Ken Fowler ihuman diagnosis

Ken Fowler ihuman diagnosis

Diagnosis: Acute kidney injury (AKI) secondary to true intravascular volume depletion and medication related side-effect
(NSAIDS) causing prerenal azotemia.

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).

• • History of nausea and anorexia with concomitant diuretic use
  • Impaired renal blood flow secondary to use of NSAID and ACE inhibitor. Ken Fowler ihuman diagnosis.

Ken Fowler iHuman Diagnosis

Diagnosis: Sudden kidney injury caused by a decrease in intravascular fluid volume and a side effect from medication (NSAIDs), resulting in pre-kidney azotemia.

When there’s a rapid rise in creatinine levels, it’s important to consider if the patient has pre-kidney azotemia, kidney-related azotemia, or an obstruction after the kidney. Factors leading to pre-kidney azotemia include dehydration, bleeding, heart failure, sepsis, anaphylaxis, hepatorenal syndrome, or medication use. Kidney-related causes include prolonged pre-kidney state, acute tubular necrosis, atheroemboli, severe hypertension, TTP, AIN, or post-infectious glomerulonephritis. Post-kidney causes involve obstructions like enlarged prostate, stones in the bladder outlet, kidney stones, or tumors blocking both ureters. In this case, since there’s no evidence of blockage or hydronephrosis in ultrasound and no signs of heart failure, bleeding, infections, or embolism-triggering procedures, the most likely cause is the use of NSAIDs for back pain while being on hypertensive medications.

Epidemiology: Between 1% and 5% of NSAID users experience kidney-related issues. In the US, this accounts for around 2.5 million people facing kidney problems annually. In Mr. Fowler’s situation, his risk was further heightened due to the diuretic and ACE inhibitor he was taking, both of which are known to increase this risk. His existing kidney insufficiency, as indicated by his elevated creatinine level of 1.1 with protein in the urine, also contributed.

NSAID Action Mechanism: NSAIDs inhibit enzymes known as cyclooxygenases (COX). This leads to reduced synthesis of prostaglandins (PG), causing temporary kidney ischemia, a drop in glomerular pressure, and kidney injury.

AKI Clinical Signs: Patients typically show a rise in plasma creatinine within 3-7 days of starting NSAID treatment. Urinalysis might reveal minor abnormalities like hyaline casts, without blood or significant protein presence (> 1 g/day).

• History of feeling nauseous and having little appetite, along with diuretic use
• Reduced kidney blood flow due to NSAID and ACE inhibitor use. Ken Fowler iHuman Diagnosis