Term
What do each of the following terms mean?
1) Acute Kidney Injury
2) Azotemia
3) Uremia
4) Oliguria
5) Anuria |
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Definition
1) Loss of renal function, assessed by GFR, over hours to days, with azotemia
2) Retention of nitrogenous waste (urea/BUN and creatinine) waste in BLOOD
3) Symptomatic renal failure (anorexia, vomiting, CNS and pericarditis can all be seen).
4) Low urine volume (24h < 400-500 mL)
5) NO urine (24h < 100 mL) |
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Term
| Why might you see elevated BUN with a normal GFR? |
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Definition
Not all nitrogenous waste elevation in the blood means AKI.
1) Protein loading
2) GI bleed (endogenous protein load)
3) Catabolic steroids like glucocorticoids (protein catabolism)
4) Tetracycline antibiotics (inhibit protein synthesis). |
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Term
| Why might you see elevated creatinine with a normal GFR? |
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Definition
Not all creatinine increases mean AKI.
1) Cemetidine and TMX decrease tubular secretion
2) Some medications interfere with the colorimetric assay |
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Term
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Definition
Based off serum creatinine and urine output
Need either
1) Serum creatinine >0.3 mg/dL for 48h
2) increase in serum creatinine by >50% within 7d
3) urine volume <0.5 mL/kg per hour for 6h
Increase in serum creatinine Urine Output
1: >0.3 mg/dL or 1.5-2X baseline <0.5 mL/kg (6-12h)
2: 2-3X baseline <0.5 mL/kg (>12h)
3: >3X baseline or >4.0 <0.3 mL/kg (>24h)
Anuria (>12h) |
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Term
| How does acute kidney injury (AKI) differ from acute kidney disease (AKD)? |
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Definition
1) AKI is defined by changes in kidney function for 7 days
2) AKD includes either
- GFR<60 ml/min for <3 months OR
- Decrease in GFR >35% or increase in serum creatinine by 50% over <3 months.
After that it is chronic kidney disease! |
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Term
| Why you see an elevation in serum plasma urea:creatinine ratio with hypotonic urine, but with NO histological changes to the kidney? |
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Definition
Prerenal Acute Kidney Injury (Azotemia) from a) True volume depletion, 2) Decreased EABV or 3) states of renal vasoconstriction.
1) Decreased renal perfusion leads to RAAS and PGE signaling, efferent arteriolar constriction and reduced RPF/maintained GFR/increased FF
**If perfusion deficit is too severe, GFR WILL drop
2) Increased sodium and urea reabsorption due to RAAS leads to dilute urine and elevated serum urea, relative to creatinine.
**Since this is Pre-renal, there are no changes to the actual kidney (at least at first)** |
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Term
| What states of decreased effective blood volume can produce Prerenal azotemia? |
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Definition
All will lead to activation of RAAS and lead to Na+/Urea reabsorption in the tubules.
1) CHF (low CO)
2) Cirrhosis
3) Nephrotic syndrome (hypoalbuminuria)
4) Sepsis |
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Term
| What clinical contexts might cause a state of renal vasoconstriction that produces pre-renal azotemia? |
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Definition
1) Hypercalcemia
2) NSAID (inhibit PGE response to Ang2 in afferent arteriole) decreasing RPF
3) Hepatorenal syndrome
- Looks like prerenal azotemia, but issue is with liver and patient needs transplant despite healthy kidney. |
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Term
Patient presents with recent history of diarrhea and vomiting.
On PE, their BP is 90/50, they have dry mucus membranes and skin turgor.
BUN:creatinine is 20:1, they are producing 500 mL/24h of concentrated urine and the Fractional Excretion of sodium is <0.01.
How do you treat this condition? |
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Definition
Prerenal Azotemia
Diarrhea and vomiting suggest real volume depletion.
