Correction

doi:10.2215/CJN.09840819

Ellison DH: Clinical Pharmacology in Diuretic Use. Clin J Am Soc Nephrol 14: 1248–1257, 2019; DOI: https://doi.org/10.2215/CJN.09630818.

Because of author error, the following corrections have been issued for this article:

The label for “Absorption Varies” in Figure 2A should have referenced Table 2, not Table 1. The corrected Figure 2 is reprinted below.
The authors have also reported the following typographical error on page 1251: “antinatriuresis” should have been “natriuresis.” The corrected word is in boldface font in situ in the paragraph below from the article.

“There are additional reasons that CKD is a loop diuretic–resistant state. Metabolic acidosis, which is frequently observed in uremia, depolarizes the membrane potential of proximal tubule cells (37), which also decreases organic anion secretion, an effect that may explain why diuretic secretion is enhanced by alkalosis (38). In addition to a shift in the dose-response curve, patients with CKD and those taking NSAIDs have a downward shift of the ceiling natriuresis, when expressed as absolute sodium excretion (rather than fractional). The mechanism for resistance attributable to NSAIDs is complex. Loop diuretic inhibition of NaCl reabsorption at the macula densa stimulates both renin secretion and prostaglandin (PG) production, the latter predominantly via cyclooxygenase-2 (39). When this happens, PG E2 feeds back on tubules, contributing to the resulting natriuresis by inhibiting NaCl transport along the thick ascending limb and collecting duct (40,41). NSAIDs block this PG-mediated natriuresis. When used chronically, NSAIDs increase the abundance and activity of NKCC2 along the thick ascending limb (42). Additionally, loop diuretics inhibit the second transporter isoform, NKCC1, mentioned above, which is also expressed by vascular smooth muscle cells; loop diuretics contribute to afferent arteriolar vasodilation by blocking this transporter (43), thus helping to maintain GFR despite a lower ECF volume. Again, this compensatory adaptation is largely dependent on PG production and can be blocked by NSAIDs. The clinical consequence of these effects is evident in the association between recent use of NSAIDs and risk for hospitalization in patients with heart failure (34). In fact, the combination of three classes of drugs that affect hemodynamics of the kidney, loop diuretics, angiotensin-converting inhibitors (or receptor blockers), and NSAIDs, is associated with AKI (44).”