Acute Kidney Injury

How is Acute Kidney Injury (AKI) defined regarding its effect on metabolic balance?

A rapid decrease in kidney function resulting in an inability to maintain acid-base, fluid, and electrolyte balance.

Azotemia.

The accumulation of nitrogenous waste and creatinine in the blood.

What clinical syndrome results from the symptomatic increase in nitrogenous waste, potentially leading to seizures or coma?

Uremia.

What is the typical duration range for Acute Kidney Injury?

Days to up to 3 months

Hospitalized patients with AKI face an increased mortality risk of up to _____.

30%.

AKI is associated with an increased risk of developing which long-term renal conditions?

Chronic Kidney Disease (CKD) and End-Stage Renal Disease (ESRD).

risk factors for AKI:

Older age, Diabetes, obesity, Sepsis, hemorrhage, volume depletion, and mechanical ventilation, Recent surgery, particularly cardiac or vascular procedures, and abdominal aneurysm reactions.

Symptoms of AKI depend on the cause and location of the renal failure (pre, intrinsic, post) but include:

Nausea, vomiting, anorexia, weight loss, Fatigue, changes in mental status, Muscle cramps, pruritus

Nephrotoxic drugs are a major ____ cause of AKI and include aminoglycosides, NSIADS, ACE/ARB

iatrogenic ; aminoglycosides, NSIADS, ACE/ARB

Prerenal AKI

Kidney injury caused by a sudden drop in blood pressure or interruption of blood flow to the kidneys from injury or illness.

Is this pre, intra, or post renal:

Anything reducing the blood flow to the kidneys: hypovolemia, massive dehydration, any type of shock, renal artery stenosis, blood clot.

pre renal

Treatment for pre renal injury

IV fluids or blood

Intrarenal AKI

Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply.

#1 cause of intrarenal injury is ______

Acute Tubular Necrosis

Postrenal AKI

Sudden obstruction of urine flow due to factors such as an enlarged prostate, kidney stones, or tumors.

Is this pre, intra, or post renal:

Blockage of urine flow from the kidney to the urethral meatus: kidney stones, BPH, cancer

postrenal

order of where you should first think kidney injury is occurring

1- prerenal

2- postrenal

3- intrarenal

Which type of AKI is suggested by physical findings such as orthostatic blood pressure, flat neck veins, hypotension or reduced body weight?

Prerenal AKI.

In a patient with AKI, the presence of edema, pulmonary rales, or an S3 gallop suggests effective volume depletion due to _____.

Cardiac dysfunction.

The presence of ascites and asterixis in an AKI patient specifically points toward which underlying pathology?

Liver dysfunction or cirrhosis.

What cardiac finding on physical exam can occur as a complication of uremia, potentially leading to cardiac tamponade?

Pericardial effusion or friction rub.

blood results of AKI

Elevated BUN and Creatinine; hyperkalemia, hyperphosphatemia, and hypocalcemia

why does Metabolic acidosis occur in AKI?

Decreased acid clearance

Which electrolyte abnormality is a primary cause of arrhythmias in AKI patients?

Hyperkalemia.

What three electrolyte elevations are typically found in AKI laboratory results?

Hyperkalemia, hyperphosphatemia, and hypocalcemia.

Describe the hematological findings associated with AKI that typically manifest over several weeks.

Low platelets and normochromic, normocytic anemia.

Why does metabolic acidosis occur in patients with AKI?

Decreased organic and nonorganic acid clearance by the kidneys.

What EKG findings are characteristic of hyperkalemia in the setting of AKI?

Peaked T waves, PR prolongation, and QRS widening.

What EKG finding is associated with hypocalcemia in AKI patients?

Long QT intervals.

For Prerenal Azotemia, the Serum BUN:Cr ratio is typically _____.

>20:1.

What is the typical urinary sodium (UNa) level in a patient with Prerenal Azotemia?

< 20, mEq/L.

A urine osmolality of > 500, mOsm/kg is most consistent with which category of AKI?

Prerenal Azotemia.

Describe the urinary sediment typically seen in Prerenal Azotemia.

Benign or hyaline casts.

For Postrenal Azotemia, the Serum BUN:Cr ratio is typically _____.

