AKI/CKD Flashcards
What is the most common cause of intrarenal AKI?
- Acute tubular necrosis (ATN)
- Primarily d/t ischemia, nephrotoxins or sepsis
- Low blood flow stimulates renin-angiotensin system = constriction of renal arterioles, further decreasing blood flow + decreased glomerular pressure
- Ischemia decreases glomerular permeability, reducing GFR to point of tubular dysfunction
- Interstitial edema, causing necrotic cells to accumulate in tubules, lowering GFR d/t debris obstruction
What are the phases of AKI?
1) Initiation phase (increase in creatinine and BUN, decrease in urine)
2) Maintenance phase (days to weeks, the longer the worse). Manifested by oliguria, fluid volume excess, metabolic acidosis, low Na+, high K+, low Ca+, high phosphate, anemia, waste accumulation causing neurological damage)
3) Recovery phase (return of BUN, creatinine and GFR towards normal range; kidneys may take awhile to return to concentrating urine)
When is oliguria classified?
Less than 400 cc/24 hours (sudden if ischemia, week if nephrotoxic drugs)
What is oliguria associated with in ATN?
- Urine with a normal specific gravity (1.010) and a high sodium concentration, and urine osmolality at about 300 mmol/kg (tubules unable to respond to autoregulatoy mechanisms)
- May include RBC’s, WBC’s and proteinuria d/t altered filtration
Why do the kidneys produce excess hydrogen in AKI?
Unable to synthesize ammonia, which is needed for hydrogen ion excretion; causes bicarbonate to decrease because it is used up in buffering the excess hydrogen ions, leading to metabolic acidosis
Why might there be excess potassium in AKI?
- Tissue trauma may cause release of potassium into extracellular fluid by damaged tissues
- Bleeding and blood transfusions can further damage cells
- Acidosis worsens hyperkalemia as hydrogen enters cells and potassium driven out (and there is likely excess hydrogen ions)
What are some symptoms of hyperkalemia?
- Weakness
- Tall, peaked T-waves
- Widening QRS
- ST depression
What are some hematological disorders with AKI?
- Anemia d/t low erythropoietin
- Uremia decreases platelet adhesion, leading to bleeding in multiple areas
- Altered WBC’s cause immunodeficiency (risk of sepsis)
What is necessary for calcium absorption in the GI tract? How is this altered in AKI?
Activated vitamin D; only functioning kidneys can activate vitamin D
How can low calcium lead to hyperphosphatemia?
Low serum calcium d/t kidney dysfunction > needs alt sources to acquire calcium > parathyroid gland secretes parathyroid hormone > bone demineralization > release of calcium > phosphate is also released > kidneys already have impaired excretion of phosphate by kidneys
What is urea?
An end product of endogenous muscle metabolism
What are reasons aside from AKI that can raise BUN levels?
- Dehydration
- Corticosteroids
- Catabolism d/t infections, fever, injury and GI bleeding
Why is a urinalysis ordered?
- Urine sediment containing abundant cells, casts or protein suggest intrarenal disorders
- Urine osmolality, Na+ and specific gravity help differentiate types of AKI
- Hematuria, pyuria and crystals may be seen with posternal AKI
What are collaborative therapies to tx AKI?
- Tx the cause
- Fluid restriction (typically 600 mL + previous 24-hour fluid loss)
- Nutritional therapy (K+, Na+ and phosphate restriction, adequate protein depending on catabolism)
- Measures to lower K+ if elevated
- Calcium supplements or phosphate-binding agents
- TPN if indicated
- Initiation of renal replacement therapy if needed
Why is an UC the first dx test?
- Allows for gross visualization of kidneys and structures
- Does not require dyes (harmful to kidneys)
