Posted: December 7th, 2022
Ken Fowler ihuman diagnosis
The presentation of a rapid increase in creatinine should prompt a consideration of whether the patient has prerenal azotemia intrarenal azotemia or postrenal obstruction. The risk factors for prerenal azotemia include: dehydration, hemorrhage, heart failure, sepsis, anaphylaxis, hepatorenal syndrome or medications. Intrarenal causes include: prolonged prerenal state, acute tubular necrosis, atheroemboli, malignant hypertension, TTP, AIN or posinfectious glomerunephritis. Ken Fowler ihuman diagnosis Post renal causes are causes of obstruction which include: BPH, bladder outlet stones, bilateral renal calculi stones and pelvic malignancies that could block both ureters. The lack of any ultrasound evidence of obstruction or hydronephrosis as well as the lack of heart failure, bleeds, infectious processes or anaphylaxis or intravascular procedures that could release emboli, the use of NSAIDS for his back pain while on his hypertensive medications is the most likely cause.
Epidemiology: Adverse renal events have been documented to occur in 1-5% of all patients using NSAIDS. In the USA, this translates to approximately 2.5 million people experiencing a nephrotoxic event annually. In Mr. Fowler’s case, he had the added use of a diuretic and ACE inhibitor which are thought to further increase this risk. Added to that was his known previously existing renal insufficiency as highlighted by his elevated creatinine of 1.1 with proteinuria Ken Fowler ihuman diagnosis.
Mechanism of Action of NSAIDS: NSAIDS inhibit the cyclooxygenase (COX) enzymes. This results in a reduction in prostaglandin (PG) synthesis which can lead to reversible renal ischemia, a decline in glomerular hydraulic pressure and AKI
Clinical manifestations of AKI: Patients present with an increase in plasma creatinine usually within 3-7 days of NSAID therapy. Urinalysis that is bland with only hyaline cases, lack of hematuria or significant proteinuria (> 1 g/day).
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