on the function of the kidney in maintaining homeostasis and how the kidney responds to declining blood pressure levels. The kidney is considered as one of the important regulatory systems for maintaining extracellular fluid volume homeostasis. Extracellular fluid volume is a key regulatory component of long-term blood pressure control influenced by controlling tubular sodium transport (Almeida et al. 2020). According to research, it was seen that high blood pressure affects approximately 67 million of the American adult population, which is equivalent to every one in three people (Iqbal & Jamal, 2023). On the other hand, blood pressure regulation is another complex and integrated mechanism. Soliman & Pollock (2021) have mentioned that the relationship between sodium excretion, circulatory system regulation, and blood pressure is a complex and important mechanism for regulating circulatory volume. The function of the kidney in this process is to regulate the circulatory volume by controlling the water and sodium balance for maintaining extracellular fluid volume or ECFV homeostasis (Iqbal & Jamal, 2023). This report aims to evaluate the homeostasis of the kidney and the way it responds to declining blood pressure levels.

Normal Anatomy And Physiology Of Body Systems

A kidney is a two-bean-shaped organ whose major function is filtration. More specifically, the kidney filters blood. They remove waste products (such as urea and creatinine) and excess water, producing urine. The kidneys help to regulate fluid balance by adjusting the amount of water reabsorbed or excreted, through which the kidney can maintain the kidney homeostat hydration of the body (Sterns, 2020). Another important function of the kidney is electrolyte regulation by maintaining the level of essential minerals (electrolytes) like sodium, potassium, and calcium in the blood. When blood pressure drops, the kidney releases renin, which converts angiotensinogen into angiotensin I (Leite et al. 2022). The angiotensin I is then converted into angiotensin II whose function is to constrict the blood vessels, which in turn triggers the release of aldosterone from the adrenal cortex. This Aldosterone further stimulates the kidneys to reabsorb the sodium, which helps in increasing and maintaining the blood pressure level. Guyton’s model refers to the relationship between renal perfusion pressure, excretion of Na, and blood pressure level as a mechanism of the regulated circulatory system (Iqbal & Jamal, 2023). The role of the kidney in managing the circulatory system or volume is to maintain a balance between sodium and water levels, which further triggers the balance between ECFV or extracellular fluid volume homeostasis, Pinter et al. (2020) have mentioned that an increase in sodium and water levels in the body can lead to an increase of ECFV which helps in increasing the blood volume. This increase in blood volume induces the atrial stretch and increases the cardiac output, which as a whole increases the systematic blood pressure level. In this situation, as per the research, it has been seen that when the arterial pressure increases, it stimulates the nephron for reduction of water and sodium reabsorption in the blood, which helps in maintaining the blood pressure level in normalcy. This scenario is known as ‘pressure natriuresis” (Baek & Kim, 2021). On the other hand, when the blood pressure level remains too low, the nephron increases the water and sodium reabsorption, which thereby increases the ECFV or extracellular fluid volume level in blood and body, which triggers the increase of blood pressure level. This is how the kidney maintains homeostasis and responds to the decline of the blood pressure level.

The Situation That Causes Homeostasis Challenge Or Dysfunction 200

In homeostasis between the kidney and decline in blood pressure, one of the key mechanisms is the renin-angiotensin-aldosterone system or RASS. This mechanism helps in regulating blood pressure, fluid balance and electrolyte homeostasis by the kidney. When the blood pressure drops, the JG cells or juxtaglomerular cells in the kidney secrete renin, which converts angiotensinogen to angiotensin I and then to angiotensin II by the ACE or angiotensin-converting enzyme (Olde Engberink et al., 2023). Angiotensin II has several effects, including vasoconstriction, which increases peripheral resistance and blood pressure; it can also stimulate the release of aldosterone, which acts on distal convoluted tubules and collecting ducts of the nephrons to increase the sodium and water reabsorption. This mechanism can further increase the blood volume and blood pressure (Leite et al., 2022). However, if the decline in blood pressure level is sustained for a prolonged time, it can cause homeostatic dysfunction and AKI or acute kidney injury. Acute Kidney Injury can be characterised by a rapid decrease in renal NAD+ level, which restricts the mitochondria from functioning properly and energy production (Morevati et al., 2022). This can cause further deterioration in kidney function and the development of chronic kidney disease, or CKD. According to research, AKI can be characterised by an abrupt decrease in GFR or glomerular filtration rate and accumulation of waste products in the blood (Kellum et al., 2021). In the context of the decline in blood pressure, AKI primarily arises from the prerenal causes. When the blood pressure drops significantly, in case of hypovolemia, shock, and sepsis, renal perfusion pressure decreases, which further reduces the blood flow of the kidney and the ability of blood filtration, as a whole causing dysfunction of homeostasis of the kidney.

