AKI and CKD (Grin) Flashcards
How is AKI defined?
By the presence of any of the following:
1. increase in serum creatinine by >0.3 within 48 hrs
2. increase in serum creatinine by >1.5 within 7 days
3. urine volume <0.5mL/kg/hour for 6 hours
Define the 3 features of the ideal substance to estimate GFR.
- Freely filtered across glomerulus
- Not reabsorbed
- Not secreted
Explain the unique features of creatinine as to why we use it to estimate GFR.
It is a metabolite of creatine phosphate in muscle.
1. Freely filtered across glomerulus
2. Not reabsorbed
3. Small amount is secreted in proximal tubule
As GFR function declines, what happens to serum creatinine?
They have an inverse relationship. As GFR declines, serum creatinine will increase.
Definition of anuria
urine output <50-100 mL/day (basically no urine output)
Definition of oliguria
urine output <400-500 mL/day (very little urine output)
Definition of azotemia
elevation of BUN with NO symptoms
Definition of “pre-renal” azotemia
elevation of BUN out of proportion in serum creatinine, specifically due to poor renal perfusion
Definition of uremia
elevation of BUN with symptoms (n/v, confusion, metallic taste in mouth, fatigue, anorexia)
What is the consequence of a disruption in the maintenance of normal volume status?
Volume overload, will present with dyspnea and edema and the severe consequence of this will be pulmonary edema.
What is the consequence of a disruption in the maintenance of normal electrolyte homeostasis?
Na retention will lead to hypertension, potentially leading to a hypertensive emergency.
Decreased K+ excretion will lead to hyperkalemia which can lead to arrhythmias and sudden cardiac death.
What is the consequence of a disruption in the maintenance of normal acid-base balance?
Metabolic acidosis will lead to dyspnea (due to respiratory compensation) and can potentially lead to arrhythmias
What is the consequence of a disruption in the maintenance of waste elimination?
increase in urea will cause uremia (elevated BUN with symptoms -n/v, altered taste, fatigue, confusion) which can lead to encephalopathy, asterixis, uremic pericarditis and uremic frost
Labs for pre-renal AKI
Urine NA < 20 mEq/L; FeNa <1%
BUN/Cr ratio >20:1
Urine Osmolality >500 mosm/kg
Which medications do you want to avoid in patients with pre-renal AKI?
NSAIDs
The body produces prostaglandins to vasodilate arterioles and autoregulate the low renal blood flow, NSAIDs inhibit prostaglandins and will worsen the AKI
What typically occurs when pre-renal AKI presents for a long time?
If pre-renal AKI present long enough, Acute tubular necrosis (ATN) will develop.
What are hypovolemic causes of pre-renal AKI?
Absolute loss of fluid due to:
Bleeding
Vomiting/diarrhea
Overdiuresis
What are hypervolemic caused of pre-renal AKI?
Congestive heart failure (relative loss of fluid)
What are systemic vasodilation causes of pre-renal AKI?
Sepsis
Systemic Inflammatory Response Syndrome (SIRS)
Cirrhosis
What are causes of acute tubular necrosis (ATN)?
Prolonged pre-renal AKI (most common cause is sepsis)
Toxins: myoglobin (rhabdomyolysis), uric acid, myeloma light chains, IV contrast
What are causes of acute interstitial nephritis (AIN)?
PPIs (omprezaloe)
NSAIDs
certain Antibiotics
AIN treatment = STOP offending medications
Explain the relationship between rhabdomyolysis and intrinsic AKI.
Rhabdomyolysis is a condition when damaged skeletal muscle breaks down rapidly; symptoms - muscle pain, weakness, dark urine.
Myoglobin can cause damage to the renal tubules (cause intrinsic AKI). Diagnosis: elevated CK, dipstick positive for blood but no RBCs on sediment
What is the diagnostic test for intrinsic AKI caused by rhabdomyolysis?
elevated creatine kinase (CK) with dipstick positive for blood, but no RBCs on sediment. Myoglobin causes a false positive on dipstick.
What is the classic triad presentation for Acute Interstitial Nephritis (AIN)?
eosinophils in urine (eosinophiluria)
fever
rash