Ninjanerd - Acute Kidney Injury Overview

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Questions and Answers

What characterizes the oliguric phase of AKI?

Normal urine output and dehydration

Decreased urine output and development of complications (correct)

Increased creatinine and return to normal kidney function

Increased urine output and hyperkalemia

In the treatment of proximal obstruction in postrenal AKI, what is an effective intervention?

Perform a percutaneous nephrostomy to drain the kidney (correct)

Increase fluid intake to stimulate urine production

Insert a Foley catheter into the bladder

Administer steroids and immunosuppressants

Which phase occurs after the polyuric phase during the progression of AKI?

Chronic phase

Oliguric phase

Recovery phase (correct)

Dehydration phase

In the polyuric phase of AKI, what significant risk can arise due to increased urine output?

Dehydration (C) Signup and view all the answers

Which of the following is a common treatment for distal obstruction in postrenal AKI?

Insert a Foley catheter to decompress the bladder (A) Signup and view all the answers

Which physical sign is typically associated with hypovolemia in pre-renal acute kidney injury (AKI)?

Dry mucous membranes (B) Signup and view all the answers

What is a common compensatory mechanism for metabolic acidosis?

Kussmaul respirations (D) Signup and view all the answers

Which of the following ecg changes is associated with hyperkalemia?

Prolonged PR interval (B) Signup and view all the answers

Which treatment should be considered for severe hyperkalemia with ECG changes?

Calcium and insulin (D) Signup and view all the answers

What is hypervolemic hyponatremia primarily caused by?

Excessive water retention (A) Signup and view all the answers

What therapeutic approach is indicated when a patient has uremia with encephalopathy?

Hemodialysis (A) Signup and view all the answers

In the treatment of intrarenal AKI caused by ATN, which intervention may be considered?

Supportive care and monitor for dialysis needs (B) Signup and view all the answers

Which factor is commonly associated with metastasis to kidney damage requiring renal replacement therapy?

Cardiorenal syndrome (A) Signup and view all the answers

Which medication class is known to potentially cause renal vasoconstriction?

ACE inhibitors (A) Signup and view all the answers

Which combination of treatments is appropriate for managing hypotension in AKI?

IV fluids and vasopressors (A) Signup and view all the answers

Which clinical manifestation is NOT typically associated with hypervolemia?

Hypotension (D) Signup and view all the answers

What is one of the first-line treatments for hypovolemic acute kidney injury?

IV fluids (D) Signup and view all the answers

In cases of acute tubular necrosis, what is the primary management strategy?

Discontinuation of nephrotoxic agents (D) Signup and view all the answers

Which physical sign can indicate potential uremia?

Asterixis (flapping tremor) (C) Signup and view all the answers

What condition is most commonly associated with acute tubular necrosis?

Ischemic renal injury (A) Signup and view all the answers

Which mechanism leads to nephrotoxic acute tubular necrosis?

Direct injury from substances (D) Signup and view all the answers

Which finding is indicative of acute interstitial nephritis?

Increased eosinophils in urine (B) Signup and view all the answers

What does an elevated urine osmolality greater than 500 mOsm/kg signify?

Prerenal AKI (D) Signup and view all the answers

What is the most common cause of postrenal acute kidney injury?

Benign prostatic hyperplasia (B) Signup and view all the answers

Which substance is known to cause nephrotoxic ATN?

Myoglobin from rhabdomyolysis (A) Signup and view all the answers

How is renal artery obstruction assessed?

Renal imaging studies (D) Signup and view all the answers

What laboratory result suggests prerenal acute kidney injury?

Low fractional excretion of sodium (D) Signup and view all the answers

Which of the following conditions can lead to ischemic acute tubular necrosis?

Hypotension (A) Signup and view all the answers

What ultrasound finding suggests proximal obstruction in the urinary tract?

Hydronephrosis (C) Signup and view all the answers

What does a post-void residual urine volume greater than 200 mL indicate?

Distal obstruction (C) Signup and view all the answers

Which type of glomerulonephritis is characterized by crescent formation?

Rapidly progressive glomerulonephritis (D) Signup and view all the answers

What classic triad suggests acute interstitial nephritis?

Fever, rash, eosinophilia (D) Signup and view all the answers

What is a common trigger for acute interstitial nephritis?

Non-steroidal anti-inflammatory drugs (B) Signup and view all the answers

What is the primary characteristic of acute kidney injury (AKI)?

Sudden decline in kidney function with a sharp drop in urine output and rapid increase in serum creatinine. (D) Signup and view all the answers

Which type of AKI results from reduced blood flow to the kidneys?

Prerenal AKI (C) Signup and view all the answers

What process primarily leads to prerenal AKI?

Reduced effective arterial blood volume (EABV). (A) Signup and view all the answers

Which of the following is a direct consequence of reduced cardiac output in the context of cardiorenal syndrome?

