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Effects of Disease on Renal Blood Flow Regulation : = Assessing Autoregulation Disruption.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Effects of Disease on Renal Blood Flow Regulation :/
Reminder of title:	Assessing Autoregulation Disruption.
Author:	Maddineni, Bhavishya.
Description:	1 online resource (63 pages)
Notes:	Source: Masters Abstracts International, Volume: 85-12.
Contained By:	Masters Abstracts International85-12.
Subject:	Chemical engineering. -
Online resource:	click for full text (PQDT)
ISBN:	9798382832715

Effects of Disease on Renal Blood Flow Regulation : = Assessing Autoregulation Disruption.
Maddineni, Bhavishya.

Effects of Disease on Renal Blood Flow Regulation :Assessing Autoregulation Disruption. - 1 online resource (63 pages)

Source: Masters Abstracts International, Volume: 85-12.

Thesis (M.S.)--State University of New York at Buffalo, 2024.

Includes bibliographical references

The renal system is essential for maintaining homeostasis within the human body by regulating the balance of fluid and electrolyte amounts. This function is performed by an intricate network of blood vessels, which ensure sufficient blood supply to the kidneys. The flow rate through these vessels is controlled by renal autoregulation, which maintains the glomerular filtration rate (GFR) and preserves kidney function, despite fluctuations in blood pressure. However, kidney diseases such as diabetic nephropathy, hypertension, and glomerulonephritis frequently result in structural and functional changes in the renal vasculature, impacting the flow rate and autoregulation.To gain an understanding of the effects of these diseases on the regulation of renal blood flow and autoregulation, it is essential to develop models that facilitate comprehension. The work in this thesis entails a thorough analysis of the simulated diameter of arterioles and the flow of blood in the kidneys across a range of different single nephron glomerular filtration rates that are relevant to varying stages of chronic kidney disease. A mathematical model is utilized to simulate two mechanisms: the myogenic response, which causes changes in the tone of vascular smooth muscle in response to variations in hydrostatic pressure, and tubuloglomerular feedback, which involves the chloride ion transport at the exit of the renal tubule. Using our mathematical model, we examined whether and to what extent autoregulation can be maintained in the clinical stages of chronic kidney disease. Such insights are crucial for developing precise therapeutic strategies that aim to mitigate the consequences of disrupted regulation of renal blood flow in the context of kidney diseases.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798382832715Subjects--Topical Terms:

555952
Chemical engineering.
Subjects--Index Terms:

Chronic kidney diseaseIndex Terms--Genre/Form:

554714
Electronic books.

Effects of Disease on Renal Blood Flow Regulation : = Assessing Autoregulation Disruption.
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504 $a Includes bibliographical references
520 $a The renal system is essential for maintaining homeostasis within the human body by regulating the balance of fluid and electrolyte amounts. This function is performed by an intricate network of blood vessels, which ensure sufficient blood supply to the kidneys. The flow rate through these vessels is controlled by renal autoregulation, which maintains the glomerular filtration rate (GFR) and preserves kidney function, despite fluctuations in blood pressure. However, kidney diseases such as diabetic nephropathy, hypertension, and glomerulonephritis frequently result in structural and functional changes in the renal vasculature, impacting the flow rate and autoregulation.To gain an understanding of the effects of these diseases on the regulation of renal blood flow and autoregulation, it is essential to develop models that facilitate comprehension. The work in this thesis entails a thorough analysis of the simulated diameter of arterioles and the flow of blood in the kidneys across a range of different single nephron glomerular filtration rates that are relevant to varying stages of chronic kidney disease. A mathematical model is utilized to simulate two mechanisms: the myogenic response, which causes changes in the tone of vascular smooth muscle in response to variations in hydrostatic pressure, and tubuloglomerular feedback, which involves the chloride ion transport at the exit of the renal tubule. Using our mathematical model, we examined whether and to what extent autoregulation can be maintained in the clinical stages of chronic kidney disease. Such insights are crucial for developing precise therapeutic strategies that aim to mitigate the consequences of disrupted regulation of renal blood flow in the context of kidney diseases.
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653 $a Diabetic nephropathy
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