Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

• AKI is characterized by a sudden decline in kidney functioning
• Two major symptoms of AKI are a sudden rise in serum creatinine levels (1.5 times higher than baseline) and a reduction in urine output
• Normal creatinine levels are less than 100 micromoles per liter; in AKI, creatinine levels climb to 200-400 micromoles per liter or above
• AKI onset is sudden, happening in hours to days, and severity ranges from mild to total kidney filtration loss
• AKI is often reversible with treatment, allowing patients to recover to their baseline functioning
• AKI is associated with high mortality rates, often affecting individuals in critical care areas or ICUs with multi-system problems
• Decreased filtration levels in AKI patients may necessitate renal replacement therapy, such as Continuous Renal Replacement Therapy (CRRT), involving 24-hour hemodialysis with one-to-one nurse monitoring
• In some cases, kidneys do not recover from AKI, resulting in permanent damage; AKI can lead to chronic kidney disease

Risk Factors for AKI

• Patients with infections are at risk due to potential septic reactions causing vasodilation, reduced blood pressure, and decreased kidney perfusion
• Septic patients are often on multiple antibiotics, some of which can be harmful to the kidneys, increasing AKI risk
• Patients with low blood pressure and those experiencing shock are at risk
• Patients undergoing surgery are at increased risk due to surgery-related drugs and potential blood loss
• Individuals with heart failure may experience lowered blood pressure to manage cardiac output, increasing AKI risk if blood pressure becomes too low
• Individuals administered nephrotoxic agents such as medications and contrast dyes are at risk; nurses should closely monitor urea and creatinine levels in these patients

Categories of AKI

• AKI is divided into pre-renal, intra-renal (intrinsic), and post-renal categories, based on the injury location
• Pre-renal injuries are caused by a sudden decrease in blood flow to the kidney before it reaches the kidney
• Intrarenal injuries are caused by direct damage to the kidney
• Post-renal injuries are due to an obstruction affecting the outflow from the kidney

Causes of Pre-Renal Injuries

• Sudden drop in blood pressure or blood flow to the kidneys can cause pre-renal injuries categorized into:
  • Hypovolemia: Loss of blood volume due to accidents or surgeries, or loss of water content due to dehydration from vomiting or diarrhea
  • Altered peripheral vascular resistance: Blood vessel tone loss as in sepsis, anaphylactic reactions, or smooth muscle relaxant medications
  • Cardiac disorders: Heart attack, dysrhythmias, or cardiac tamponade causing decreased cardiac output and subsequent drop in blood pressure

Intrarenal or Intrinsic Injuries

• Prolonged renal ischemia, or prolonged lack of blood flow to the kidney, can cause intrarenal injury if pre-renal factors are not addressed and reversed
• Nephrotoxic drugs can cause damage; Aminoglycosides are particularly harmful to kidneys
• Exposure to chemicals, including ethylene glycol (antifreeze), is harmful
• Acute hemolysis and rhabdomyolysis can cause intrarenal injury including:
  • Hemolysis is the breakdown of red blood cells
  • Rhabdomyolysis is the breakdown of muscle tissue
  • Both release heme, a nephrotoxic particle that is filtered through the glomerulus into the tubules, causing damage
  • Hemolysis causes include blood transfusion reactions
  • Rhabdomyolysis causes include injury to a large muscle (traumatic accident, motor vehicle collision), or falls in the elderly
• Glomerulonephritis, inflammation in the glomerulus causes kidney injury

Post-Renal Injuries

• Obstruction of urine flow after it leaves the kidney may involve:
  • Kidney stones
  • Tumors
  • Scar tissue narrowing the urinary tract (after repeated urinary tract infections or STIs)
  • External force pressing on the urinary tract (enlarged prostate compressing the urethra, or a tumor in the pelvis)