Decreased effective arterial blood volume (EABV). (C) Signup and view all the answers

How does decompensated cirrhosis contribute to prerenal AKI?

By decreasing oncotic pressure and fluid leak from the blood vessels which reduces EABV. (D) Signup and view all the answers

Which of the following conditions can lead to hypovolemia and ultimately prerenal AKI?

Diarrhea, diuresis, dehydration, and blood loss. (C) Signup and view all the answers

How do NSAIDs contribute to reduced renal blood flow?

By inhibiting prostaglandin production, causing afferent arteriole vasoconstriction. (B) Signup and view all the answers

What is the effect of ACE inhibitors and ARBs on glomerular pressure?

They cause efferent arteriole vasodilation, decreasing glomerular pressure. (C) Signup and view all the answers

Study Notes

Acute Kidney Injury (AKI)

AKI is a sudden decline in kidney function, marked by a sharp drop in urine output and a rapid increase in serum creatinine.
AKI is categorized into three types: prerenal, intrarenal, and postrenal.
Prerenal AKI is primarily caused by reduced blood flow to the kidneys, leading to decreased glomerular filtration rate (GFR).
Intrarenal AKI results from damage to the nephrons, the functional units of the kidneys, impairing filtration and reabsorption.
Postrenal AKI is caused by urinary tract obstruction, creating a backflow of urine and raising pressure within the nephrons, hindering filtration.

Pre-renal AKI

Reduced effective arterial blood volume (EABV) is the core mechanism of prerenal AKI.
Causes of EABV reduction include:
- Cardiorenal syndrome: Heart failure (systolic or diastolic dysfunction) lowers cardiac output, decreasing EABV and renal perfusion.
- Hepatorenal syndrome: Decompensated cirrhosis, marked by reduced albumin production, decreases oncotic pressure and causes fluid leakage from blood vessels, further reducing EABV. Portal hypertension-linked systemic vasodilation, especially in splanchnic vessels, compounds this reduction in EABV.
- Hypovolemia: Various factors (diarrhea, diuresis, dehydration, blood loss) lower preload, stroke volume, and ultimately cardiac output, leading to reduced EABV.
- Hypotension and shock states: Severe hypotension (septic, cardiogenic, or hypovolemic shock) dramatically reduces mean arterial pressure (MAP), the pressure driving kidney blood flow, thus decreasing EABV.
Other contributing factors include:
- Increased renal vasoconstriction: Medications like NSAIDs, tacrolimus, ACE inhibitors, and ARBs can cause this.
  - NSAIDs inhibit prostaglandin production, which typically dilates afferent arterioles, causing vasoconstriction.
  - ACE inhibitors and ARBs dilate efferent arterioles, decreasing glomerular pressure.
- Renal artery obstruction: Atherosclerosis and fibromuscular dysplasia narrow the renal artery, reducing kidney blood flow. Bilateral renal artery stenosis, particularly with ACE inhibitor use, significantly contributes to severe AKI.

Intrarenal AKI

Acute tubular necrosis (ATN) is the most common intrarenal AKI type (85-90% of cases). ATN results from damage to tubular cells, leading to sloughing and obstruction of the tubular lumen, harming filtration and reabsorption.
Ischemic ATN: Prolonged reduced renal perfusion, often from untreated prerenal AKI (hypotension or hypovolemia), limits oxygen to the tubular cells, causing cell death.
Nephrotoxic ATN: Direct tubular cell injury from various substances:
- Medications: Aminoglycosides, vancomycin, amphotericin B, and contrast dye.
- Pigments: Myoglobin (rhabdomyolysis) and hemoglobin (hemolysis).
- Crystals: Uric acid (tumor lysis syndrome) and immunoglobulin light chains (multiple myeloma).
Other intrarenal AKI types include:
- Acute interstitial nephritis (AIN): Triggered by medications (NSAIDs, beta-lactams, PPIs), leading to interstitium inflammation and tubular cell damage. Fever, rash, and elevated eosinophils in urine and blood are key diagnostic signs.
- Glomerulonephritis (GN): Inflammation of the glomerulus due to various causes (ANCA-associated vasculitis, anti-GBM disease, infectious GN, immune complex diseases, thrombotic microangiopathy). GN often shows hematuria, proteinuria, and AKI. Rapid GN progression with significant glomerular thickening and crescent formation is called rapidly progressive glomerulonephritis (RPGN), common in ANCA vasculitis and anti-GBM disease.
  - Thrombotic microangiopathy (TMA) causes microthrombi formation, leading to glomerular obstruction, frequently presenting with a triad of hemolytic anemia, thrombocytopenia, and AKI.

