Acute renal failure 12/13 Flashcards
The hallmark of acute renal failure?
Azotemia (increased BUN and creatinine) often with oliguria/anuria.
Increased BUN indicates ………
Acute renal failure.
Acute renal failure is divided in 3 azotemias, which are based on etiology. Name them.
Prerenal, postrenal and intrarenal azotemia.
Decreased Renal Blood Flow leads to ….
hypoperfusion-> Prerenal azotemia.
Prerenal azotemia mechanism?
Decreased RBF (e.g. hypotension due to HF) –> decreased GFR . Body conserve volume –> oliguria. Increased BUN/creatinine ration because urea is absorbed, but creatinine not.
RESULT: Decr. GFR, azotemia, oliguria
BUN:Cr ratio in acute renal failure?
> 15.
Increased BUN/creatinine ratio because urea and fluids are absorbed, but creatinine not.
What causes prerenal azotemia?
Decreased renal blood flow.
What about tubular function in prerenal?
Intact. (fractional excretion of sodium (FENa) <1 proc.,
UNa< 20 mEq/, and urine osmolality (osm) > 500 mOsm/kg.
Why there is acute tubular necrosis?
Due to ischemia or toxins –> injury and necrosis of tubular cells.
Mechanism of intrarenal azotemia?
Tubular cell injury and necrosis –> necrotic cells plug tubules –> obstruction –> decreased GFR
What causes intrarenal azotemia (ischemic and toxic)?
Ischemic - dereased blood flow –> necrosis of tubules.
Severe hemorrhage, severe renal vasoconstriction, hypotension, dehydration, shock.
Nephrotoxic –> toxic agents result in necrosis of tubules.
Ethylene glycol (assoc with oxalate crystals in urine),
myoglobinuria (due to crush injury to muscle),
radiograph contrast,
drugs (sulfonamides, methicilin, aminoglyciosides - most common),
heavy metals (eg lead),
organic solvents (methyl alcohol, chloroform, carbon tetrachloride).
urate (due to tumor lysis syndrome)
Which part of kidney is the most susceptible for ISCHEMIC injury?
PCT and ascending thick part of Henle in medulla.
Which part of kidney is the most susceptible for toxic injury?
PCT
What ATN is preceded by prerenal failure?
Ischemic
What is the most common cause of ARF?
Acute tubular necrosis (intrarenal azothemia)
ATN. What casts?
brown, granular casts in the urine.
What is used prior chemotherapy to prevent ATN?
Hydration and allopurinol –> decrease risk of urate-induced ATN.
ATN clinical features?
Oliguria with brown, granular casts
Decreased BUN and Cr
hyperkalemia (due to decr. renal excretion) with metabolic acidosis
ATN is reversible, sometimes need dialisis due to electrolyte imbalances that may be fatal.
.
How long can persist oliguria prior recovery? ATN
2-3 weeks. tubular cells (stable cells) take time to reenter the cell cycle and regenerate.
ATN. Dysfunctional epitelium results in decreased ….
decr. reabsorbtion of BUN (serum BUN:Cr ration <15), decreased reabs. of Na (FENa > 2 proc.) and inability to concentrate urine (urine osm < 500 mOsm/kg).
decr. reabsorbtion of BUN (serum BUN:Cr ration <15), decreased reabs. of Na (FENa > 2 proc.) and inability to concentrate urine (urine osm < 500 mOsm/kg).?
ATN
Intact. (fractional excretion of sodium (FENa) <1 proc., and urine osmolality (osm) > 500 mOsm/kg.?
Prerenal
Postrenal, decrease outflow results in 3
decr. GRG, azotemia, oliguria
Postrenal. due to?
obstruction of urinary tract downstream from the kidney eg ureters
Postrenal. Early stage of obstruction? FENa, BUN/Cr
Increased tubular pressures ,,forces” BUN into the blood (serum BUN/Cr ratio > 15); tubular function remains intact (FENa < 1 proc. and urine osm>500 mOsm/kg).
Postrenal. Late stage of obstruction? FENa, BUN/Cr
with long-standing obstruction, tubular damage ensues, resulting in decreased reabsorption of BUN (serum BUN:Cr ration < 15), decreased reabsorption of sodium FENa > 2 proc., and inability to concentrate urine (urine osm < 500 mOsm/kg)
Acute interstitial nephritis. causes? what type of azotemia?
Drug-induced hypersensitivity involving the interstitium and tubules.
Results in ARF (intrarenal azotemia)
Acute interstitial nephritis. Drugs?
NSAIDs, penicillin, diuretics
Acute interstitial nephritis. presentation?
oliguria, fever, rash days to weeks after starting a drug. eosinophils may be seen in the urine
Acute interstitial nephritis. what cells in the urine?
Eosinophils may be seen in the urine
Acute interstitial nephritis. when resolves?
with cessation of drug
Acute interstitial nephritis. may progress to what?
renal papillary necrosis
Renal papillary necrosis. definition?
necrosis of renal papillae.
Renal papillary necrosis. presentation?
gross hematuria and flank pain
Renal papillary necrosis. causes?
