Acute Kidney Injury/Rhabdo Flashcards
Functions of the Kidney
Regulation of ionic composition
Sodium, potassium, calcium, chloride, phosphate
Regulation of blood pH, osmolarity, and glucose
Regulation of blood volume
Conserving or eliminating water
Regulation of blood pressure
Secreting renin
Release of erythropoietin & calcitriol
Excretion of wastes
Nitrogenous waste products (ammonia, uric acid, urea, creatinine, and amino acids), excess quantities of salts and water
Major Function of the Kidney
Filter blood plasma and separate wastes from the useful chemicals
Eliminates the wastes in urine while returning the useful chemicals to the bloodstream
Renal Corpuscle
Component of each nephron
Site where blood filtration begins
Passive process by high hydrostatic pressure of the glomerular capillaries
Consists of:
Glomerulus (cluster of capillaries)
Bowman’s capsule
Two-layered capsule that encloses the glomerulus
Blood flows into the glomerulus via the afferent arterioles → water and solutes pass through the capillary endothelium, through the basement membrane, and through the epithelium → Bowman’s space → renal tubule
Remaining blood leaves the glomerulus through efferent arterioles
Glomerular Filtration Rate (GFR)
General and dependent on
The volume of fluid filtered by the kidneys in a minute
Measure of your kidney function
Dependent upon:
The net filtration pressure
Vasodilation of the afferent arterioles mediated by prostaglandins
Vasoconstriction of the efferent arterioles mediated by angiotensin II
Available surface area for filtration
Filtration membrane permeability
Angiotensin II vasoconstricts the glomerular arterioles; greater effect on the efferent arterioles than the afferent arterioles → increased glomerular filtration pressure
Increased circulating volume from the affects of aldosterone → increased blood pressure and renal perfusion
Angiotensin II stimulates the release of antidiuretic hormone (ADH), which will reabsorb water from the collecting ducts → increased circulating blood volume and renal perfusion
Renal Tubule
Duct that leads away from the glomerular capsule
Divided into 4 regions:
Proximal convoluted tubule (PCT)
Nephron loop
Distal convoluted tubule (DCT)
Collecting duct
Each has a unique absorptive properties
Acute Kidney Injury (AKI)
general and epi
Characterized by abrupt deterioration in kidney function (within 48 hours) based on an elevation in serum creatinine level with or without reduction in urine output
Spectrum of injury from mild to advanced → requiring renal replacement therapy
Often reversible
Classified as pre-renal, intrinsic/intra-renal, or post-renal
Epidemiology:
7% of hospitalized patients
2/3 of ICU patients → Mortalityis 50%‒70% in AKI associated withsepsis and multiple organ failure
Previously referred to as acute renal failure (ARF) and acute renal insufficiency
AKI
Staging Criteria
Kidney Disease: Improving Global Outcomes (KDIGO) criteria for AKI
Stage 1
≥ 0.3 mg/dL increase in serum creatinine within 48 hours,or
Increase in serum creatinine > 1.5–1.9 times baseline in the past 7 days,or
Urine volume/urine output < 0.5 mL/kg/hr for 6–12 hours
Stage 2
Serum creatinine 2.0‒2.9 times baseline,or
Urine volume/urine output < 0.5 mL/kg/hr for ≥ 12 hours
Stage 3
Serum creatinine 3 times baseline,or
Serum creatinine ≥ 4 mg/dL,or
Initiation of renal replacement therapy,or
Decrease in estimatedGFR
< 35 mL/min/1.73 m2in individuals < 18 years of age,or
Urine volume/urine output < 0.3 mL/kg/hr for ≥ 24 hours,or
Anuria for ≥ 12 hours
DONT MEMORIZE
Multiple staging systems for AKI
Staging is based on serum creatinine, urine output, and/or changes in GFR
Kidney Disease: Improving Global Outcomes (KDIGO) criteria is the currently preferred staging system
Other staging systems:
Risk, Injury, Failure, Loss, and End-stage kidney disease (RIFLE) classification system
The Acute Kidney Injury Network (AKIN) criteria
International Renal Interest Society (IRIS) guidelines for AKI (Grade I-V)
AKI
RF
Older age >75 years
Hypovolemia – dehydration or blood loss
Nephrotoxic drugs
Rhabdomyolysis
Sepsis
Chronic disease:
Diabetes mellitus
Liver failure
Heart failure
Kidney disease (acute on chronic kidney injury)
AKI
Pre-renal Causes
Most common type of AKI
70% of community-acquired cases
Caused by decreased renal perfusion
Reduced circulating volume (GI losses, blood loss, diuretic use, osmotic diuresis – DKA, insensible loss – burns)
Reduced cardiac output (heart failure)
Systemic vasodilation (septic shock)
Medications
ACE inhibitors, ARBs, NSAIDs
Obstruction of the renal artery (thrombosis/embolus, stenosis, or aneurysm)
