Intrarenal acute kidney injury (acute renal failure) - causes, symptoms & pathology

Summary

Acute kidney injury (AKI) occurs when the kidneys suddenly reduce their function, previously referred to as acute renal failure. AKI is classified into prerenal, postrenal, and intrarenal causes. This video focuses on intrarenal AKI, which affects the kidneys' internal structures like tubules, glomeruli, or interstitium. Key causes include acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis, leading to impaired filtration, reduced urine output, and accumulation of waste in the blood. Understanding the underlying mechanisms can aid in diagnosing and treating AKI effectively.

Takeaways

• 🩺 Acute Kidney Injury (AKI) is a condition where kidney function decreases rapidly, typically within a few days.
• 🔄 AKI is categorized into three types: prerenal (before the kidneys), postrenal (after the kidneys), and intrarenal (within the kidneys).
• 💡 The kidneys play an essential role in filtering blood, removing waste, regulating electrolytes, maintaining fluid balance, and producing hormones.
• ⚠️ Acute Tubular Necrosis (ATN) is the most common cause of intrarenal AKI and occurs due to ischemia (lack of blood supply) or nephrotoxins (harmful substances).
• ⚗️ Nephrotoxins like antibiotics, heavy metals, and chemotherapy drugs can cause tubular epithelial cells to die, leading to tubular blockage and impaired filtration.
• 🔬 Glomerulonephritis (GN) is another form of intrarenal AKI caused by immune complexes attacking the glomeruli, leading to inflammation and reduced filtration.
• ⚡ Damage to the glomeruli in GN results in proteinuria (protein in the urine), hematuria (blood in the urine), and a decrease in glomerular filtration rate (GFR).
• 🔥 Acute Interstitial Nephritis (AIN) is inflammation of the kidney’s interstitium often triggered by medication or immune responses, causing damage to the tissue.
• 💧 A key sign of AKI is oliguria (reduced urine output), along with azotemia (high levels of nitrogen-containing compounds) due to impaired filtration.
• 🧪 Diagnostic indicators of intrarenal AKI include changes in the blood urea nitrogen (BUN) to creatinine ratio, fractional excretion of sodium (FENa), and urine osmolality.

Q & A

What is acute kidney injury (AKI) and how does it differ from acute renal failure (ARF)?

Acute kidney injury (AKI) refers to a sudden decrease in kidney function that can develop over a few days. It is a broader term than acute renal failure (ARF) because it includes subtle decreases in kidney function, whereas ARF typically refers to a more severe form of kidney failure.

What are the three types of AKI, and what distinguishes them?

The three types of AKI are prerenal, postrenal, and intrarenal. Prerenal AKI occurs when the cause is before the kidneys, often due to reduced blood flow. Postrenal AKI is caused by obstructions after the kidneys, like urinary blockages. Intrarenal AKI results from direct damage within the kidneys, affecting structures like the tubules, glomeruli, or interstitium.

What is the role of the kidneys in the body?

The kidneys regulate blood composition by removing waste, balancing electrolyte levels, regulating water volume, and producing hormones. Blood is filtered through the glomeruli, and the filtrate passes through the renal tubules, where reabsorption and secretion processes refine it before urine is produced.

What causes acute tubular necrosis (ATN) and what are its effects on the kidneys?

Acute tubular necrosis is caused by either ischemia (lack of blood supply) or nephrotoxins that damage the epithelial cells lining the tubules. When these cells die, they can slough off and block the tubules, reducing glomerular filtration rate (GFR) and causing oliguria (low urine production) and azotemia (high nitrogen-containing compounds in the blood).

What are some common nephrotoxins that can lead to acute tubular necrosis?

Common nephrotoxins include aminoglycoside antibiotics, heavy metals like lead, myoglobin from damaged muscles, ethylene glycol (antifreeze), radiocontrast dye, and uric acid buildup during tumor lysis syndrome.

What is the typical course of recovery from acute tubular necrosis if the underlying cause is treated?

If the underlying cause of acute tubular necrosis is addressed, the tubular cells can regenerate over a few weeks, leading to potential recovery of kidney function.

What is glomerulonephritis and how does it affect kidney function?

Glomerulonephritis (GN) is inflammation of the glomerulus, often due to antigen-antibody complexes depositing in the tissue. This activates the immune system, causing inflammation and damage to the glomerular cells, leading to proteinuria (protein in the urine), hematuria (blood in the urine), reduced GFR, oliguria, hypertension, and edema.

What causes acute interstitial nephritis, and what are its symptoms?

Acute interstitial nephritis is caused by immune cell infiltration in the interstitium, often due to a type I or type IV hypersensitivity reaction to medications like NSAIDs, penicillin, or diuretics. Symptoms include oliguria, eosinophils in the urine (eosinophiluria), fever, and rash. If untreated, it can progress to renal papillary necrosis.

What are the main indicators of kidney dysfunction in intrarenal AKI?

Indicators include a reduced GFR, oliguria, azotemia, hyperkalemia (high potassium levels), metabolic acidosis, and changes in urine characteristics, such as high urine sodium concentration and low urine osmolality.

What diagnostic ratios or measurements can help assess kidney function in AKI?

The blood urea nitrogen (BUN) to creatinine ratio, which is normally between 5:1 and 20:1, helps assess kidney function. In intrarenal AKI, the ratio falls below 15:1. The fraction of sodium excreted in the urine (FENa) and urine osmolality can also be used to evaluate kidney function.