Homeostatic Impact

The kidney plays an important role in maintaining homeostasis, particularly in response to changes in blood pressure. However, physiological dysfunction, such as acute kidney injury or AKI can cause a sudden decrease or decline in blood pressure level, which has a profound impact on multiple body systems, particularly on the endocrine and renal systems. According to research, the kidney releases EPO or erythropoietin, in response to the hypoxia, which stimulates the production of RBC or red blood cells (Bhoopalan et al., 2020). AKI or acute kidney injury, can restrict EPO production, which can lead to the onset of anaemia. On the other hand, the sudden disruption in RAAS and ADH or antidiuretic hormone secretion, can affect the fluid and electrolytic balance, which further can influence the endocrine function and systematic homeostasis (Iovino et al., 2021). In the case of the renal system, homeostatic dysfunction can restrict the elimination of waste products from the body and balance the fluid. In the case of a dysfunction of the kidney, homeostasis can reduce the kidney’s ability to filter the blood, which results in the accumulation of metabolic waste products like urea and creatinine and causes electrolytic imbalance or hyperkalemia. This scenario can disrupt the overall systematic equilibrium and affect the other organs that play an important role in maintaining stability in fluid and electrolyte levels.

Anatomical And Physiological Adaptations

When kidney dysfunction impairs homeostasis, the body needs to adopt anatomical and physiological adaptations to mitigate the effect of homeostatic dysfunction of the kidney at the time of declining blood pressure level.

The physiological adaptation includes renin-angiotensin-aldosterone system (RAAS) activation, which responds at the time of decreased renal perfusion and reduced blood pressure level. At that time, the kidney used to release renin, which initiates the RAAS pathway. This system helps in increasing the blood pressure level through vasoconstriction, mediated by angiotensin II, which further promotes sodium and water reabsorption through aldosterone (Gelen et al., 2021). Another physiological adaptation includes the release of ADH or antidiuretic hormone, the posterior pituitary releases the ADH to increase the water reabsorption, which aims to counteract the loss of fluid and helps in stabilising the blood volume and pressure (Almeida et al., 2020). The anatomical adaptation includes the remodelling of the nephron and hypertrophy of renal tubules. Prolonged dysfunction of the kidney can lead to the enlargement of the renal tube, which is known as hypertrophy. This anatomical adaptation can trigger the reabsorption of sodium and water despite kidney dysfunction and stimulate waste production by maintaining homeostasis despite the impaired function of the kidney. On the other hand, nephron remodelling refers to the fact that, in chronic kidney dysfunction, the nephron, which is the functional unit of the kidney, has undergone many structural changes like glomerulosclerosis and tubular atrophy (Ren & Dai, 2020). This change enhances the filtration capacity of the kidney. This adaptation, both physiological and anatomical, can boost the reabsorption of water and counteract the fluid loss. For example, the hypertrophy of renal tubules and nephron remodelling can improve filtration and waste excretion despite the impaired function of the kidney. On the other hand, the release of ADH can help in stabilising blood pressure by increasing blood volume and vascular resistance. Similarly, RAAS activation can enhance sodium and water reabsorption, which in turn can help in maintaining blood pressure levels