Pathophysiology of Pre-Renal AKI

• Low blood flow disrupts the normal balance of pressures in the glomerulus
• Loss of glomerular hydrostatic pressure results in a drop in the overall filtration rate
• The kidney attempts to compensate by activating the renin-angiotensin-aldosterone system
• Less urine is formed and less waste product is excreted

Pathophysiology of Intrarenal AKI

• Lack of blood flow or exposure to a nephrotoxic agent injures the epithelial cells lining the tubules
• Injured epithelial cells slough off and collect in the renal tubules, obstructing filtrate movement and increasing intratubular pressure
• Imbalance in filtration pressures drops the overall GFR, leading to reduced urine output and the development of azotemia
• Dead cells slough off and move through the tubules, clumping together to form casts excreted in the urine

Pathophysiology of Post-Renal AKI

• Physical obstruction of filtrate outflow from the kidney
• Intratubular pressure rises to push against the obstruction, eventually dropping GFR
• Tubules are not initially damaged in post-renal injury

Clinical Course of AKI: Pre-Renal vs. Post-Renal

• Early recognition allows quick return to normal kidney function
• Pre-renal requires normalizing blood pressure
• Post-renal requires removing obstruction
• Failure to intervene quickly can lead to intrarenal injury involving nephron damage

Clinical Course of Intrarenal Injury: Three Phases

• Initiation phase: Begins with a precipitous event, such as a hemolytic reaction, prolonged ischemia, or exposure to a nephrotoxic agent
• Maintenance Phase: Lasts for days to weeks, with symptoms related to a drop in GFR
  • Anuria (no urine production) indicates the most severe type of intrarenal injury
  • Oliguria (less than 400 mL of urine per day), is a more common presentation
  • Non-oliguric urine continues but is very dilute with low specific gravity
  • Fluid accumulation leads to increased blood pressure, edema, and weight gain
  • Electrolyte and acid-base imbalances occur, similar to chronic kidney disease
  • Injured kidney fails to maintain erythropoietin production, leading to anemia
  • Waste products accumulate
• Recovery Phase: Return of normal kidney functioning as urine production resumes
  • Improvement in blood work trending urea and creatinine towards the patient's baseline
  • Diuretic phase involves producing larger amounts of urine (up to 5 liters per day) for 1-3 weeks
  • Kidney's ability to concentrate urine is not yet regained, resulting in fluid and electrolyte excretion and potential imbalances
  • Assess for hypovolemia, hypotension, and dehydration
  • Monitor blood work for hyponatremia and hypokalemia
  • Full return to baseline may take up to 12 months

Glomerulonephritis

• Glomerulonephritis is a group of diseases causing inflammation in the glomerulus or kidney's filtration membrane
• An immune-mediated condition and is often an abnormal response to an infection elsewhere in the body
• Can develop after a strep infection, pneumonia, hepatitis, or mononucleosis virus
• Symptoms are due to loss of filtration of inflamed glomerular tissue including:
  • loss of red and white blood cells in the urine.
  • fluid retention
  • a drop in urine output

Types of Glomerulonephritis

• Acute : Has the same disease progression as previous slides with acute drop in filtration followed by an oliguric phase, then a recovery phase.
• Rapidly progressive. Initial acute injury does not resolve, but rather progresses to kidney failure in a relatively short period of time (weeks to months)
• Chronic. Acute injury seems to resolve but low levels of inflammation persist over years
• Nephrotic syndrome is an atypical presentation which features a loss of large amounts of protein in the urine

Acute Post Streptococcal Glomerulonephritis

• Develops 5 to 21 days after a strep infection (most commonly in the throat or on the skin), impacting children ages 3-7 mostly
• Antigen antibody complexes deposit in the glomerulus
• Injury causes activation of white blood cells to rush to the area which creates decreases the lumen where blood can enter and be filtered, decreasing GFR
• Ruptured capillaries will leak cells out into the urine leading to hematuria.
• Urine is usually described as smoky or tea-colored
• Drop in GFR causes fluid retention; manifest as edema appearing first in areas of low pressure/around the eyes, and results in rising blood pressure
• Urine analysis reveals large molecules (white/red blood cells and protein), and erythrocyte casts