Hypotension and dry membranes confirms this. Labs indicate increased urea reabsorption (BUN:creatinine) and FEna is consistent with Prerenal azotemia (rather than ATN)
1) Correct volume deficit with crystalloid solution
2) STOP diuretics, NSAIDS (PGE effect), ACE-i and ARBs
3) If cardiac disease, use Inotropes to supplement. |
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Term
| What is the Fractional excretion of sodium and how is it useful to distinguish between causes of AKI? |
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Definition
1) FEna= Sodium clearance/ Creatinine clearance
= [(U * Una)/Pna]/ [(U* Ucr)/Pcr]
Prerenal azotemia is <0.1
ATN is >0.2 |
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Term
A patient presents with fluctuating periods of polyuria and oliguria, but normal serum creatinine. There is also hydronephoris (dilation of renal collecting system)
What is the natural history of this disease? |
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Definition
Partial bilateral obstructive uropathy (Postrenal AKI)
**If it was complete, you would see anuria **
1) Obstruction initially increases pressure in bowman's space, relative to glomerular capillaries, decreasing GFR and Increasing RPF (decreased FF)
2) Rapid decline in RPF follow with further decrease in GFR
3) Later, intratubular pressure will return to normal, but RPF and GFR remain decreased. |
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Term
A patient presents complaining of increased urinary frequency, urgency and incomplete voiding.
She says she has been having some flank pain and has seen some blood in her urine as well.
On PE, you discover a distended, palpable suprapubic mass and some adenopathy.
Labs reveals BUN:creatinine of 21:1 and there are some RBC casts in the urine.
How do you treat? |
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Definition
H/X is consistent with bladder outlet obstruction (post-renal AKI)
The distended suprapubic mass is probably the bladder and her labs confirm hematuria and azotemia.
Treatment is mechanical relief (do it 1-2 weeks to prevent CKI)
**Look out for post-obstructive diuresis!** |
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Term
| How can you diagnose lower tract obstruction in post-renal AKI? |
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Definition
| Post-void residual bladder volume > 100mL will suggest voiding dysfuction and lower tract obsruction (bladder outlet or urethra rather than ureter or renal pelvis) |
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Term
| What are the 5 major categories of Intrinsic Acute Kidney Injury? |
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Definition
Classified by pathologic compartment!
1) Acute tubular necrosis (ATN)- 85% of the time!!
2) Acute interstitial nephritis (AIN)
3) Acute glomerulonephritis (AGN)
4) Acute vascular syndrome
5) Intratubular obstruction. |
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Term
What are the major etiologies of acute tubular necrosis?
What is the pathophysiological basis? |
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Definition
1) Most common intrinsic AKI!
- Ischemic, Nephrotoxic, or possibly septic
2) Loss of tubular epithelial cell morphology and polarity
- Membrane transport proteins migrate to incorrect membranes, disrupting tubular transport
- Necrosis/Apoptosis and cell sloughing can obstruct tubule and damage BM
- Renal vasoconstriction, Tubular obstruction and Back-leak across denuded BM lead to LOSS of GFR
- Endothelial injury/Inflammation also occurs but RENAL FUNCTION ULTIMATELY RETURNS |
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Term
| What are the 4 phases of ischemic acute tubular necrosis? |
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Definition
1) Initiation (acute ischemic event)
2) Extension (Ischemia ends, but endothelial injury, vasoconstriction and inflammation lead to continue injury)
3) Maintenance (resolution of endothelial injury and initiation of tubular repair, but continued inflammation)
4) Recovery (proliferation and re-differentiation of epithelium and recovery of GFR). |
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Term
Patient presents with a h/x of NSAID use and previous episodes of hypotension.
Labs reveals BUN:Creatinine of 8:1, Isosthenuric urine, and FEna> 0.02. You also see Una is >40 mmol/L
There are "muddy brown" casts in the urine as well as tubular epithelial cells and epithelial casts.
How do you treat? |
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Definition
H/X suggests possibly nephrotoxicity. BUN:creatinine suggests some azotemia, but not to the degree that would be expected in prerenal or postrenal AKI (>20).
FEna suggests some sodium wasting, as opposed to prerenal AKI (<0.01) and granular casts with tubular epithelial cells are classic for Acute Tubular Necrosis.
Isosthenuric urine means it is not concentrated or dilute, which also fits ATN.
No pharmacological treatment is available, but you can perform Acute Dialysis to support patients with severe renal injury.
