Ken Fowler iHuman Diagnosis

Ken Fowler iHuman Diagnosis

Diagnosis: Mr. Fowler’s condition is characterized as Acute Kidney Injury (AKI), primarily resulting from two key factors: true intravascular volume depletion and medication-related side effects, specifically the use of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) leading to prerenal azotemia.

When encountering a sudden elevation in creatinine levels, it becomes essential to consider whether the patient is experiencing prerenal azotemia, intrarenal azotemia, or postrenal obstruction as the underlying cause. Prerenal azotemia, in Mr. Fowler’s case, is associated with risk factors such as dehydration, hemorrhage, heart failure, sepsis, anaphylaxis, hepatorenal syndrome, or certain medications. Intrarenal causes encompass prolonged prerenal states, acute tubular necrosis, atheroemboli, malignant hypertension, thrombotic thrombocytopenic purpura (TTP), acute interstitial nephritis (AIN), or postinfectious glomerulonephritis.

Introduction to Qualitative Nursing Research

Postrenal causes, indicating obstruction, can be attributed to conditions like benign prostatic hyperplasia (BPH), bladder outlet stones, bilateral renal calculi, or pelvic malignancies that obstruct both ureters. Given the absence of ultrasound evidence of obstruction, heart failure, bleeding, infectious processes, anaphylaxis, or invasive procedures that could result in emboli, Mr. Fowler’s use of NSAIDs in conjunction with his hypertensive medications emerges as the most probable cause of his condition.

Epidemiology:

Adverse renal events associated with NSAID usage have been reported in 1-5% of all NSAID users. In the United States, this corresponds to roughly 2.5 million individuals experiencing nephrotoxic events annually. In Mr. Fowler’s case, the concomitant use of a diuretic and an ACE inhibitor is believed to further elevate this risk. Additionally, his previously documented renal insufficiency, indicated by an elevated creatinine level of 1.1 with proteinuria, contributes to his susceptibility to renal complications.

Mechanism of Action of NSAIDs:

NSAIDs exert their effects by inhibiting the cyclooxygenase (COX) enzymes, leading to a reduction in prostaglandin (PG) synthesis. This can result in reversible renal ischemia, a decline in glomerular hydraulic pressure, and subsequently, AKI.

Clinical Manifestations of AKI:

Patients typically exhibit an increase in plasma creatinine levels, typically within 3-7 days of NSAID therapy initiation. Urinalysis tends to reveal bland findings, characterized by the presence of only hyaline casts, without indications of hematuria or significant proteinuria (>1 g/day).

Clinical Presentation:

– History of nausea and anorexia, exacerbated by concurrent diuretic use.
– Impaired renal blood flow, stemming from NSAID and ACE inhibitor use, contributes to the development of AKI in Mr. Fowler’s case.