Demand management of procalcitonin requests in the biochemistry emergency laboratory

Abstract

Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit the synthesis of prostaglandins, which comprise an important compensatory mechanism for maintaining renal blood flow, glomerular filtration, and water and electrolyte homeostasis in the setting of a number of pathophysiologic states including chronic kidney disease (CKD). CKD patients are, therefore, at risk for adverse renal side effects of NSAIDs, including acutely worsened renal function, hyperkalemia, hyponatremia, sodium retention, and exacerbation of hypertension. Although these effects are generally reversible on discontinuation of the drugs, patients with CKD must be monitored closely while taking NSAIDs.Evidence suggests that heavy cumulative NSAID consumption is capable of causing chronic kidney injury with manifestations similar to those seen in classic analgesic nephropathy, including chronic interstitial nephritis and papillary necrosis. The pathogenesis of this disorder is probably renal medullary ischemia resulting from diversion of blood flow to the cortex that occurs with suppression of prostaglandin synthesis. CKD due to NSAIDs is probably rare.Extra caution is indicated when (1) committing patients to high-dose, long-term NSAID therapy or (2) recommending NSAID therapy of any duration to patients with CKD or other risk factors for adverse renal side effects including advanced age, use of diuretics, congestive heart failure, cirrhosis, and hypertension.As with NSAIDs, opioid analgesics must be considered from two standpoints: their ability to cause chronic kidney injury, which appears rare if it occurs at all, and the susceptibility of patients with chronically impaired renal function to the hemodynamic and neurotoxic effects of opioids, a problem commonly confronted in the clinic.