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NUR 133: exam 3 review sheet|Acute Kidney Management (Fall 2025)

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NUR 133: exam 3 review sheet Acute Kidney Management

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Voorbeeld van de inhoud

Acute Kidneyof
Injury (AKI) - pg 1549-1565, 1569-1573 Renal
Management AKI - pg 1581-1589
pgChronic Kidney Disease / End-Stage Renal Disease (ESRD)
1576-1581
Renal Replacement Therapy
Hemodialysis
Continuous - pg Replacement
Renal 1589-1602 Therapy (CRRT)
Peritoneal Dialysis
Kidney Transplant - pg 1607-1612



Renal
What do the kidneys do?
● Filters waste of blood including ketones, proteins, electrolytes
● Acid/base balance — can create Bicarb if needed
● Regulates Blood Pressure — RAAS System, fluid balance
● Releases hormone (Erythropoietin) for bone marrow to release RBC
Lab Values
● BUN - 7-18 mg/dL
● Potassium - 3.5-5; usually high in a renal patient
● Glomerular Filtration Rate (GFR) - 125ml/min (180 L/day); amount of blood going through the kidney; will usually be decreased in a renal patient
● Creatinine - 0.6-1.2 mg/dL; usually high in a renal patient
● Creatinine Clearance - inverse relationship to Creatinine (creatinine clearance is usually low); looks at how much creatinine the patient is actually excreting

Acute Kidney Injury - Overview
● A rapid/sudden REVERSIBLE loss of renal function due to damage to the kidneys — begins with kidney insufficiency where kidneys function but not well
● Life threatening metabolic conditions can occur — Metabolic acidosis, F&E imbalances
● An increase of 50% in BUN/Cre from baseline is classified as AKI; this does not mean they stop producing urine

Signs and symptoms
● Critically ill/lethargic; dry/dehydrated
● CNS symptoms — drowsiness, headache, muscle twitching (caused by f&e imbalances especially in sodium & calcium), seizures (sodium)
● Increase in BUN and creatinine — 50% increase above baseline indicates AKI;

, ○ Means the kidneys are not working properly and excreting BUN and Creatinine
● Urine Output -
Oliguria - decreased urinary production Anuria - not producing urine

Goals/Care
● Replace renal function temporarily to reduce complications
○ Dialysis to remove the fluid from the body when the kidney can not do it by itself
○ Give drugs to manage BP
○ Give Erythropoietin for RBC production if counts are low
● Monitor BUN/Creatinine; dosage of drugs because the kidneys are responsible for clearing drugs…if the kidneys are impaired they can not
effectively clear drugs → overdose

Glomerular Filtration - The fluid that filters through the glomerulus into Bowman's capsule
● Glomerular Filtration Rate - The quantity of the glomerular filtrate formed in all nephrons
● Looked at to see if the body is producing enough urine after looking at BP and BUN/Cre
○ Normal Value - 125ml/min (180 L/day)
Assessment and Diagnosis Prevention
● Monitor urine output - normal is 30mL/hr ● Assess renal function
● AKI results in decreased glomerular filtration rate and oliguria ● Adequate hydration - assess I&O
● Monitor Lab Values - ● Treat shock promptly - when a person can not maintain organ perfusion
○ BUN - 7-18 mg/dL ● Monitor CVP, BP
○ Creatinine - 0.6-1.2 mg/dL ● Nephrotoxic agents - Aminoglycoside antibiotics, NSAIDS, radiocontrast
○ Potassium - 3.5-5 (monitor for (dye in scans)
hyperkalemia→dysrhythmias)
○ Phosphate & Calcium
● Metabolic Acidosis - bc kidney can’t excrete toxins
● Anemia - due to impact in erythropoietin production; monitor h&h
Causes / Categories of AKI
● Cardiac - Hypovolemia, Hypotension, reduced cardiac output and heart failure
● Urinary - Obstruction of the kidney or lower urinary tract (tumor, kidney stones, clots,
bladder cancer) obstruction of renal arteries or veins
Pre - caused by conditions or substances that interfere with blood flow to the kidneys; *most
common in an ICU setting*
● Low blood pressure, reduced blood flow, low blood volume
Intra - caused by conditions that affect the structure and function of the kidneys
● Nephrotoxicity (d/t exposure to toxic substances such as alcohol, drugs, heavy metals,
fuels, and solvents & certain pharmaceutical drugs), Inflammation / allergic reaction to

, drugs, Atheroembolic Kidney Disease
Post - caused by problems with the flow of urine as it leaves the body
● This may occur in the bladder (urethral obstruction) or the tubes that lead from the kidneys into the bladder (ureters).
● Neurological — the brain isn’t sending a signal to the kidneys to release the urine
Acute Tubular Necrosis (ATN) -
● Damage to the kidney tubules that is the most common cause of AKI
● Most common form of AKI - Intratubular obstruction, Tubular back leak, Vasoconstriction, Changes to glomerular permeability
● Causes ↓ in GFR, Azotemia (toxic levels in the urine), F&E imbalances

Phases - can progress over months
1. Initiation - Initial insult up until oliguria develops
○ Ex - MI leading to a decrease in Cardiac Output; Hypovolemia; Sepsis
2. Oliguria (less than 400mL/24 hours or 0.5 mL/kg/hr) - Increase in serum concentration of urea, Cr, uric acid, potassium and magnesium
○ After injury, we now see a progressively decreasing urine output
○ Diuretics won’t help to excrete urine because the kidneys aren’t working to create urine
3. Diuresis - increase in urine output, means that some recovery/function has improved; GFR has started to recover, labs values stabilize, monitor dehydration
4. Recovery - Signals the improvement of renal function; sustained level of improvement, lab values are normalized

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