8-19 Acute Renal Failure DSA Flashcards by Stephen Schaffner

What are the essentials of Dx for acute kidney injury? (very general)

Sudden increase in BUN or creatine
Oliguria can be associated
Sx and signs depend on cause

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What is the RIFLE criteria?

describes 3 progressive levels of acute kidney injury

risk, injury, failure

Based on serum creatine or decline in urinary output

2 outcome measures: loss and ESRD

In other words, takes signs of acute kidney injury, quantifies magnitude of problem

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How are risk, injury, and failure defined with the RIFLE criteria?

risk = 1.5x increased serum creatine

injury = 2x increase in serum creatine

failure = 3x increase in serum creatine

or-
0. 5mL/kg/hr decline in urinary output over 6, 12, or 24 hours, respectively

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What is an additional criteria for quantifying damage/outcomes with acute kidney injury?

AKIN criteria, which is close to RIFLE

change in serum creatine > or = 0.3 mg/day

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What are the signs and symptoms you should look out for with AKI?

Nonspecific Sx, oft due to uremia

uremia causes:

nausea, vomiting, malaise, altered senses

Also look for HTN and altered fluid homeostasis

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You are examining a patient who is complaing of oliguria. If they have AKI, what might you hear when you ausculate their heart? Why?

pericardial friction rub

uremia can cause pericardial effusions, resulting in cardiac tamponade (yikes!)

Might also hear arrhythmias, d/t hyperkalemia

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Continuing with your evaluation of your patient with suspected AKI, what might you hear in their lungs?

rales in presence of hypervolemia

(Hypervolemia causes what kind of AKI? That’s right, post-renal)

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Your patient is pretty much a trainwreck with their acute kidney injury (AKI), and you’re suspecting acute kidney failure. What symptoms are associated with acute kidney failure?

Abdominal pain - nonspecific, diffuse

ileus dysfxn

platelet dysfxn

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What sort of hematological problems are associated with acute kidney failure?

platelet dysfxn

leads to bleeding and clotting disorders

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You want to ask your patient with acute kidney failure some questions regarding their stomach pain, but find their mental status altered. What neurological Sx are present? What do you do now?

asterixis - flapping tremor

confusion

seizures

Patient pretty out of it, better order labs at this point.

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Your patient is out of it, but lab work coming in is indicating acute kidney failure. What do you expect to see?

Elevated BUN, serum creatine

Hyperkalemia –> peaked T waves, PR prolonged, widened QRS on EKG

hypocalcemia –> long QT segment on EKG

Anion gap, or normal anion gap metabolic acidosis –> decreased acid clearance

Hyperphosphatemia

Anemia, platelet dysfxn

To sum: increased BUN, serum creatin, K+, PO4. Decreased Ca++, RBCs. Metabolic acidosis, platelets messed up.

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What would you expect with prerenal azotemia as far as:

etiology

serum BUN/Cr

Una

FEna (%)

Urine osmolality (mosm/kg)

urinary sediment

etiology - poor renal perfusion

serum BUN/Cr - >20:1

Una - <20

FEna (%) - <1

Urine osmolality (mosm/kg) - >500

urinary sediment - hyaline casts

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What would you expect for postrenal azotemia as far as:

etiology

serum BUN/Cr

Una

FEna (%)

Urine osmolality (mosm/kg)

urinary sediment

etiology - obstruction of urinary tracy

serum BUN/Cr - >20:1 (according to Lange)

Una - variable

FEna (%) - variable

Urine osmolality (mosm/kg) - <400

urinary sediment - normal or red cells, white cells or crystals

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What would you expect with acute tubular necrosis as far as:

etiology

serum BUN/Cr

Una

FEna (%)

Urine osmolality (mosm/kg)

urinary sediment

etiology - ischemia, nephrotoxins

serum BUN/Cr - <20:1

Una - >20

FEna (%) - >1 (when oliguric)

Urine osmolality (mosm/kg) - 250-300

urinary sediment - granular (muddy brown) casts, renal tubular casts

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What would you expect with acute glomerulonephritis as far as:

etiology

serum BUN/Cr

Una

FEna (%)

