Acute Kidney Injury

Question 1

AKI and Critical Illness Sepsis

1. How common is it?
2. What is it often part of?
3. What do 5% require?

Answer 1

1. 5-20% of critically ill patients; sepsis pts
2. Multi-System Organ Dysfunction Syndrome
   3.

Question 2

Acute Kidney Injury Causes

1. Prerenal
2. Intrinsic Renal
3. Postrenal

Answer 2

1. Absolute drop in blood volume, relative drop in blood volume (ECV), renal artery stenosis of occlusion, NSAID/ACE-I/ARB mechanism
2. Vascular, Acute Glomerular Disease, AIN, ATN
3. Bladder outlet obstruction, bilateral ureteral obstruction, unilateraly ureteral obstruction (solitary kidney)

Question 3

Common Causes of AKI

1. Prerenal Azotemia and Ischemic ATN accounts for what % of AKI cases?
2. Are these two totally different diseases?
3. Define Prerenal Azotemia
4. What can it complicate?
5. How can pre-renal Azotemia be corrected?
6. What can it progress to?

Answer 3

1. 75%
2. continuum of the same pathologic process
3. appropriate physiological response to renal hypoperfusion
4. true hypovolemia or low effective circulating volume (ECV)
5. by reversing the cause;
6. ischemic ATN

Question 4

Normal Renal Autoregulation

1. What is the overall goal?
2. What 2 things does a drop in BP or ECV lead to? What mediates each?
3. What antagonizes each?

Answer 4

1. to keep GFR constant
2. Vasodilatation of preglomerular arterioles via Prostaglandin I2, NO
3. Vasoconstriciton of postglomerular arterioles via Angiotensin II
4. COX I/II (NSAIDS) inhibit pre-glomerular vasodilatation
5. ACE-Is/ARBs inhibit post-glomerular vasoconstriction

Question 5

Post-renal Failure

1. Risk Factors (3)
2. What needs to occur to improve/recover renal function?
3. Post-intervention sequelae?
4. How is it diagnosed?

Answer 5

1. Older men w/prostate disease, solitary kidney, intra-abdominal (pelvic) cancer
2. prompt ID and intervention
3. post obstructive diuresis (>4L/day); hyperkalemic, hyperchloremic Renal Tubular Acidosis (can be chronic)
4. Phyiscal Exam, renal ultrasounds, measurement of post void residual volume (beside bladder scan or urinary catheterization)

Question 6

What are the four categories of Intrinsic Renal Failure?

Answer 6

1. Vascular (malignant HTN, other)
2. Acute Glomerular Disease
3. Acute interstitial necrosis
4. Acute tubular necrosis

Question 7

Causes of Acute Tubular Necrosis (ATN)

1. most common
2. second most common
3. other causes

Answer 7

1. sepsis
2. surgery
3. Nephrotoxic exposures: anti-microbial agents, anti-neoplastic agents, recreational drugs, tubular hemoglobinuria (massive hemolysis), tubular myoglobinuria (rhabdomyolysis), tubular proteins (myeloma), tubular crystals (urate, oxalate)

Question 8

ATN

1. Risk Factors
2. Pathogenesis

Answer 8

1. Advanced age, pre-existing chronic kidney disease, HTN, cardiac disease, liver disease, peripheral vascular disease, DM
2. Injury to vascular/tubular components; then Repair:
   death/exfoliation of proximal tubular cells (–>epithelial cell casts)
   Appearance of poorly differentiated epithelial cells
   Proliferation of surviving proximal tubular cells
   Normal differentiation of tubular cells

Question 9

Classic Clinical Features of ATN

1. What happens to urine?
2. 2 phases

Answer 9

1. Dirty or Muddy brown urine
2. Oliguric phase: HTN, volume overload, hyperkalemia, acidosis
3. Polyuric phase: volume depletion, hypotension, hypernatremia,

Question 10

Vascular Causes of AKI (5)