- chronic analgetic abuse (long-term phenacetin or aspirin use)
- DM
- Sickle cell trait or disease
- severe acute pyelonephritis
what is difference between prerenal and intrarenal due to decr. blood flow?
prerenal - HYPOPERFUSION
intrarenal - HYPOPERFUSION WITH ISCHEMIA
liver disease with portal hypertension–> effect on kidney
Vasoconstriction -> prerenal azotemia. hepatorenal syndrome
intrarenal. what is classification based on the damaged site?
tubular (85 proc.)
glomerular - GN
interstitial (interstitial nephritis)
Hemolytic intravascular anemia - what ATN?
toxic
Bence Jones protein light chains - what ATN?
toxic
Aminoglycosides - effect PCT cells? 3
impair lisosomal function, protein synthesis and mitochondrial activity –> ATN.
Aminoglycosides - histology of PCT?
FOCAL tubular epithelial necrosis with casts that obstruct the tubular lumen –> lead to rupture of the basement membrane.
Aminoglycosides -> damage to PCT –> electrolytes?
loss of reabsorptive capacity –> electrolyte wasting
Aminoglycosides -> damage to PCT. if very severe, what syndrome?
Fanconi
Aminoglycosides -> if damage to Distal CT occurs–> ?
loss of concentration capacity with poliuria (nonoliguric renal failure).
Is ethylen glycol toxic to kidney?
No, its not toxic.
Toxic are its metabolites.
ethylen glycol metabolized to —-> 2?
glycolic acid and oxalic acid —> cause toxicity.
ethylen glycol what symptoms?
as intoxication of alcohol: altered mental status innitially
Renal failure - 24-72h post ingestion (oliguria, flank pain).
ethylen glycol. what causes obstruction?
glycolic and oxalic acids crystalizes –> obstruction -> ATN
ethylen glycol. what crystals on biopsy?
oxalate
ethylen glycol. histology?
proximal tubular ballooning and vacuolar degeneration (cia tiesiog nekrozei budingi pokyciai) with morphologically normal glomeruli.
ethylen glycol. What all findings?
altered mental status
renal failure
high anion gap metabolic acidosis
increased osmolar gap, calcium oxalate in the urine
ethylen glycol. why acidosis and high osmolar gap?
elevated anion gap metabolic acidosis - due to acid. metabolite formation.
high osmolar gap - due to uncharged parent alcohol
contrast induced pehropathy (CIN). what is damage?
direct citotoxicity of intravenous contrast on tubular cells -> diffuse necrosis of PCT cells.
prevention: avoids NSAIDs, give smallest possible volume of contrasts, give periprocedural intravenous saline
Hemoglobin. prolonged seizure –> renal injury?
prolonged seizure –> rhabdomyolysis –> kindney injury
Cristaline induced kidney injury due to ….
acyclovir or sulfonamide.
urinalysis - needle shaped or rosette-shaped crystals
vancomycin - when injury?
after prolonged course (days). single dose would not cause injury. Also, no cristals
intrarenal due to GN. mechanism?
immune complex deposition –> activation of complement –> attracts iimune cells (macrophages, neutrophils) –> release of LYSOSOMAL ENZYMES – >inflammation and damage to podocytes –> increased membrane permeability -> filtration of huge molecules -> proteinuria and hematuria
GN. Damage to podocytes -> fluid leakage –> what result?
REDUCED PRESSURE DIFFERENCE –> lower GFR -> oliguria
more fluids in body –> volume overload -> edema and hypertension
less filtration –> azotemia
AIN - renal biopsy?
inflammatory interstitial infiltrate and edema
cells: lymphocytes, macrophages, eosinophils
AIN - what hypersensitivity?
type I and IV.
AIN - urinalysis?
sterile pyuria (EOSINOPHILS), WBC, WBC casts
however, eosinphils are not specific finding - it may be also in prostatitis or transplant rejection
renal papillary necrosis.
- analgetic nephropathy - findings?
papillary necrosis and tubulointerstitial nephritis
renal papillary necrosis.
Why DM?
DM -> metabolic abnormalities eg nonenzymatic glycosylation -> changes in vessels -> renal vasculopathy -> subsequent hypoperfusion
renal papillary necrosis.
why pyelonephritis/urinary tract obstruction?
edematous interstitium of pyelonephric kidney compresses the medullary vasculare -> ischemia.
renal papillary necrosis. why gross hematuria?
due to sloughed papillae
renal papillary necrosis. why flank pain?
due to ureteral obstruction
renal papillary necrosis. macroscopically?
Gray-white or yellow necrosis of the distal two-thirds of the renal pyramids is seen macroscopically
what vascular diseases can cause ATN? 5
HUS, TTP, Hypertensive emergency, vasculitis or scleroderma renal crisis, renal vein thrombosis/atheroemboli/renal infarction
postrenal - what side obstruction?
BILATERAL
postrenal - causes?
ACQUIRED OBSTRUCTIONS:
- BPH
- iatrogenic - catheter-assoc. injuries
- Tumors - bladder, prostate, cervical, metasteases, intraabdominal turmors
- stones
- bleeding with subsequent clot formation
Neurogenic bladder - eg due to multiple sclerosis, spinal cord lesions, peripheral neuropathy
Congenital malformations - posterior urethral valves
posterenal. unilateral obstruction. what creatinine?
!!!As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels.
also, if one kidney is okay, GFR ir maintained
posternal - UG?
distended bladder, high postvoidal residual volumes, bilater hydrophrosis, and/or obstructing stones
posternal. If bladder outlet obstruction - what management?
urgent relief of UT obstruction: cateterization, suprapubic cateterizatio
posternal. If ureteral or renal pelvic obstruction - what management?
urgent urology consultation to relieve obstruction
Management: ureteral stenting; percutaneous nephrostomy
