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mini lecture about Acute kidney injury


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Acute Kidney Injury:

Acute Kidney Injury Dr Mohammed Abdelsattar

Def Oliguria Anuria :

Def Oliguria Anuria May present as Uremia ( malaise, anorexia, nausea, vomiting ), but is usually asymptomatic . abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products urinary  output less than 400ml/day  passage of less than 100  ml   of urine in a day



Prerenal azotemia:

Prerenal azotemia Result from decrease renal perfusion Normalization of renal function When perfustion is restored   . occure following hemorrhage , shock Intravascular volume depletion , cong heart failure  . fractional excretion of Na of < 1% and an elevated urine osmolarity


Aet : 1-Decreased circulatory volume Hypovolemia 2-Decreased local blood flow to kidney Renal artery stenosis , Drug, Hepatorenal syndrome 3- Diminished cardiac output CHF ,Arrhythmias, tamponade

Acute tubular necrosis:

Acute tubular necrosis Acute tubular necrosis is a kidney disorder involving damage to the tubule cells of the kidneys, which can lead to  acute kidney failure . .Usually occurs after an ischemic event or exposure to nephrotoxic agents. . muddy brown casts and FeNa >2% .Accounts for some 50% of cases of AKI in hospitalized patient   Risks for acute tubular necrosis include: Blood transfution reaction Injury or trauma that damages the muscles Low blood pressure (hypotension) that lasts longer than 30 minutes Recent major surgery Septic shock due to severe infection .

Acute Interstitial nephritis :

Acute Interstitial nephritis form of nephritis affecting the interstitium of the kidneys surrounding the tubules ass with triad


AIN .The most common cause is reaction to a drug as penicillin and cephalexin , and nonsteroidal anti-inflammatory drugs or Infection or malignancy or systemic immune dse .The time between exposure to the drug and the development of acute tubulointerstitial nephritis can be anywhere from 5 days to 5 months . Esinophillia is non specific may be seen in pyelonephritis or prostatitis or cystitis


ttt Withdraw of the drug with treatment for acute renal failure, if necessary. Dietary restriction of fluids, sodium, and protein. Corticosteroids may accelerate recovery

Contrast Induced Nephropathy:

Contrast Induced Nephropathy Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration Cr peak in 3-5 d and return to normal in 7-10 d


RF: CKD DM Old age>75y Class IV CHF

Prevention of CIN::

Prevention of CIN: .Use the lowest possible dose of contrast medium in patients at risk for CI-AKI. (Not Graded) . i.v . volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions  . oral NAC on the day before and of the procedure if creatinine clearance is estimated to be less than 60 mL /min

Post renal causes:

Post renal causes Obstruction anywhere in the urinary tract .Bladder outlet obstruction can be seen with bladder scan and relieved with catheterization . Ureteral obstruction and hydronephrosis may be seen on ultrasound and noncontrast CT Order: Order: UA, Uosm , Una , Ucr , BMP, Uurea (if on diuretics)

PowerPoint Presentation:

A postvoid residual volume of 100 mL or more suggests obstructive uropathy , and the cause should be further investigated. Relief of the obstruction is the mainstay of therapy


Sources: KDIGO guidelines AKI Nephrology secrets Acute Kidney Injury - Mini Lecture(university of California)

Thanks dr Mohammed A.Gwad for his efforts:

Thanks dr Mohammed A.Gwad for his efforts جزآكم الله خيرا

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