Renal: Acute and Chronic Kidney Disease Flashcards
(51 cards)
Why is it important to detect acute kidney injury ASAP?
So you can treat it aggressively = PREVENT irreversible damage and death
What is AKI?
Severe and sudden decline in renal function (GFR) = kidneys inability to regulate fluid balance, maintain electrolyte/acid-base balance, and excrete nitrogenous waste
Causes of AKI (6)
1) Ischemic = decreased renal blood flow (tubule swelling, obstruction and cell death) = decreased GFR = hypovolemia, decreased CO, renal vasoconstriction, systemic hypotension and vasodilation, thrombosis
2) Toxic = concentrate or metabolize toxin = analgesics/NSAID’s, ACE inhibitors, antibiotics (aminoglycosides), amphotericin B, heavy metals, contrast agents, ethylene glycol, lilies, grapes, raisins, etc.
3) Infection - bacterial pyelonephritis, lepto, tick-borne (Lyme, RMSF, Ehrlichia)
4) Immune-mediated = glomerulonephritis or amyloidosis
5) Neoplasia - lymphoma in cats, adenocarcinoma in dogs
6) Post-renal, obstructive
7) Sepsis = UNCOMMON IN VET MED
Causes of AKI and decreases in GFR (4)
- Tubular obstructions from debris
- Increased tubular permeability
- Alterations in renal blood flow
- Decreased glomerular capillary permeability
Three main phase of AKI
1) Initiation
(Extension)
2) Maintenance
3) Recovery
When does the initiation phase of AKI occur? Signs?
> Time from renal insult AKI begins
*Tx now can prevent AKI development
*Clinical detection can be difficult = not azotemic, may have decreased urine concentrating ability
+ May see tubular injury on U/A = casts, proteinuria, glucosuria
Duration, signs, and timeline of the maintenance phase of AKI?
> Develops after tubular lesions are established
+ Azotemia/uremia, increased/decreased urine output
*Removal of inciting cause = doesn’t restore renal function
- Lasts days to several weeks
Therapy during maintenance phase of AKI?
Supportive - maintain hydration and electrolyte balances, keep patient alive until the nephrons can repair and hypertrophy
Duration, signs, and timeline of the recovery phase of AKI?
*Renal lesions are repaired, renal function improves
+ Extreme polyuria = GFR increases due to nephron hypertrophy and repair
- May take weeks to months
*Can be complete and result in adequate/normal renal function
What does the reversibility of the AKI depend on? (2)
- Severity and type of injury
- Rapidness and efficacy of removal of the underlying cause
What are we trying to find and focus on with AKI?
FIND THE TREATABLE CONDITIONS and treat them!
> Examples:
+ Hypovolemia or hypotension
+ History of NSAID’s or ACE inhibitor use
- Animals with decreased concentrating ability = Addison’s, hypercalcemia, pyometra, drugs (pheno, furosemide, glucocorticoids)
Reason for hospital caused acute kidney injury
Anesthesia in high risk patients = decreased renal perfusion and hypotension
Clinical signs of AKI
\+ Acute onset of anorexia or vomiting \+ Painful kidneys \+ Azotemia = increased BUN, creatinine, phosphorus \+ Isosthenuria \+ Granular or cellular casts \+ Glucosuria
What do pre/post-renal components, lepto, pyelonephritis, hypercalcemia, ethylene glycol toxicity, lily poisoning, or history of NSAID/ACE-i use have in common?
THEY ARE TREATABLE and you may help avoid AKI
Five things you should do with AKI patients
- Take a good history for toxin or drug exposure
1) Tx aggressively with fluids - r/o pre-renal
2) Culture urine - pyelonephritis
3) Tx for lepto
4) Tx with penicillin/amoxicillin or doxycycline while C&S and lepto are pending
5) Perform imaging = abdominal U/S or rads
Where and what do we use for fluid rehydration in AKI patients?
- Ideal = jugular catheter
- Most patients = 0.9% NaCl, LRS, Normosol-R = isotonic
- Patients w/ acidosis or cardiac abnormalites = hypotonic (0.45% NaCl)
Monitor for signs of overhydration, which include…?
\+ Increased RR and HR \+ Restlessness \+ Chemosis or runny nose \+ Increased body weight \+ Decreased PCV/TP \+ Increased central venous pressure \+ Severe cases = peripheral or pulmonary edema, respiratory distress
What other monitoring piece of equipment (other than clinical signs, imaging, infectious dz testing) is helpful in AKI patients?
Indwelling urinary catheterization to measure urine output
*Monitor urine output every 2 hrs and electrolyte/acid-base every 4-6 hours
What happens with K+ in AKI patients and what do we do to correct it?
> Hyperkalemia due to the decreased production or urine (oliguria or anuria)
- Should be accomplished by aggressive fluid therapy and diuresis
- Severe elevations = prevent cardiotoxic effects with Ca++ gluconate, shift K+ into cells with dextrose/insulin/Na+ bicarb
What happens with acid-base balance in AKI patient and what do we do to correct it?
> Metabolic acidosis = inability to excrete H+ or uremic acids (worse with anuria or oliguria)
- Should be accomplished with aggressive fluid therapy and diuresis
- Severe acidosis = bicarb (BE CAREFUL!)
What happens with Ca++ in AKI patients and what do we do to correct it?
> Hypercalemia or hypocalcemia
- Can be the cause or effect or AKI
- Tx = supportive = saline diuresis or furosemide (hyper) -OR- add Ca++ (hypo)
What happens with P in AKI patients and what do we do to correct it?
Hyperphosphatemia - fluid therapy diuresis
What do the ins and outs of urine production add to?
Ins = outs + 20 mL/kg/day (insensible losses)
What is absolute oliguria?
< 1 mL/kg/hour
