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Chapter 15: NSAIDs and the Kidney: Acute Kidney Injury

Mark A. Perazella

INTRODUCTION

ESSENTIALS OF DIAGNOSIS

  • Nonsteroidal anti-inflammatory drug (NSAID)-associated acute kidney injury (AKI) develops predominantly in patients with underlying risk factors.

  • Clinical presentations can be asymptomatic or associated with uremic symptoms, edema (pulmonary and peripheral), hypertension, or electrolyte and acid–base disturbances.

  • Elevated blood urea nitrogen (BUN) and serum creatinine (Cr) concentrations are present.

  • An elevated BUN/Cr ratio (>20) is often noted.

  • Hyponatremia (serum [Na+] <135 mEq/L), hyperkalemia (serum [K+] >5.5 mEq/L), and nonanion gap metabolic acidosis (serum [HCO3–] <20 mEq/L) are common.

  • Urine [Na+] <10–20 mEq/L and FENa+ <1.0% characterize NSAID-associated AKI.

  • AKI is generally reversible with discontinuation of NSAIDs and treatment of concurrent disease processes.

  • Severe AKI from NSAIDs may require dialysis.

GENERAL CONSIDERATIONS

A. Epidemiology of Nonsteroidal Anti-inflammatory Drug Use

NSAIDs are employed widely to treat pain, fever, and inflammation. Other potential uses for these drugs include treatment and prevention of colonic polyposis and Alzheimer-type dementia. The first NSAID discovered was sodium salicylate in 1763. In 1950, phenylbutazone was introduced into clinical practice. It was efficacious, but its use faded due to bone marrow toxicity. Subsequently, indomethacin entered the market in the 1960s. More than 20 NSAIDs from seven major classes, including the selective cyclooxygenase (COX)-2 inhibitors (Table 15–1), are available in the United States. In addition to prescription NSAIDs, a large percentage of the general population consumes over-the-counter NSAIDs. Annually, more than 50 million patients ingest these drugs on an intermittent basis, while some 15–25 million people in the United States use an NSAID on a regular basis. Importantly, the elderly patients who are at risk for multiple complications of NSAID therapy constitute a growing population that has a prevalence of NSAID use as high as 15–20%.

Table 15–1.Classes of nonsteroidal anti-inflammatory drugs.
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Table 15–1. Classes of nonsteroidal anti-inflammatory drugs.
Class Trade Name Total Dose/Day (Dosing Interval)
Carboxylic acids
Aspirin Aspirin 2.4–6.0 g (qid)
Salsalate Disalcid 1.5–3.0 g (bid)
Choline magnesium Trilisate 1.5–3.0 g (bid–tid)
Diflunisal Dolobid 0.5–1.5 g (bid)
Acetic acids
Indomethacin Indocin 75–150 mg (bid–qid)
Tolmetin Tolectin 400–2400 mg (bid–tid)
Sulindac Clinoril 200–400 mg (bid)
Diclofenac

Voltaren, Cataflam

Arthrotec

100–150 mg (bid)

100 mg (bid)
Etodolac Lodine 400–1200 mg (bid–qid)
Ketorolac Toradol

Oral 40 mg (qid)

Intravenous 60–120 mg (qid)
Propionic acids
Ibuprofen Motrin, Rufen 800–3200 mg (qid)
Naproxen

Naprosyn, Anaprox

Alleve

500–1000 mg (bid)

450 mg (bid)
Ketoprofen Orudis 225 mg (tid)
Flurbiprofen Ansaid 200–300 mg (bid–tid)
Fenoprofen Nalfon 1200–2400 mg (qid)
Oxaprozin Daypro 1200 mg (qd)
Enolic acids
Piroxicam Feldene 10–20 mg (qd)
Phenylbutazone Butazolidin 300–600 mg (tid)
Fenamates
Mefenamic acid Ponstel 1000 mg (qid)
Meclofenamate Meclomen 150–400 mg (tid–qid)
Naphthylkanones
Nabumetone Relafen 1000–1500 mg (bid–tid)
COX-2 inhibitors
Celecoxib Celebrex 100–400 mg (qd–bid)

B. Epidemiology of Nonsteroidal Anti-inflammatory Drug-Associated Acute Kidney Injury

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