Urine osmolality (mosm/kg)

urinary sediment

etiology - immune complex mediated, pauci-immune, anti-GBM related

serum BUN/Cr - >20:1

Una - <20

FEna (%) - <1

Urine osmolality (mosm/kg) - variable

urinary sediment - red cells, dysmorphic red cells and red cell casts

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What would you expect with acute interstitial nephritis as far as:

etiology

serum BUN/Cr

Una

FEna (%)

Urine osmolality (mosm/kg)

urinary sediment

etiology - allergic rxn, drug rxn, infection, collagen vascular disease

serum BUN/Cr - <20:1

Una - variable

FEna (%) - less or greater than 1

Urine osmolality (mosm/kg) - variable

urinary sediment - white cells, white cell casts, with or without eosinophils

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What is prerenal azotemia caused by? How often is it the cause of AKI? Is damage permanent?

Caused by renal hypoperfusion

Cause of 40-80% of acute kidney injury/insult

Damage doesn’t occur if hypoperfusion is fixed quickly

Acute kidney injury with permanent damage happens if ischemia occurs

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What happens with renal medullary hypoxia leading to ischemia?

Hypoxia

Increased Na+ to macula densa

Increased renal arteriolar vasoconstriction

Ischemia-induced rearrangement of cytoskeleton in renal tubule cells

Loss of polarity, integrins, adhesion in renal tubular cells

tubule cells slough off

Tubules are filled with crap and obstructed

Tubule damage

acute renal failure

add complicating factors too: NSAIDs, myoglobin ppt, BJ proteins, hypovolemia, sepsis

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What are some things that can cause renal hypoperfusion?

Things that cause volume depletion:

hemorrhage

GI losses

dehydration

excessive diuresis

extravascular space sequestration

pancreatitis

burns

trauma

peritonitis

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What medications can affect renal perfusion and GFR?

(RAS blockers)

ACE inhibitors - efferent arteriolar constriction, decreased GFR

NSAIDs - reduce afferent arteriolar vasodilation, really bad with cirrhosis and HF

Epinephrine

norepinephrine

high dose dopamine

anesthetic agents

cyclosporine

Also, renal aa stenosis

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Why is FEna helpful in diagnosing acute kidney injury?

Decreased GFR = kidney absorbs more Na+ and water if tubules intact

So, prerenal causes will have low excreted Na+ or low FEna

Oligura + intrinsic kidney dysfxn will excrete more Na+, or high FEna

Accuracy may vary if measured during active half life of diuretics

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What causes post-renal acute kidney injury? Why are they important to detect?

urinary flow from 1 or both kidneys obstructed

single is problematic if other kidney can’t compensate - ie CKD

Important to find because they are reversible

What general pathologies does postrenal azotemia cause?

increased intraluminal pressure –> kidney parenchymal damage

Effects on RBF and tubular fxn

decreased GFR

What are some causes of obstruction in postrenal AKI?

Structural causes:

BPH (most common in men)urethral obstruction, bladder dysfxn or obstruction, obstruction of ureters or renal pelvises

bladder, prostate or cervical cancer

Other:

retroperitoneal fibrosis

neurogenic bladder

blood clots

b/l ureteral stones

urethral strictures

b/l papillary necrosis

With postrenal AKI, what are some common symptoms?

anuric or polyuria lower abdominal pain Might be able to palpate structural problem - enlarged prostate

How does labwork change over time with postrenal AKI?

Indices can look like prerenal problem at first, but ability to concentrate urine goes away as tubules get damaged, so urine sodium increases sediment is usually benign

What are the possible sites of injury with intrinsic AKI? What percentage of AKI does this type cause?

Responsible for up to 50% of AKI Sites include: tubules interstitium vasculature glomeruli

What are the essentials for Dx'ing acute tubular necrosis?

AKI Ischemia, or toxic insult Urine sediment with pigmented granular casts and renal tubular epithelials

What are the 2 major causes for acute tubular necrosis?

Ischemia Nephrotoxin exposure

Ischemia-mediated acute tubular necrosis is characterized by what?

inadequate GFR RBF inadequate to maintain parencymal cellular perfusion

What type of AKI is acute tubular necrosis often associated with? What kind of medical intervention?

