Acute Kidney Injury Flashcards
1
Q
What are 3 basic features of renal failure?
A
- Impairment of the GFR
- Elevation of BUN/creatinine
- Decreased GFR leads to accumulation of substances/drugs normally excreted by the kidney
2
Q
What is AKI?
A
- Acute kidney injury = acute renal failure
- Rapid deterioration of renal function (hours to days, but <1 month)
- Greater than .5 mg/dl INC in creatinine or increase of 50% over baseline value
- Sometimes decreased urine output but not always (can have normal urine output, but GFR is down)
- Inability of kidney to regulate electrolytes/water
3
Q
What are the definitions of oliguria and anuria?
A
- Oliguria: <400 (or 500) ml urine output in 24 hours
- Anuria: <100 ml urine output in 24 hours
4
Q
How is AKI usually discovered?
A
- Usually asymptomatic and discovered and routine labs
- Most cases are reversible if underlying disease is treated
5
Q
What are the 3 categories of AKI? Distribution?
A
6
Q
What elements are critical in the eval of AKI?
A
- Careful history
- Review of hospital chart
- Medications
- Physical examination
- Examination of the urine
7
Q
Normal or few RBCs, WBCs
A
- Prerenal acute kidney injury
- Arterial thrombosis or thromboembolism
- Preglomerular vasculitis
- HUS or TTP
- Scleroderma crisis
- Postrenal AKI
8
Q
Granular casts
A
- Acute tubular necrosis (muddy brown casts)
- Glomerulonephritis or vasculitis
- Interstitial nephritis
9
Q
RBC casts
A
- Glomerulonephritis or vasculitis
- Malignant HTN
- Rarely interstitial nephritis
10
Q
WBC casts
A
- Acute interstitial nephritis or glomerulonephritis (RBC casts much more common in latter)
- Severe pyelonephritis (kidney inflammation due to bacterial infection)
- Allograft rejection
- Marked leukemic or lymphomatous infilitration
11
Q
Eosinophiluria
A
- Allergic interstitial nephritis (AB’s, NSAIDs)
- Atheroembolic disease
12
Q
Crystalluria
A
- Acute uric acid nephropathy
- Calcium oxalate (ethylene glycol toxicity)
- Acyclovir
13
Q
What are the 5 critical urine chemistry tests for prerenal vs. ischemic intrinsic AKI?
A
- Urine osmolality: Pre >500 (high AVP); In <300-350
- Urine Na conc (UNa x PCr)/(UCr x PNa): Pre <20; In >25
- FENa: Pre <1%; In >1%
- Urine sediment: Pre - hyaline casts; In - muddy brown granular casts/RTE’s
- BUN/Cr: Pre >20:1; In 10-15:1
14
Q
What is going on here? Describe the potential causes, presentation, and dx.
A
- Renal ultrasound with dilated calyces, indicating obstruction of urine flow
-
Potential causes:
1. Prostate disease (most common in old men -> BPH)
2. Pelvic or retroperitoneal malignancies (i.e., advanced cervical cancer)
3. Eurogenic bladder (bladder does not respond, or give signal that it is full) - Voiding complaints
- Physical exam: may have distended bladder
- U/A unremarkable
- Diagnosis: by ultrasound
15
Q
What do you see here?
A
- Normal renal ultrasound -> don’t see the calyces at all
16
Q
What is the most common type of AKI? What can cause it?
A
- Pre-renal AKI: kidney still intact, but decreased BF to kidney
- Volume depletion (GI, renal, 3rd space loss, bleeding, etc.)
- Congestive heart failure (bad pump)
- Shock from fluid losses, sepsis,
- Heart failure
- Hepatorenal syndrome (pts with cirrhosis)
- Renal artery stenosis
- Drugs that impair auto-regulation (NSAIDS)
17
Q
What is the pathophysiology of pre-renal AKI?
A
- Body tries to compensate, but ends up causing a dramatic reduction in renal BF, GFR, and urine flow
- Hypovolemic/decreased CO -> RAAS, AVP (non-osmotic stimulus), SNS -> body is trying to maintain BP and restore homeostasis
18
Q
What do you see here?
A
- Hyaline cast: common in pre-renal AKI, but also seen in normal urine
- Fairly non-specific
21
Q
What is the pathophysiology of hepatorenal syndrome?
A
- Very low urine sodium -> may be <10
23
Q
What’s going on here?
A
Renal artery stenosis
24
Q
What drugs can cause pre-renal AKI? How?
A
- ACEI’s, ARB’s, NSAID’s
-
ACEI/ARB’s: can cause a form of pre-renal AKI in pts w/bilateral renal artery stenosis
1. DEC levels, blocking of angiotensin II impairs renal auto-regulation (constriction of efferent arterioles in RAS) -
NSAID’s: block prostaglandin synthesis
1. Prostaglandins dilate the afferent arteriole
2. Can lead to AKI in some pts with: 1) true volume depletion, 2) CHF, 3) cirrhosis
3. Cox-2 inhibitors have similar intra-renal effects: also can cause AKI
25
Q
What does this graph show?
A
- Impaired auto-regulation of renal BF in patients taking angiotensin II antagonists (ACEI’s, ARB’s)
28
Q
What are the primary sites of tubular injury in ATN? Why?
A
- Less oxygen moving from cortex down to the medulla
- Proximal tubule S3 segment and TAH of LOH most likely to suffer ischemic injury because most active transport going on here
30
Q
What do you see here?
A
Muddy granular casts (suggestive of ATN, or other type of intra-renal AKI)
31
Q
How does ATN happen?
A
- Loss of cell-cell polarity and integrin-mediated tethering (diffusion of integrin and ATPase to apical surface)
- Loss of cytoskeletal attachments, actin polymerization
- Blebbing, loss of brush border, swelling
- See image -> gives you muddy, brown granular casts and backflow (INC creatinine and other waste products)
38
Q
What is this? Describe the disease process.
A
- Acute interstitial nephritis
- “Allergic” rxn in kidney-infiltration of interstitium with granulocytes (often eosinophils)
- Most commonly caused by ABs (e.g. penicillins, cephalosporins, sulfa, beta-lactam ABs), NSAIDS
- Symptoms: fever, rash, joint pain, INC eosinophils on CBC; possibly only renal dysfunction
- UA: pyuria, +/- urine eosinophils (need special stain)
- Scenario: normal renal function, put on some drug (normally, AB), measure renal function several days later and creatinine rise -> acute interstitial nephritis
- Probably the best course to take them off of the drug eliciting the problem
