Critical Care Medicine-Renal, Electrolyte and Acid Base Disorders>>>>>Acute Renal Failure
Question 1#

A 62-year-old male presents to the hospital complaining of nonradiating back pain for the past 2 days. He has a past medical history of hypertension, hyperlipidemia, and chronic back pain for which he takes ibuprofen, atorvastatin, and hydrochlorothiazide. He mentions that he tried to take a few extra doses of analgesics which did not seem to help, and it seems like his regular water pill is not working either. His vitals are as follows:

• Heart rate (HR) 110 bpm
• respiratory rate (RR) 18/min
• blood pressure (BP) 95/54 mm Hg
• SpO₂ 98%
• temp 37.3°C

and laboratory work as follows:

• WBC 5.08 k/µL
• hemoglobin (Hb) 14 g/dL
• hematocrit (Hct) 37%
• platelet (Plt) count 290 k/µL
• Sodium (Na) 143 mmol/L
• potassium (K) 4.3 mmol/L
• CO 18 mmol/L
• chloride (Cl) 109 mmol/L
• BUN 30 mg/dL
• serum creatinine (Scr) 2.0 mg/dL
• Anion gap is 16 mmol/L

Which of the following etiologies for acute renal injury (AKI) should ALWAYS be excluded first?

A. Dehydration
B. Nonsteroidal anti-inflammatory overdose
C. Septic shock
D. Chronic anemia

Correct Answer is A

Comment:

Correct Answer: A

Renal blood flow constitutes 20% of cardiac output. A large part of the renal perfusion (80%-90%) goes to renal cortex where glomerular filtration occurs. Prerenal azotemia as a consequence of reduction in renal perfusion, accounts for approximately 70% of the community-acquired and 40% of hospital-acquired cases of AKI. As this is a reversible process, most of the time, once the underlying inciting process is addressed, prerenal etiology (eg, vomiting, dehydration, and hemorrhage) should be excluded in all cases of AKI. 

The renin-angiotensin-aldosterone system (RAAS) becomes activated secondary to a decrease in renal blood flow with subsequent increase in sodium reabsorption at the level of the proximal and distal tubule induced by angiotension II and aldosterone, respectively. As a result, the urine sodium concentration is less than 20 mmol/L and fractional excretion of sodium (FENa ) is less than 1%. Medications like nonsteroidal antiinflammatory drugs (NSAIDs) or RAAS inhibitors which interfere with the renal autoregulatory mechanisms could worsen prerenal azotemia, which seems likely in this patient.

Patients with NSAID overdose typically present with a wide spectrum of gastrointestinal symptoms, altered mental status, and arterial blood gas consistent with an anion gap metabolic acidosis. C and D are unlikely due to lack of neurological symptoms and patient not being in shock, respectively. Prerenal etiology should be excluded in all cases of AKI due to its reversible nature in the majority of cases. 

Reference:

1. Elhassan E, Schrier R. Acute kidney injury. In: Vincent JL, Abraham E, Moore FA, Kochanek PM, Fink MP, eds. Chapter 109: Textbook of Critical Care. 7th ed. 773-783.