Oft assoc with prerenal AKI Can happen as a result of surgery, oft exacerbated by surgery-mediated hypoperfusion and anaesthetic-mediated vasodilation

What are some major exogenous nephrotoxins?

Radiographic contrast media Cyclosporine Aminoglycosides - can remain in kidney tissue for a month streptomycin is least nephrotoxic Amphotericin B \>2-3g Vancomycin intravenous acyclovir cephalosporins

What are some endogenous nephrotoxins?

heme containing products uric acid paraproteins - cancer proteins in blood

What is myoglobinuria?

Consequence of rhabdomyolysis --\> leads to acute tubular necrosis myoglobin released by necrotic mm myoglobin filtered across glomerulus, absorbed by tubule cells, then is toxic to tubule cells

What can cause myoglobinuria?

crush injury mm necrosis d/t: prolonged unconsciousness seizures cocaine EtOH abuse

In a patient with myoglobinuria, what will a urine dipstick test reveal?

result will show hemoglobin due to globin part of myoglobin (false positive) urine is dark brown with no RBCs

What other lab markers on a metabolic panel will be off with a patient with myoglobinuria?

hyperkalemic hyperphosphatemic hyperuricemic Hypocalcemia

What can cause hemoglobin in the urine?

massive intravascular hemolysis - ie transfusion rxn, hemolytic anemia

What can cause hyperuricemia?

rapid cell turnover and lysis - chemotherapy for germ cell neoplasms, leukemia, lymphoma AKI occurs with uric acid crystal deposition in tubules

If a patient is showing acute tubular necrosis due to endogenous nephrotoxins and is not being treated for cancer at the moment, what should you be suspicious for?

Multiple Myeloma - puts off Bence-Jones proteins, causing tubular obstruction and toxicity - also see hypercalcemia and RTA II (proximal)

What are the stages of acute tubular necrosis?

1. Initial Injury 2. Maintenance 3. Recovery

What are the essentials of diagnosis for interstitial nephritis?

Fever transient maculopapular rash acute or chronic kidney injury pyuria (including eosinophiluria), WBC casts, & hematuria

Acute interstitial nephritis can occur due to what?

Drugs - most common infectious disease immunological disorders idiopathic condition

What drugs most commonly cause acute interstitial nephritis?

PCN cephalosporins sulfonamides sulfonamide-containing diuretics NSAIDs rifampin phenytoin allopurinol proton pump inhibitors

What are the clinical features associated with interstitial nephritis?

fever rash arthralgias peripheral blood eosinophilia

What urine findings are associated with interstitial nephritis?

urine contains: WBCs RBCs WBC casts modest proteinuria

What are the essentials to dx'ing glomerulonephritis?

Hematuria dysmorphic red cells RBC casts mild proteinuria dependent edema and HTN AKI

How common is acute glomerulonephritis as a cause of AKI?

Not very common - ~5%

Pathologically, what is generally seen with glomerulonephritis?

Inflammatory glomerular lesions - mesangioproliferative focal and diffuse proliferative crescentic lesions larger % of glomeruli involved, the worse the outcome

How do you categorize acute glomerulonephritis?

Serologic analysis - anti-GBM Ab - ANCAs - other immune markers of disease

When causes immune complex deposition to occur?

IgA nephropathy - Berger's disease peri-infectious or post-infectious glomerulonephritis endocarditis lupus nephritis cryoglobulinemic glomerulonephritis MPGN

In addition to immune complex deposition, what other entities can cause glomerulonephritis?

Anti-GBM-associated acute glomerulonephritis/Goodpasture's Pauci-immune acute glomerulonephritis Other vascular causes - acute HTN emergencies, thrombotic microangiopathies, HUS, TTP

What are the signs and symptoms of glomerulonephritis?

HTN edema - periorbital and scrotal regions abnormal urinary sediment

What laboratory findings are associated with glomerulonephritis?

Dipstick and microscope: hematuria, moderate proteinuria, RBCs, red cell casts, WBCs FEna usually low low complement with some ASO titers Anti-GBM Ab titers ANCAs Antinuclear Ab titers cryoglobins hepatitis serology blood cultures