Urinary Tract Infections (UTIs)

• Normally the urinary tract is sterile, but bacteria can try to enter the urinary tract on a regular basis, resulting in an infection.
• Ascending infections start with bacteria entering the urethra, moving up into the bladder
• Infection spreading above the bladder (ureters/kidneys) is rare but possible

Terminology of UTIs

• UTIs are classified by part of the urinary tract an infection involves
• Lower urinary tract (urethra and bladder) "cystitis"
• Upper urinary tract (ureters and kidneys) "pilonophritis". Pylo refers to the renal pelvis where urine enters the kidney
• Most UTIs are caused by E. coli, Gram negative bacteria from feces
• Bacteria entering the urethra are flushed out during the emptying of the bladder via the "flushing effect"

Risk Factors for UTIs

• Female anatomy is attributed to the fact female anatomies have a shorter route for bacteria to reach the bladder.
• Those with immobility or are in urinary stasis
• Not emptying the bladder regularly so that any bacteria trying to get in is removed can cause increased infection risk

What Can Cause Urinary Stasis

• Enlarged prostates
• Urethral narrowing from scarring or recurrent infections,
• Congenital abnormalities and how the ureters are attached to the bladder.
• Blood and nerve supply damage due to a condition like stroke
• Kidney stones

Clinical Manifestations of a Lower UTI

• Tissue that is red swollen and inflamed
• Experience dysuria
• Urinary frequency occurs when the inflamed bladder has less space for the urine to accumulate
• Urge to void is very strong
• Discomfort in the bladder area/suprapubic area.
• Urine may be cloudy or have a whitish hue, milky appearance or be fowl smelling due to presence of bacteria and pus

Urinalysis (UA) - Testing of Urine

• Lower UTI findings are bacteria/pus/small amounts of blood attributed to that irritated tissue.
• In pylonephritis also have lower UTI symptoms and fever, chills and malaise as well as significant pain
• Plus the additional of cell casts (cellular debris that comes when things are dying inside the tubules of the kidneys)

Complications from Frequent Infections (Pylonephritis)

• Can cause long term damage or scar tissue, decreasing the ability of kidneys to filter properly over time
• Chronic Kidney Disease

Renal Calculi/Kidney Stones

• Mineral salts in urine become so concentrated that they can't stay in the solute and start to precipitate out solid stone structures.
• Mineral salts mix in the solute.

Terminology About Kidney Stones

• Renal Calculi - Kidney Stones
• Calculus - Stone
• Lithiasis - Stone Formation
• Nefrolithiasis - Stones in the urinary tract
• Stone Types: Calcium Phosphate, Calcium Oxalate, Uric Acid, Cysteine and Struvite (Magnesium Ammonium Phosphate)
• Clinical Manifestations: Pain depending on the location which stone is in
• Kidney in renal pelvis complains of flank pain, which can be described as the pain in the back over top of where the kidneys would sit
• Stone moving into the ureters presents intensifies with renal colic. Excruciating pain usually radiating and tightening the ureters
• For men the pain radiates towards the scrotum and women towards the labia hematuria

Polycystic Kidney Disease

• Common genetic disease, where healthy kidneys are taken over by cycts
• Cycts compress the healthy kidney tissue, resulting in loss of renal function
• Kidneys are enlarged, causing pain due to the cycts pressing on renal tissue and can cause hematuria
• UTI occurs along with rising blood pressure
• Can lead to renal failure that needs possible dialysis or renal transplant

Bladder Cancer

• Risk factors include history of smoking
• Repeated exposure from chemicals
• Frequent injury/infection to the bladder

Bladder Cancer Manifestations

• Painless blood in the urine, which can be visibly seen or only seen under microscope
• Tumor Obstruction/Infection has similar sxs as a UTI
• These are frequent and urgent UTIs