Prognosis depends upon severity of renal failure (oliguric is worse than non-oliguric), but most get better in 2-4 weeks (not perfect, though). |
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Term
Patient presents with Fever, Rash and Eosinophilia. She has just started taking a Furosemide for a UTI.
Her UA shows non-nephrotic proteinuria, hematuria and pyuria, with WBC casts and eosinophils.
What would you find on pathology and how do you treat? |
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Definition
Fever, Rash and Eosinophelia is classic triad for Acute Interstitial Nephritis and her history of recent drug use fits classic drug-induced form.
Labs are also consistent with AIN and pathology would find lymphocytic infiltrate in the kidney interstitium with eosinophils (this is an immune reaction, Type IV hypersensitivity)
REMOVE the drug |
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Term
| A patient's UA shows RBC casts and hematuria. Why order a kidney biopsy? |
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Definition
RBC casts and hematuria are "Nephritic Urine sediment" which suggests acute glomerulonephritis.
Biopsy is required to distinguish between
1) Post-strep
2) Post-infectious
3) Endocarditis-associated
4) Systemic vasculitis
5) Thrombotic microangiopathy (HUS or TTP)
6) Rapidly-progressing GN. |
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Term
On a renal biopsy, you see biconcave, needle-shaped clefts in the arcuate artery.
What happened? |
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Definition
Atheroembolic disease resulting in AKI (RARE)
1) Cholesterol cleft embolism from the aorta to the kidney
**Might also see micro-infarcts of the digits (blue-toe syndrome)** |
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Term
| What are the common causes of Intratubular Obstruction? |
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Definition
RARE in itself.
1) Uric acid in tumor lysis syndrome
2) Calcium oxylate in ethylene glycol ingestion.
3) Drug crystals (acyclovir)
4) Proteinacious material in light chain cast nephropathy in multiple myeloma. |
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Term
What kinds of Urine sediment do you see in each of the following forms of AKI?
1) Prerenal
2) Post-renal
3) ATN
4) AIN
5) AGN
6) Vascular
7) Intralobular obstruction |
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Definition
1) Normal
2) Normal or RBC's
3) Muddy brown "granular casts" with tubular epithelium
4) WBC's; RBC's; Eosinophils
5) RBC's; RBC casts (nephritic sediment)
6) Eosinophils if atheroembolic
7) Crystals of immunoglobulin light chains (Bence-Jones Proteins) in urine. |
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Term
What is the BUN:Cr range in each of the following?
1) Prerenal
2) Post-renal
3) ATN
4) AIN |
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Definition
<20 means you are dealing with instrinsic disease and <10 means it is AIN.
**If >20, and Una >20 it is postrenal (sodium wasting), otherwise it is prerenal (sodium retention)
1) >20:1
2) >20:1
3) <10:1
4) <20:1 |
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Term
What FEna do you see in each of the following forms of AKI?
1) Prerenal
2) Post-renal
3) ATN
4) AIN
5) AGN |
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Definition
1) <0.01 because of sodium retention
2) Variable
3) >2% (wasting)
4) >1%
5) <1% |
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Term
What syndrome is characterized by each of the following (BUN:Cr, Una, FEna, urine sediment)
1) >20:1, >20, variable, normal
2) <10:1, >40, >2%, muddy brown "granular"
3) <20:1, >20, >1%, WBC/RBC casts and Eosinophils
4) >20:1, <20, <0.01, normal |
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Definition
1) Postrenal obstructive AKI
2) Acute Tubular Necrosis
3) Acute interstitial nephritis
4) Prerenal AKI |
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Term
How do you manage each of the following AKIs?
1) Prerenal azotemia
2) Obstructive uropathy
3) Intrinsic AKI |
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Definition
1) Volume repletion and stop diuretics, NSAID/ACEI/ARB and give inotropes for cardiac support as needed
2) Bladder cath for lower tract and Percutaneous nephrostomies or ureteral stents for upper tract
3) Supportive with fluid management, diuretcs
Replace kidney IFF
- Volume overload is unresponsive to diuretic
- Metabolic acidosis unresponsive to bicarbonate
- Persistent Hyperkalemia
- Pericarditis and encephalopathy
- Severe azotemia (BUN> 80-100 mg/dL) in absence of uremic symptoms. |
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