>20:1

Cause of Intrinsic: Acute Tubular Necrosis (ATN)

Ischemia or nephrotoxins

What specific urinary sediment finding is pathognomonic for Acute Tubular Necrosis (ATN)?

Granular (muddy brown) casts or renal tubular casts.

The Serum BUN:Cr ratio in Acute Interstitial Nephritis (AIN) is typically _____.

< 20:1.

Cause of Intrinsic: Acute Glomerulonephritis

Immune-mediated, pauci immune, anti-GBM related

The Serum BUN:Cr ratio in Acute Glomerulonephritis is typically _____.

>20:1

What are the characteristic sediment findings in the urine of a patient with Acute Glomerulonephritis?

Red cells, dysmorphic red cells, and red cell casts.

Which urinary sediment findings are associated with Acute Interstitial Nephritis (AIN)?

White cells and white cell casts, with or without eosinophils.

Cause of Acute Interstitial Nephritis (AIN)

Allergic reaction, infection, or drugs

Patients with prior kidney disease are particularly susceptible to AKI when exposed to which diagnostic substance?

Contrast dyes.

Which class of antibiotics, including Gentamicin, is a major cause of nonoliguric ATN in hospitalized patients?

Aminoglycosides.

When do Aminoglycosides typically cause ATN relative to the start of therapy?

During the first 2 weeks of therapy.

Contrast-induced AKI typically presents as oliguric ATN within _____ hours after the study.

24-48 hours.

Episodes of hypotension specifically suggest the possibility of _____ AKI or _____ ATN.

Prerenal ; Ischemic.

Which two anesthetic agents are identified as potential causes of nonoliguric ATN?

Methoxyflurane and enflurane.

Patients with prior cardiac or vascular surgery are at a higher risk for developing which specific renal pathology?

Acute Tubular Necrosis (ATN).

What is the estimated mortality rate for AKI in the ICU setting when dialysis is required?

Up to 70%.

List the three main risk factors for increased mortality in AKI patients.

Advanced age, severe underlying illness, and multisystem organ failure.

What are the two leading causes of death in patients with AKI?

Infection and fluid/electrolyte imbalance.

In the context of systemic illness, a skin rash in an AKI patient might indicate SLE, vasculitis, or _____.

SLE, vasculitis, or Acute interstitial nephritis (AIN).

What is the primary physiological mechanism that characterizes pre-renal Acute Kidney Injury (AKI)?

It results from a decrease in renal blood flow and perfusion to the kidney.

_____ is the most common cause of AKI both outpatient and in the hospital

Prerenal

What are the three broad categories of causes for pre-renal AKI?

Hypovolemia, hemodynamic/fluid shifts, and arterial occlusion involving the renal vasculature.

Examples how pre renal AKI caused by redcuted arterial blood volume due to hypovolemia

hemorrhage, skin burns, sweating, diarrhea, vomiting, diuretics, glucosuria

Examples of causes of pre-renal AKI through alterations in hemodynamics and fluid shifts.

sepsis, anaphylaxis, third spacing, meds

How does 'third spacing' contribute to pre-renal AKI?

It causes reduced effective arterial blood volume through fluid shifts, such as in peritonitis or severe burns.

Under what anatomical condition can unilateral atherosclerosis of the renal artery cause pre-renal AKI?

When the atherosclerosis occurs in a patient with a solitary functioning kidney.

How does hypoperfusion in pre-renal AKI affect the reabsorption of sodium and water in a functioning kidney?

It leads to enhanced reabsorption of sodium and water to compensate for low volume. which results in oliguria (decreased urine output), high urine osmolality, and low urine sodium.

What is the typical urine volume status found in patients with pre-renal AKI?

Oliguria, which is a significant decrease in urine output.

What is the characteristic BUN:Cr ratio found in pre-renal AKI?

A ratio >20:1 .

Why does the BUN:Cr ratio increase to > 20:1 in pre-renal states?

Slowed flow through the tubules results in increased urea reabsorption while creatinine remains relatively constant.

What is the expected urine sodium ( U_Na ) level in a patient with pre-renal AKI?

< 20 meq/L .

What urine osmolality value is indicative of pre-renal AKI?

> 500 mosm/kg .

What type of microscopic findings are characteristic of the urine sediment in pre-renal AKI?

