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
19
Q
What are some of the diagnostic clues for pre-renal AKI?
A
- FeNa = UNa PCr/ PNa UCr: < 1 % suggestive of pre-renal
-
Urinary Na: pre-renal if < 25 (this is what you are going to look for)
1. Kidneys are structurally intact, so when RAAS levels go up, they cause reabsorption of Na from CD, so there should be minimal Na in urine - Urine Osm: pre-renal if >500 -> due to high AVP levels
20
Q
What is hepatorenal syndrome?
A
- Special case of pre-renal AKI in end-stage cirrhosis
- Decreased blood pressure despite increased ECFV
- Kidneys structurally intact and urinalysis usually normal (might see some hyaline casts)
- Worsening azotemia and progressive oliguria
- Survival limited unless patient receives liver transplant
21
Q
What is the pathophysiology of hepatorenal syndrome?
A
- Very low urine sodium -> may be <10
22
Q
How do you diagnose hepatorenal syndrome?
A
- Diagnosis of exclusion: must rule out other causes (NSAIDS, nephrotoxic drugs, IV contrast)
- Urine sodium very low (<10) -> need to see this
-
Trial of volume infusion to rule-out simple pre-renal condition (albumin, saline, etc., depending on the condition of the patient)
1. Hepatorenal syndrome will not improve with a volume infusion (b/c ECFV already elevated)
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
What does this graph show?
- Impaired auto-regulation of renal BF in patients taking angiotensin II antagonists (ACEI's, ARB's)
26
What are the 3 potentially damaged areas in intra-renal AKI? Describe some of the causes w/in each.
- Structures of the kidney are damaged or dying
- _Glomerular_: Post-strep GN, Lupus, RPGN, Hepatitis related, IgA nephropathy
- _Tubular_: Acute Tubular Necrosis (ATN) (prolonged hypotension, medication toxicity, toxins), Acute Interstitial Nephritis
- _Vascular_: vasculitis
27
What are the 2 big categories of ATN? Histology?
- _Two big categories_:
1. Ischemic injury
2. Toxic injury from radio-contrast or meds
- _Histologically_:
1. Tubular necrosis w/denuding of renal tubular epithelial cells
2. Most ischemic injury in proximal tubules and thick ascending limbs of loop of Henle
3. Occlusion of tubular lumens with cells/casts
28
What are the primary sites of tubular injury in ATN? Why?
- 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_
29
What are the clinical clues for ATN?
- _Clinical clues_:
1. Muddy brown granular casts on urinalysis
2. Urine Na \>20
3. Fractional excretion of Na \>1%
30
What do you see here?
Muddy granular casts (suggestive of ATN, or other type of intra-renal AKI)
31
How does ATN happen?
- 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)
32
How do you manage ischemic ATN?
- Restore perfusion
- Avoid nephrotoxins
- Supportive care
33
What therapeutic agents may cause intra-renal AKI?
- _ATN_: aminoglycosides, amphotericin B
- _Acute interstitial nephritis_ (allergic rxn) caused by: penicillins, cephalosporins, sulfonamides, NSAIDS
34
Aminoglycoside toxicity
- 10-20% receiving drug will have rise in creatinine
- Accumulates in _proximal tubule cells_ (damages the tubules)
- Drug inhibits normal lysosomal function
- Toxicity associated with higher dose and longer duration of therapy
- ATN
35
How might you prevent aminoglycoside toxicity?
- Once daily dosing
1. Results in high urinary concentrations which exceed the reabsorptive capacity of the proximal tubule
- Careful monitoring of drug levels and minimizing duration of therapy
- Get them off of this drug, and only use it for the shortest duration
36
Contrast nephropathy
- _AKI_ caused by contrast agents (CT scans, heart catheterizations, other angiograms, etc.)
- Direct vasoconstrictive effects on arterioles and tubular toxicity
- _Risk Factors_: pre-existing renal disease, heart failure, hypovolemia, high dose of contrast, multiple closely spaced studies (this happens)
37
How might you prevent contrast nephropathy?
- Lower dose of contrast (least possible)
- Avoidance of closely spaced studies
- Avoid volume depletion by giving IV fluids (esp. in ER -\> before whisking off to CT scanner, get patient euvolemic)
- Avoid other nephrotoxins (NSAIDS, Ace I)
38
What is this? Describe the disease process.
- **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
39
How can you prevent AKI?
- Avoid nephrotoxins: sometimes we have to use these to save patient’s life
- Assure good renal perfusion before contrast studies and surgery
1. Hypovolemia could be due to: pancreatitis, burn victims, GI bleed, etc.
40
What is the supportive care for AKI?
- Avoid further injury
- Watch volume status and electrolytes carefully
- Dialysis in some cases
- Wait