Pre-renal cause
NSAIDs
Vasodilation of the afferent arterioles mediated by prostaglandins
NSAIDs block the production of prostaglandins → vasoconstriction and possible AKI
Vasoconstriction of the efferent arterioles mediated by angiotensin II
ACEi/ARBs block the effects of angiotensin II (vasoconstriction) → vasodilation of the efferent arterioles (renal protective)
In patients with renal artery stenosis, the introduction of an ACEi/ARBs can lead to a drop in glomerular filtration pressure
AKI
Intrinsic/Intra-renal Causes
Caused by direct damage to the glomeruli and/or tubulointerstitial structures
Acute tubularnecrosis(ATN)
Damage to the tubular cells
Caused by a lack of blood flow to the kidneys and nephrotoxic agents
Acute interstitial nephritis
Inflammatory cell infiltration into the kidney interstitium
Caused by medications,infections, orautoimmune diseases
Vascular disease
Atherosclerosis and vasculitis
Glomerular disease
Glomerulonephritis (presents withhematuria) or nephrotic syndrome(presents withproteinuria)
AKI
Post-renal Causes
Caused by inadequate drainage of urine distal to the kidneys (obstruction) leading to back pressure on the kidneys and hydronephrosis
May occur at any point in its course from therenal pelvisto theurethra
Causes of obstruction
Urinary calculi
Benign prostatichyperplasia (BPH) or prostate cancer
Bladder outlet obstruction
Urethral stricture
Gynecologic tumors (ovarian cancer, uterinefibroids,cervical cancer)
A single stone will lead to AKI in a patient with 1 functioning kidney, but unlikely in patients with 2 functioning kidneys
Effects of AKI on Electrolytes & Acid-Base Balance
Hyperkalemia
Due to decreased renal excretion ofpotassium
Increases theprobability ofcardiac arrhythmias
Hyperphosphatemia
Due to decreased renal excretion ofphosphate
Metabolic acidosis
Inability of thekidneysto excreteacids
Exacerbateshyperkalemia
Increases theprobabilityofcardiac arrhythmias
Hyperkalemia
AKI
Labs
Urinalysis – proteinuria, hematuria, casts
Urine output
Oliguria < 400 mL per day of urine
Anuria < 100 mL per day of urine
CBC with differential
CMP
Compare current BUN/creatinine to prior results
Electrolyte imbalances
Other lab tests to further evaluate underlying cause
AKI
imaging
Doppler US to evaluate for renal artery stenosis
Non-contrast CT scan of abdomen and pelvis to rule out obstruction
AKI
Biopsy
Reserved for patients in whom prerenal and postrenal causes of AKI have been excluded
AKI
Tx
Based on the etiology of AKI
Stop any offending agents (medications) if identified as the cause of AKI
Adjust all essential medications for renal dosing
Avoid iodinated contrast media and gadolinium
If prerenal withhypovolemia
Treat withIV fluids (isotonic solution - normal saline or Lactated Ringer’s)
Ifprerenal with fluid overload treat withdiuretics
If postrenal with obstruction
Foley catheter to relieveurinary retention
Specialist consultation to treat underlying conditions (urology or gynecology)
AKI
Tx electrolyte imbalance
Treat electrolyte and acid-base imbalances urgently
Hyperkalemia
≥ 6.5 mEq/L (severe)
If EKG changes are present
Calcium gluconate 10 mL of 10% solution given IV over 5 minutes to reduce the risk of cardiac arrhythmias
Insulin and dextrose given IV to shift potassium out of circulation and into the cells
Loopdiureticsto allow for renal loss ofpotassium
Sodium polystyrene sulfonate (Kayexalate) can be given to lower potassium levels gradually
Metabolic acidosis
Treat with oral or IVsodium bicarbonate
Rhabdomyolysis
general and causes
Condition characterized by muscle necrosis and the release of intracellular contents into circulation (especially myoglobin)
Prompt recognition and treatment are vital because severe disease can be associated with life-threatening acute kidney injury (AKI) and electrolyte imbalances
Causes:
Any form of muscle damage can result in rhabdomyolysis
Broadly divided into three categories:
Traumatic or muscle compression
Non-traumatic exertional
Non-traumatic, non-exertional
Rhabdo
Traumatic or muscle compression
Crush injuries
Victims of prolonged restraint, torture, or physical abuse
Surgical procedure with prolonged muscle compression
Acute lower-limb compartment syndrome
High-voltage electrical injury
Rhabdo
Non-traumatic exertional causes
Extreme exertion or exertion under conditions in which muscle oxygenation is impaired
Marked physical exertion when one or more of the following risk factors is present:
Patient with the sickle cell trait
Patient is physically untrained
Exertion occurs in extremely hot, humid conditions (heatstroke)