Answer 10

1. Vasculitits
2. Thromboembolic disease
3. HUS/TTP
4. Malignant HTN
5. Scleroderma renal crisis

Question 11

Malignant HTN

1. Causes what?
2. BP?
3. What can happen?

Answer 11

1. AKI
2. > =180/120
3. impending/progressive organ dysfunction: HTN encephalopathy
   Intracerebral hemorrhage
   ACS (acute MI, unstable angina)
   Acute LV dysfunction w/ pulmonary edema (new S4, rales)
   Dissecting aortic aneurysm
   Eclampsia

Question 12

Acute Glomerular Disease

1. Causes
2. When is it commonly seen?

Answer 12

1. neoplastic disorders, infections, autoimmunity, drugs, genetic abnormalities, idiopathic
2. uncommon acutely, more commonly seen in subacute and chronic kidney disease

Question 13

Glomerular Diseases: Nephritic pattern

1. Histo
2. Urinary sediment
3. Proteinuria

Answer 13

1. inflammatory changes
2. active sediment (cells/casts)
3. variable

Question 14

Glomerular Diseases: Nephrotic pattern

1. Histo
2. Urinary sediment
3. Proteinuria

Answer 14

1. cooler findings, far less inflammation
2. inactive urine sediment
3. severe proteinuria

Question 15

Acute Interstitial Nephritis

1. Most common cause?
2. Classic triad
3. What helps make the diagnosis?

Answer 15

1. medications (70%)- PPIs, NSAIDs, antimicrobials (PCNs, cephalosporins); also due to Autoimmune disorders (SLE), infections
2. fever, peripheral eosinophilia, rash; all 3 only seen 10% of time; usually at least 1 present
3. may help make diagnosis, PPV and NPV are low though

Question 16

AKI Workup: What questions are important in the history?

Answer 16

antecedent illness/trauma?
changes in oral intake?
vomiting and/or diarrhea?
suspicion on insensible water loss (high fevers, rapid breathing, excess sweating)?
New medications/dosage changes?
Recent medical procedures/IV dye use?
Rash, joint pain, pulmonary symptoms?

Question 17

AKI Workup: What needs to be looked for in a chart review?

Answer 17

weight trends
intake/output trends
BP trends
O2 sat trends
Operative/anesthesia notes (labile BP/HR/O2 during case, estimated blood loss, urine output, IV fluids given)

Question 18

AKI Workup: Physical Exam

1. Too wet? signs
2. Too dry? signs
3. urine color
4. Assessment for urinary retention
5. Signs of vasculitic process

Answer 18

1. abdominojugular reflux, S3 gallop, ascites, peripheral edema and rales are TOUGH to interpret
2. dry mucuous membranes, skin tenting (only useful if positive in adults), neck veins flat at 0 degrees, signs of shock (orthostatic or frank
   hypotension)
3. bloody, dirty/muddy, dark yellow/concentrated
4. fullness/dullness on suprapubic exam, enlarged prostate on digital rectal exam
5. characteristic rash, synovitis, pulmonary findings

Question 19

AKI Workup: Lab Review

1. 3 important tests
2. Others

Answer 19

1. Renal indices (BUN/Creatinine)
2. Urinalysis (critically important)
3. Urine indices(electrolytes/creatinine)
4. infectious labs (CBC, cultures, serologies), complement levels, autoimmune serologies, urine eosinphils

Question 20

AKI Workup: Imaging Review

1. What is most helpful?
2. What else can be done? Why?

Answer 20

1. renal ultrasound

2. CXR, CT, MRI: evidence of infection, volume overloaded state, postrenal obstruction

Question 21

Pre-renal Azotemia

1. Urinalysis
2. Urine Specific Gravity
3. Urine Osmolality
4. Urine Sodium
5. Fractional Excretion of Na
6. Fractional Excretion of Urea

Answer 21

1. Hyaline casts
2. 1.020
3. > 500
4. <35%

Question 22

Acute Tubular Necrosis

1. Urinalysis
2. Urine Specific Gravity
3. Urine Osmolality
4. Urine Sodium
5. Fractional Excretion of Na
6. Fractional Excretion of Urea

Answer 22

1. 1.010
2. > 300
3. > 40
4. > 2%
5. > 35%

Question 23

Why is Creatinine a poor indication of function in AKI?

