Vancomycin-Associated Acute Kidney Injury with a Steep Rise in Serum Creatinine

Abstract

Background: Vancomycin-associated (VA) acute kidney injury (AKI) is being increasingly recognized. A distinct pattern of rapid rise in serum creatinine (sCr) during VA-AKI has occasionally been observed. However, such scenarios remain underreported. Methods: We conducted an online survey at the American Society of Nephrology Communities forum and reviewed publications of VA-AKI via PubMed or Google searching for cases of precipitous AKI (those with rise in sCr ≥1.5 mg/dL/day) attributable to vancomycin. Results: We identified 12 original cases compiled from 6 different hospitals and 4 published cases (n = 16; 38% women, age 43.5 ± 16 years, weight 108 ± 23 kg, body mass index 35 ± 7 kg/m²) of precipitous AKI observed shortly after large cumulative doses of VA (8.8 ± 5 g). The median steepest 24-h rise in sCr was 2.6 mg/dL (range 1.5–3.5 mg/dL) and the slope of the initial 48-h sCr rise was greater than that of a control AKI (non-VA, n = 48) group (2.03 ± 0.1 vs. 0.62 ± 0.0 mg/dL/day; p < 0.0001). The steep rise in sCr in the VA-AKI was not accompanied by anuria. Overt rhabdomyolysis was absent in all cases. Further, in 3 precipitous VA-AKI cases, simultaneous serum cystatin C values did not rise precipitously, suggesting that the reductions in glomerular filtration rate were overestimated by the sCr increase. Conclusions: VA-AKI can manifest with a precipitous rise in sCr shortly after a high cumulative dose of vancomycin. True toxic tubular injury overrepresented by the sCr rise is postulated.

Association of vancomycin plus piperacillin–tazobactam with early changes in creatinine versus cystatin C in critically ill adults: a prospective cohort study

“…Serum creatinine, the standard kidney function biomarker, is subject to proximal tubular secretion, which accounts for 10-40% of creatinine clearance in healthy adults and up to 60% in patients with chronic kidney disease (CKD) [12]. Notably, both VN and PT bind to renal transporters that mediate creatinine secretion [13][14][15][16][17][18][19]. Thus, the association with creatinine defined AKI may represent pseudotoxicity, mediated by effects on tubular secretion of creatinine without toxic effects on kidney parenchyma.…”

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“…Hepatitis C-Associated Glomerulonephritis. A glomerular pattern of injury encountered in patients with cirrhosis due to HCV is that of membranoproliferative GN (44). Cryoglobulinemia is often present.…”

“…Staphylococcal infections requiring treatment with vancomycin are not uncommon in cirrhosis. Vancomycin is known to cause toxic acute tubular injury in the general population, and it can present clinically as a precipitous rise in serum creatinine (44). Vancomycin nanospheres have been described to precipitate intratubular obstruction, an entity named vancomycin cast nephropathy (45).…”

Hepatorenal Syndrome Type 1: From Diagnosis Ascertainment to Goal-Oriented Pharmacologic Therapy

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