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Acute Kidney Injury II: Pathophysiology

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of...

Physiology of the Genitourinary System I: Renal Blood Flow and Glomerular Filtration

Physiology of the Genitourinary System I: Renal Blood Flow and Glomerular Filtration

The kidneys are vital organs responsible for regulating blood filtration, waste excretion, and fluid balance, all of which are crucial for maintaining homeostasis. Renal physiology examines renal blood flow, glomerular filtration, and urine formation, ensuring the body’s internal environment remains stable.Renal Blood FlowThe kidneys receive about 20-25% of the cardiac output, typically around 1200 mL of blood per minute in an average adult. Blood flows into the kidneys through the renal...

Renal Corpuscle

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The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
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Acute Kidney Injury I: Introduction

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Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...

Nephrons

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Related Experiment Video

Updated: Sep 25, 2025

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice

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Published on: February 2, 2024

Hepatorenal Syndrome: Pathophysiology.

Timea Csak¹, David Bernstein²

¹Sandra Atlas Bass Center for Liver Diseases, Northwell Health, 400 Community Drive, Manhasset, NY 11030, USA.

Clinics in Liver Disease

|April 29, 2022

Summary

Hepatorenal syndrome (HRS) is a severe kidney dysfunction in advanced liver disease, characterized by poor blood flow to the kidneys. Systemic inflammation plays a significant role in its development and progression.

Keywords:

Hepatorenal syndrome Kidneys Mortality Pathophysiology Systemic inflammation

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Area of Science:

Nephrology
Hepatology
Internal Medicine

Background:

Hepatorenal syndrome (HRS) is a critical complication of advanced liver disease, leading to functional renal failure.
It is associated with high mortality rates due to complex circulatory dysfunction and renal hypoperfusion.
Current treatments targeting circulatory dysfunction show limited efficacy.

Purpose of the Study:

To summarize the current understanding of hepatorenal syndrome pathophysiology.
To highlight the role of circulatory dysfunction and systemic inflammation in HRS.

Main Methods:

Literature review of existing studies on hepatorenal syndrome.
Synthesis of current knowledge on HRS pathophysiology, focusing on circulatory and inflammatory mechanisms.

Main Results:

Renal hypoperfusion, driven by vasoconstriction from circulatory dysfunction, is central to HRS.
Splanchnic and peripheral arterial vasodilation, along with cirrhotic cardiomyopathy, cause effective arterial hypovolemia.
Systemic inflammation is increasingly recognized as a key contributor to HRS, affecting both vascular and renal systems.

Conclusions:

Understanding the complex pathophysiology of HRS, including circulatory dysfunction and inflammation, is crucial.
Further research is needed to develop more effective therapeutic strategies for HRS.
Addressing systemic inflammation may offer a novel therapeutic target for managing HRS.