16 ) Acute kidney injury

Question 1

prerenal acute kidney injury etiology ?

Answer 1

any condition leading to decreased renal perfusion

Hypovolemia
Volume depletion: e.g., hemorrhage, vomiting, diarrhea,

Decreased circulating volume: e.g., hepatorenal syndrome, cirrhosis, liver failure, nephrotic syndrome,

Hypotension: e.g., sepsis, dehydration, cardiogenic shock (decreased cardiac output)

Renal artery stenosis

Drugs affecting glomerular perfusion: e.g., cyclosporine,

Question 2

intrinsic acute kidney injury etiology ?

Answer 2

any disease that leads to severe direct kidney damage.

Acute tubular necrosis (causes ∼ 85% of intrinsic AKIs): most commonly caused by sepsis, infection, ischemia

Glomerulonephritis (e.g., rapidly progressive glomerulonephritis

Vascular
Hemolytic uremic syndrome (HUS)
Thrombotic thrombocytopenic purpura

acute tubulointerstitial nephritis

Question 3

what is the etiology of post renal acute kidney injury ?

Answer 3

any condition that results in bilateral obstruction of urinary flow

Congenital malformations posterior urethral valves

Acquired obstructions
Benign prostatic hyperplasia (BPH)
tumors 
stones 
neurogenic badder - MS

Question 4

what are the 4 phases of AKI ? !

Answer 4

Initiating event (kidney injury)
= hours to days 

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Oliguric or anuric phase (1-3wks) 
(maintenance phase)
oliguria = < 400 mL per 24 hours
anurea =  < 50 ml/24 hrs = anuria
azotemia 

complication = pulmonary edema , hyperkalemia , metabolic acidosis , asterisks

=========
Polyuric/diuretic phase
- 2 wks

Generally, the glomeruli recover faster than the tubular system,
Glomerular filtration returns to normal, which increases urine production (polyuria), while tubular reabsorption remains disturbed.

==========
recovery phase = months to years
Kidney function and urine production normalize

Question 5

clinical features of AKI ?

Answer 5

Reduced skin turgor

Oliguria or anuria
============
Signs of volume depletion
 (in prerenal AKI caused by volume loss)
Orthostatic or frank hypotension and tachycardia

Signs of fluid overload

Hypertension
Heart failure
Shortness of breath

===========

Signs of uremia
Anorexia, nausea
Encephalopathy, asterixis
Pericarditis
Platelet dysfunction

======
azotemia
gastrtis
colitis 
Asterixis 
decreased alertness and confusion
==========

Signs of renal obstruction (in postrenal AKI)
Distended bladder
Incomplete voiding
Pain over the bladder or flanks

========

Fatigue,

In severe cases: seizures or coma

Question 6

acute tubular necrosis usually take place where ?

Answer 6

straight segment of the proximal tubule and the straight segment of the distal tubule (i.e., the thick ascending limb)

= most susceptible to ischemic changes

Question 7

etiology of acute tubular necrosis ?

Answer 7

Ischemic: Injury occurs secondary to decreased renal blood flow:

Severe hypotension,

Thromboembolism

Thrombotic microangiopathy

Toxic:
Injury occurs directly due to nephrotoxic substances.

Contrast-induced nephropathy

Medication: aminoglycosides, cisplatin, amphotericin,
Pigment nephropathy

Myoglobinuria due to rhabdomyolysis (crush syndrome)

Question 8

diagnosis of tubular necrosis ?

Answer 8

Blood findings: azotemia, hyperkalemia, and metabolic acidosis
Urinary findings
↑ Fractional excretion of sodium (FENa)

Urinary sediment
Muddy brown granular casts
Epithelial cell casts
Free renal tubular epithelial cells (due to denudation of the tubular basement membrane)

Question 9

diagnosis of AKI

Answer 9

stage 1
serum creatinine increase by 0.3mg/dl within 48hr
urine output less than 0.5 ml/kg/h for 6-12hr

stage 2

serum creatinine 2-2.9 times higher than baseline
urine output less that 0.5ml/kg/hr for more than 12 hrs

========
stage 3
more than or equal 3 times higher
urine output less than 0.3ml/kg/hr for or at 24hrs

prerenal

Elevated serum creatinine concentration
Serum BUN:creatinine ratio > 20:1

Low urine sodium concentration (< 20 mEq/L)
Low fractional excretion of sodium (FeNa < 1%)

High urine osmolality (> 500 mosm/kg) and specific gravity (> 1.010)

intrinsic

blood:
Elevated serum creatinine concentration and rapidly rising serum creatinine level
BUN:creatinine ratio < 15:1

Hyperkalemia,
metabolic acidosis, hyperphosphatemia, hypocalcemia,
hyperuricemia, and/or dyslipidemia

anemia - due to decreased EPO

urine
Renal tubular epithelial cells or granular, muddy brown, or pigmented casts
Urine dipstick is positive for blood but negative for RBCs in rhabdomyolysis

post renal
Elevated serum creatinine concentration in bilateral obstruction

how you test fo rtsones and blocks

Question 10

treatment ?

Answer 10

Prerenal
Replete volume with normal saline in patients with hypovolemia

Administer diuretics in patients with hypervolemia who are hemodynamically stable and not anuric

Intrinsic
Replete volume with normal saline in suspected ATN or contrast-induced renal dysfunction

Consider corticosteroid or immunosuppressive therapy in RPGN or interstitial nephritis.

Treat infection.

Postrenal: Remove outflow obstructions with Foley catheter insertion, an indwelling bladder catheter, nephrostomy, or stenting