Answer 23

1. AKI is not a steady state condition
2. Depends on clearance rate, rate of production, volume of distribution, all of which change in AKI
3. Bottom line: poor estimate of GFR

Question 24

1. Causes of High (>10:1) BUN:Creatinine Ratios
2. Causes of Normal (10:1) BUN:Creatinine Ratios
3. Causes of Low (<10:1) BUN:Creatinine Ratios

Answer 24

1. Prerenal Azotemia, Decreased Urea load, Obstructive uropathy, ureteroenterostomy, decreased muscle mass
2. Normal, CKD, ATN
3. Decreased urea load,inhibition of creatinine secretion, increased creatinine load, interference with creatinine measurement, increased muscle mass

Question 25

BUN: Creatinine Ratio >10:1 1. What causes Prerenal Azotemia? 2. What causes an increased urea load? 3. Other cause? 4. Why does decreased muscule mass cause it? 5. Which causes lead to increased urea?

Answer 25

1. true hypovolemia or decreased ECV 2. GI bleeding (protein load, inc urea abs), glucocorticoids (lead to catabolic state), tetracycline, hypercatabolic states, high protein diet 3. Ureteroenterostomy 4. drops creatinine due to muscular atrophy 5. Prerenal azotemia, increased urea load, ureteroenterostomy

Question 26

BUN: Creatinine Ratio

Answer 26

1. low protein diet, liver failure 2. cimetidine, probenecid, trimethoprim (common) 3. ingesting cooked meat, rhabdomyolysis 4. ketosis, isopropyl alcohol ingestion (metabolized to acetone), cefoxitin, flucytosine 5. anabolic steroids, muscular development

Question 27

AKI Management: 3 things

Answer 27

1. search for and correct cause of prerenal azotemia or postrenal obstruction (improve ECV when possible) 2. stop/avoid nephrotoxic agents 3. adjust dosages of medications in relation to renal clearance 4. Watch intake/output, daily weight, volume status closely 5. Manage complications (electrolyte derangement-high K, low Na, high Phos, metabolic acidosis, pulmonary edema) 6. Nutritional support (ensure adequate carb (prevents protein breakdown) and protein (not too much) 7. Aggressively manage infections (skin care, catheter care) 8. Hemodialysis when needed

Question 28

Hemodialysis in AKI 1. When should it be done? 2. Indications (there's a mnemonic)

Answer 28

1. controversial, too early better than too late 2. AEIOU: Acidosis (severe/refractory) 3. Electrolyte derangement (usually severe hyperkalmemia) 4. Intoxication syndrome (severe, dialyzable cause) 5. Overload (significant pulm edema) 6. Uremia (significantly symptomatic)

Question 29

AKI Prognosis 1. What happens to most pts? 2. What happens 5-16% of time? 3. What can be seen following AKI? 4. When is mortality highest?

Answer 29

1. most recover, complete recovery not always the cacse 2. progresses to irreversible condition 3. progressive chronic kidney disease 4. if they require RRT +/- Multi System Organ Dysfunction; mortality >= 50%

Question 30

Prevention of AKI 1. What needs to be promoted? 2. What should be avoided? 3. What should be given with IV contrast? 4. What is Tumor Lysis Syndrome? 5. How should it be managed?

Answer 30

1. adequate volume status, cardiac output 2. nephrotoxic agents in at risk pts (ex use NSAIDs, ACE-Is, ARBs cautiously) 3. prophylactic care: saline infusion, bicarbonate infusion, N-acetylcysteine (antioxidant) 4. large lymphoid or solid tumor burden; death of tumor cells delivers large uric acid load to kidneys 5. prevention with allopurino, rasburicase, alkaline diuresis (reduces likelihood of urate cystal formation)