Postrenal AKI

Postrenal AKI is characterized by urinary tract obstruction, causing urine backflow and rising pressure within the kidneys. Obstruction can be proximal or distal.
Proximal obstruction: Renal pelvis or ureters. Common cause is nephrolithiasis (kidney stones), often requiring bilateral obstruction to cause AKI (except in solitary kidney). Other causes include tumors, masses like ovarian or rectal cancer.
- Ultrasound: Hydronephrosis (dilated renal pelvis) and unilateral ureteral dilation suggest proximal obstruction.
Distal obstruction: Bladder or bladder outlet.
- Neurogenic bladder (lack of bladder muscle contraction): Spinal cord disease, stroke, Parkinson's disease impair bladder contraction.
- Medications (anticholinergics): Inhibit bladder muscle contraction, causing urine retention.
- Benign prostatic hyperplasia (BPH): Enlarged prostate hinders urine flow. Prostate cancer may also contribute to obstruction.
- Ultrasound: Distended bladder, hydronephrosis point to distal obstruction. Post-void residual > 200 mL confirms distal obstruction.

Diagnosis of AKI

Initial steps: Assess serum creatinine levels (rise of 0.3 mg/dL or more in 48 hours or 1.5 times baseline over 7 days). Evaluate urine output (oliguria < 400 mL/24 hours).
Identifying the cause:
- Postrenal AKI: Renal/bladder ultrasound to assess for hydronephrosis, ureteral dilation, and bladder enlargement. History of flank pain, hematuria, nausea, vomiting, or urinary tract infection. Post-void residual > 200 mL. Foley catheterization can alleviate distal obstruction.
- Intrarenal and Prerenal AKI:
 - Urine sodium (UNa) < 1% and low FeNa suggest prerenal AKI (kidneys reabsorbing sodium).
 - Urine osmolality (> 500 mOsm/kg), Urine urea nitrogen/creatinine ratio (> 20:1) indicate prerenal AKI (kidney conserving water and urea).
 - Urine microscopy: Muddy brown casts (ATN). White cell casts/high eosinophils (AIN). Red cell casts or high proteinuria (GN). FePP stress test can differentiate.
History and physical examination:
- Pre-renal AKI: Volume status. Medications: ACE inhibitors, ARBs, NSAIDs.
- Intrarenal AKI: History of nephrotoxicity, rhabdomyolysis, tumor lysis syndrome, etc. Fever, rash, eosinophilia (AIN).

Complications of AKI

Metabolic acidosis: Hydrogen ion retention, reduced bicarbonate reabsorption, elevated anion gap (especially in severe uremia). Compensation: Kussmaul respirations. Consequences: Worsened hyperkalemia, decreased myocardial contractility, vasodilation, and lowered blood pressure.
Hyperkalemia: Decreased potassium excretion due to reduced GFR. ECG changes: Peaked T waves, prolonged PR interval, absent P waves, widened QRS ( > 120 msec), and sine wave pattern (risk of ventricular fibrillation/cardiac arrest).
Hypervolemia: Water and sodium retention. Clinical manifestations: Pulmonary/pleural effusions, edema, hypertension. Consequences: Impaired oxygenation, shortness of breath, increased heart failure risk. Hypervolemic hyponatremia results from excess water retention.
Uremia: Retention of waste products, primarily urea. CNS effects: Confusion, lethargy, asterixis, nausea, vomiting. Pericarditis. Platelet dysfunction (epistaxis, bleeding).

Treatment of AKI

Addressing complications: Metabolic acidosis (sodium bicarbonate), hyperkalemia (loop diuretics, potassium binders, calcium, insulin, albuterol), hypervolemia (loop diuretics), uremia (hemodialysis)
Underlying causes:
- Hypovolemia: IV fluids.
- Cardiorenal syndrome: Inotropes, diuretics, vasodilators.
- Hepatorenal syndrome: Albumin, vasopressors, octreotide.
- Hypotension/shock: IV fluids, vasopressors.
- Renal artery obstruction: Revascularization (angioplasty, stenting).
- Medication-related AKI: Discontinue offending agents.
Dialysis: Indications include complicated AKI. Types: CRRT, intermittent hemodialysis. Access: Central venous catheters.
Pre-renal AKI treatment: Address underlying causes; hypovolemia with fluids, cardiorenal with inotropes/diuretics/vasodilators, and hypotension/shock with fluids/vasopressors.
Intrarenal AKI treatment: Supportive care, remove nephrotoxic agents.
Postrenal AKI treatment: Proximal obstruction (stents, nephrostomy); distal obstruction (Foley catheter).

Understanding the Progression of AKI

AKI progresses through three phases:
- Oliguric phase: Reduced urine output, increased creatinine, and complications (hyperkalemia, metabolic acidosis, uremia).
- Polyuric phase: Increased urine output, potentially leading to dehydration and hypokalemia.
- Recovery phase: Gradually restored kidney function (months/years).

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Description

This quiz covers the key aspects of Acute Kidney Injury (AKI), including its types: prerenal, intrarenal, and postrenal. Understand the mechanisms behind prerenal AKI and how factors like blood flow and heart function affect kidney health. Test your knowledge on kidney physiology and dysfunction.