AKI

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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

Staging:

Staging

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::

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:

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:

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::

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::

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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