Normal heat loss through sweating is impaired (anticholinergic medications or heavy football equipment)
Pathologic hyperkinetic states:
Grand mal seizures
Delirium tremens (DTs): severe type of withdrawal from alcohol
Psychotic agitation
Amphetamine overdose
rhabdo
Nontraumatic, non-exertional causes
Prolonged immobilization
Alcohol use
Drug use
Illicit: heroin, cocaine, LSD, methadone
Prescription: statins, colchicine, daptomycin
Toxins
Snake venom, mushroom poisoning, carbon monoxide
Infections
Viral – influenza A & B, coxsackievirus
Inflammatory myopathies (dermatomyositis)
Electrolyte abnormalities
Hypokalemia
Hypophosphatemia
Electrolyte balance
intra/extracellular fluid
Intracellular fluid
Potassium (K⁺) – main cation
Magnesium (Mg2⁺)
Proteins
Phosphates (HPO₄²-/H₂PO₄-) – main anion
Electrically balance the intracellular cations along with the negatively chargedproteins
Extracellular fluid
Sodium (Na⁺) – main cation
Controls ECF volume and water distribution in the body – water follows sodium
Calcium (Ca²⁺)
Chloride (Cl-) and Bicarbonate (HCO₃-):
Chloride is the most abundant anion in the ECF
Anions balance the extracellular cations
rhabdo
Patho
Muscle injury
Influx of extracellular sodium and calcium into the myocytes; water follows sodium distorting the integrity of the intracellular space
↑ intracellular calcium causes a sustained myofibril contraction → ATP depletion within these cells
Activation of lipases and proteases → damage of the myocyte cellular membrane
Release of intracellular components (creatine kinase (CK), myoglobin, potassium, phosphate) that enter the bloodstream
Myoglobinuria and electrolyte abnormalities cause end-organ complications
Most common systemic complication is renal failure
Rhabdo
S/Sx
Triad
Clinical presentation is variable
Classic triad - Present in < 10% of patients
Weakness
Myalgia
Tea-colored urine
Muscle pain
Affects proximal muscle groups, such as shoulders, thighs, lower back, and calves
Oliguria (output of < 500 mL/day) or anuria (output of 0-100 mL/day)
Other signs and symptoms based on the inciting event and complications
Fever is present in patients with infection
Altered mental status in cases of intoxication
rhabdo
labs
Suspected based on history and clinical signs and symptoms
Labs (confirmatory)
↑creatine kinase (CK)
Key biomarker for rhabdomyolysis
>5x the upper limit of normal
Elevated at 12 hours after insult
Peaks at 24‒72 hours
Back to normal in about 5 days
↑ Myoglobin
Hard to detect in serum due to shorthalf-life
Red-to-brown urine without genitourinary symptoms
Suspect myoglobinuria → positive test for blood on the urine dipstick, but no RBCs on microscopic examination
Electrolyte abnormalities
Hyperkalemia: serum potassium (K+) level > 5.0 mEq/L
Hyperphosphatemia
Hyperuricemia: release of purines from the damaged muscle
Hypocalcemia: results from hyperphosphatemia
Metabolicacidosis
↑ lactic acid from damaged/ischemic muscles
↑ LDH due to tissue damage
Acute renal injury
↑ BUN and creatinine
Myoglobin is cytotoxic to nephrons and scavenges nitric oxide leading to worsening renal injury
rhabdo
ECG
Electrocardiography (ECG)
To look for cardiac dysrhythmias (secondary to electrolyte abnormalities)
Possible findings ofhyperkalemia
Peaked T waves
Flattened to loss of P waves
Wide QRS interval
Sine wave pattern
Possible finding withhypocalcemia
QT prolongation
rhabdo
Tx
Initial approach
Airway, breathing, circulation (ABC) assessment for all patients with trauma history
Exclude and treat other potential injuries (compartment syndrome, vascular compromise, fractures, dislocations, and wounds)
Removal of offending agents (if medication is suspected)
Aggressive intravenous fluid resuscitation
Lactated Ringer’sor saline (0.9%‒0.45%)
Caution for fluid overload in the anuric patient
Manage electrolyte abnormalities
Rhabdo
monitoring
CK levels every 6 hours until levels are consistently decreasing
Basic metabolic panel at least every 4 hours to monitor
Electrolyte abnormalities
Renal function
Hourly urine output (urinary catheterization may be necessary)
Electrocardiogram and cardiac monitoring if K+is > 6.0 mEq/L
Rhabdo
Key points
The classic triad of symptoms (myalgias, muscle weakness, and tea-colored urine) is present in<10% of cases
Myoglobinuria → positive test for blood on the urine dipstick, but no RBCs on microscopic examination
A CK level of>5 times the upper limit of normal is typically required for diagnosis
Treatment is supportive with IV hydration as well as concurrent treatment of the inciting cause and any resulting complications
