Acute Renal Failure Flashcards
Synonyms for acute renal failure
Acute renal insufficiency
Acute kidney injury
What are common causes of hospital acquired AKI?
Decreased renal perfusion
Meds
Radiographic contrast agents
Post-op
Sepsis
** Higher increase in S creat = more severe dz
How do we define AKI? Stages I, II, III
AKI Stage I: increase of serum creat by >/= 0.3 mg/dl
or increase to >/= 150-200% from bsln
- also urine output <0.5 ml/kg/hr for >6 hours
AKI Stage II: increase of serum to >/= 200-300% from bsln
- also urine output <0.5 ml/kg/hr for >12 hours
AKI Stage III: increase of serum creat to >300% from bsln
or >/= 4.0 mg/dl after a rise of at least 44 umol/L
or treatment with renal replacement therapy
- also urine output <0.3 ml/kg/hr for >24 hours or anuria for 12 hrs
Normal creatinine
0.6-1.2
Why is creatinine the best measure of renal function?
As GFR goes down, level of substances normally not in the blood go up: so if BUN and serum creat are elevated in blood test, you know they have kidney injury
Creatinine is slightly better marker than BUN
What are the 3 major patterns of acute kidney injury?
Post-renal azotemia (obstruction)
Pre-renal azotemia (perfusion problem)
Intrinsic renal failure (ATN = acute tubular necrosis, most common)
- also AIN: acute interstitial nephritis, AGN: acute glomerular nephritis, vascular dz
Post-renal Azotemia
ARF caused by obstruction to the outflow of urine
Can occur at any level from the urethra to pelvis of the kidneys
Common causes: prostatic enlargement (benign hypertrophy, cancer), gynecologic malignancies, kidney stones
Anuria (100cc/day) suggests obstruction
You must exclude obstruction in every case of ARF!!!
How can radiological tests help you distinguish what the underlying cause for post-renal azotemia?
i.e. ultrasonogram bc no contrast required. normal kidney = white in cortex, dark in medulla
If it’s urinary obstruction, you’ll get hydronephrosis & the collecting system expands: giant dilated collection system, so it looks dark in the middle!
If it’s a kidney stone, you’ll see a white kidney stone in the ultrasonogram
Also note that unilateral obstruction does not cause progressive severe ARF: if it’s progressive, where the creat goes up every day, then you have bilateral obstruction
What is pre-renal azotemia?
An oliguric condition associated with decreased GFR and retention of nitrogenous wastes caused by decreased perfusion of the kidney
Volume depletion
Volume overload
It’s potentially rapidly reversible
Decreased renal perfusion –> increased proximal Na reabsorption (AngII) & distal Na reabsorption (aldo)
What are the urinary findings in pre-renal azotemia?
Low urinary Na+ conc and low FeNa
Large increase in BUN, high BUN/Pcreat
Increased urine osmolality >400 mOsm/L & urinary specific gravity
What is acute tubular necrosis?
Most common pattern of intrinsic ARF
Physiologic Syndrome not morphologic: sometimes you get very little damage morphologically
Can be due to ischemic injury (longer and more severe insult than in prerenal azitemia) or nephrotoxins
Classic oliguric and diuretic phases
Nonoliguric ATN
ATN casts= bloody brown things, patients with ATN have a lot of these
What are the urinary findings in acute tubular necrosis
High urinary Na+ conc and high FeNa
Unchanged BUN/plasma creat ratio in blood
Fixed urine osmolality
What are the mechanisms of ATN?
Ischemic damage
Nephrotoxic damage
More than one mechanism may be involved in each model of ARF
Causes reduced RBF, modifying hormones & ultimately leads to: vasoconstriction, back leak, tubular obstruction, decreased glomerular permeability
Why is GFR reduced in ATN?
Vasoconstriction
Back leak of tubular fluid
Intratubular obstruction
Altered Glomerular permeability
What is the role of renin-angiotensin system in ARF?
JGA hyperplasia
Increased plasma renin & AII levels in ARF
Experiments with blockers of Renin-AII system
Tubulo-glomerular feed back theory