Benign or hyaline casts.

What are the three main management priorities for treating pre-renal AKI?

Correcting volume status, monitoring potassium levels, and avoiding nephrotoxic agents.

What defines the physiological cause of post-renal Acute Kidney Injury?

It results from an obstruction of urinary flow anywhere along the urinary tract.

Which demographic of patients is most commonly affected by post-renal AKI due to prostatic hyperplasia?

Elderly men.

At what point in the kidney does post-renal obstruction potentially begin?

It starts at the renal calyces or renal pelvis.

How is the clinical prognosis of post-renal AKI generally described?

It is generally considered reversible once the obstruction is relieved.

What medication class is explicitly listed as a cause of post-renal AKI due to its effect on bladder function?

Anticholinergic medications.

List four types of malignancies that commonly cause post-renal AKI via obstruction.

Bladder, prostate, cervical, and endometrial cancers.

What retroperitoneal processes can lead to extrinsic compression and post-renal AKI?

Abscesses, fibrosis, and carcinomas.

Under what specific obstructive condition would a patient with post-renal AKI present with anuria?

When there is a complete obstruction of urinary flow.

Why do some patients with partial post-renal obstruction present with polyuria?

Tubular dysfunction occurs, leading to an inability to reabsorb salt and water loads.

What specific physical examination findings should be assessed if post-renal AKI is suspected?

Enlarged prostate, distended bladder, or a mass on the pelvic exam.

In the initial phase of post-renal AKI, what is the expected BUN:Cr ratio?

Greater than 20:1 .

What is the characteristic urine osmolality in post-renal AKI?

< 400 mOsm/kg .

Describe the typical appearance and possible constituents of urine sediment in post-renal AKI.

Usually normal-appearing, but may contain RBCs, WBCs, or crystals.

What is the purpose of bladder catheterization in the diagnostic workup of post-renal AKI?

To evaluate for obstruction and place a stent if necessary.

Which imaging modality is primarily used to assess for hydroureter and hydronephrosis in AKI?

Ultrasound.

Foley catheter

placed through the urethral meatus and goes into the bladder where it stays in place by a balloon that is inflated.

Straight catheter

straw like tube that is inserted into the bladder to empty it one time, not left in.

What clinical phenomenon must be monitored after reversing a urinary obstruction?

Post-obstructive diuresis.

What is the primary risk to avoid during the treatment of post-obstructive diuresis?

Volume depletion.

At what point in the diagnostic evaluation should Intrinsic Acute Kidney Injury (AKI) be considered?

Intrinsic AKI should be considered only after pre-renal and post-renal causes have been ruled out.

What percentage of AKI cases are typically attributed to intrinsic etiologies?

Intrinsic AKI accounts for 10% to 40% of cases.

What are the 3 primary sites of injury for Intrinsic AKI.

glomeruli, the tubules, and the interstitium.

Identify the four broad processes that result in intrinsic renal injury.

The processes are vascular, glomerular, interstitial, and tubular injury.

_______is the most common cause of intrinsic AKI

ATN

In the context of Acute Tubular Necrosis (ATN) pathophysiology, what leads to decreased GFR following tubular cell sloughing?

The sloughed-off cells block the tubule, creating high intratubular pressure that opposes filtration.

What is the characteristic microscopic finding in the urine sediment of a patient with ATN?

The sediment typically contains "muddy brown" granular casts.

What are the muddy brown casts seen in ATN

death and sloughing of tubular epithelial cells which then block the tubule

Pt with pneumonia who is coughing up blood with a BP 60/20, despite treatment pt starts to develop acute renal failure with muddy brown casts in the urine =

ATN

Why are renal tubular cells uniquely susceptible to ischemic injury?

They have a very high metabolic rate and are highly sensitive to oxygen deprivation.

Ischemic ATN: Occurs when tubular cells,

which have a very high metabolism and are highly sensitive to oxygen deprivation, do not receive adequate oxygenation. This is often linked to shock or involvement of renal blood vessels (e.g., HUS, TTP).

Toxic (Nephrotoxic) ATN: Results from

exposure to substances that are directly poisonous to tubular cells.

Name the three clinical phases of Acute Tubular Necrosis.

The three phases are initial injury, maintenance, and recovery.