Abstract:AKI, a frequently transient condition, is not accepted by the US Food and Drug Association as an end point for drug registration trials. We assessed whether an intermediate-term change in eGFR after AKI has a sufficiently strong relationship with subsequent ESRD to serve as an alternative end point in trials of AKI prevention and/or treatment. Among 161,185 United States veterans undergoing major surgery between 2004 and 2011, we characterized in-hospital AKI by Kidney Disease Improving Global Outcomes creatin… Show more
“…AKI was also staged according to KDIGO creatinine-based criteria from the date of first antibiotic exposure during hospitalization [21]. Baseline creatinine was defined as the mean of outpatient serum creatinine levels 7-365 days prior to hospitalization [22]. For our analyses, we only considered AKI events occurring after 48 h following the start of vancomycin administration.…”
Background: To determine the association of vancomycin with acute kidney injury (AKI) in relation to its serum concentration value and to examine the risk of AKI in patients treated with vancomycin when compared with a matched cohort of patients receiving non-glycopeptide antibiotics (linezolid/daptomycin). Methods: From a cohort of > 3 million US veterans with baseline estimated glomerular filtration rate ≥60 mL/min/1.73 m2, we identified 33,527 patients who received either intravenous vancomycin (n = 22,057) or non-glycopeptide antibiotics (linezolid/daptomycin, n = 11,470). We examined the association of the serum trough vancomycin level recorded within the first 48 h of administration with subsequent AKI in all patients treated with vancomycin and association of vancomycin vs. non-glycopeptide antibiotics use with the risk of incident AKI. Results: The overall multivariable adjusted ORs of AKI stages 1, 2, and 3 in patients on vancomycin vs. non-glycopeptides were 1.1 (1.1–1.2), 1.2 (1–1.4), and 1.4 (1.1–1.7), respectively. When examined in strata divided by vancomycin trough level, the odds of AKI were similar or lower in patients receiving vancomycin compared to non-glycopeptide antibiotics as long as serum vancomycin levels were ≤20 mg/L. However, in patients with serum vancomycin levels > 20 mg/L, the ORs of AKI stages 1, 2, and 3 in patients on vancomycin vs. non-glycopeptide antibiotics were 1.5 (1.4–1.7), 1.9 (1.5–2.3), and 2.7 (2–3.5), respectively. Conclusions: Vancomycin use is associated with a higher risk of AKI when serum levels exceed > 20 mg/L.
“…AKI was also staged according to KDIGO creatinine-based criteria from the date of first antibiotic exposure during hospitalization [21]. Baseline creatinine was defined as the mean of outpatient serum creatinine levels 7-365 days prior to hospitalization [22]. For our analyses, we only considered AKI events occurring after 48 h following the start of vancomycin administration.…”
Background: To determine the association of vancomycin with acute kidney injury (AKI) in relation to its serum concentration value and to examine the risk of AKI in patients treated with vancomycin when compared with a matched cohort of patients receiving non-glycopeptide antibiotics (linezolid/daptomycin). Methods: From a cohort of > 3 million US veterans with baseline estimated glomerular filtration rate ≥60 mL/min/1.73 m2, we identified 33,527 patients who received either intravenous vancomycin (n = 22,057) or non-glycopeptide antibiotics (linezolid/daptomycin, n = 11,470). We examined the association of the serum trough vancomycin level recorded within the first 48 h of administration with subsequent AKI in all patients treated with vancomycin and association of vancomycin vs. non-glycopeptide antibiotics use with the risk of incident AKI. Results: The overall multivariable adjusted ORs of AKI stages 1, 2, and 3 in patients on vancomycin vs. non-glycopeptides were 1.1 (1.1–1.2), 1.2 (1–1.4), and 1.4 (1.1–1.7), respectively. When examined in strata divided by vancomycin trough level, the odds of AKI were similar or lower in patients receiving vancomycin compared to non-glycopeptide antibiotics as long as serum vancomycin levels were ≤20 mg/L. However, in patients with serum vancomycin levels > 20 mg/L, the ORs of AKI stages 1, 2, and 3 in patients on vancomycin vs. non-glycopeptide antibiotics were 1.5 (1.4–1.7), 1.9 (1.5–2.3), and 2.7 (2–3.5), respectively. Conclusions: Vancomycin use is associated with a higher risk of AKI when serum levels exceed > 20 mg/L.
“…7 Information on medication use, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), loop or thiazide diuretics, potassium-sparing diuretics, β-blockers, and other antihypertensive medications, were extracted from VA Pharmacy dispensation records. 18 …”
Background
Recent studies suggest that potassium levels may differ by race. The basis for these differences and whether associations between potassium levels and adverse outcomes differ by race is unknown.
Study Design
Observational study.
Setting & Participants
Associations between race and potassium as well as the interaction of race and potassium with outcomes were investigated in the Racial and Cardiovascular Risk Anomalies in Chronic Kidney Disease (RCAV) study, a cohort of US veterans (N=2,662,462). Associations between African ancestry and potassium were investigated in African Americans in the Atherosclerosis Risk in Communities (ARIC) Study (N=3,450).
Predictors
Race (African American vs non-African American) for cross-sectional analysis; serum potassium as a continuous variable (for longitudinal analysis).
Outcomes
For cross-sectional analysis: potassium level; for longitudinal analysis: mortality and end-stage renal disease (ESRD) via linkage with the Veterans Affairs Vital Status File and the US Renal Data System.
Results
The RCAV cohort was 18% African American (N=470,985). Potassium levels were, on average, 0.162 mmol/L lower in African Americans compared to non-African Americans, with differences persisting after adjustment for demographics, comorbidities, and potassium-altering medication use. In the ARIC study, higher African ancestry was related to lower potassium levels (-0.027 mmol/L per each 10% African ancestry). In both race groups, higher and lower levels of potassium were associated with mortality. Compared to a potassium of 4.2 mmol/L, the mortality risk associated with lower levels of potassium was lesser in African Americans vs non-African Americans, whereas mortality risk associated with higher levels was slightly greater. For ESRD, risk-relationships were weaker, with no difference by race.
Limitations
No data on potassium intake.
Conclusions
African Americans had slightly lower serum potassium levels than non-African Americans. Consistent associations between potassium and percent African ancestry may suggest a genetic component to these differences. Higher and lower serum potassium levels were associated with mortality in both racial groups.
“…At the time of a post-discharge clinical review, future subsequent renal decline is uncertain, whereas the extent of nonrecovery can already be observed. Moreover, because the trajectory of renal decline can vary from a gradual to a catastrophic loss of function, 5 both hard outcomes (e.g., de novo long-term renal replacement therapy [RRT] or CKD stage 4) and intermediate outcomes (e.g., a 30% drop in kidney function) 6 are important for clinicians and their patients to understand when planning care.Figure 1 Renal progression after acute kidney injury (AKI) caused by renal decline (red solid line) or nonrecovery (pink dashed line). A patient with AKI who has incomplete post-episode recovery has a high risk of developing advanced chronic kidney disease (CKD) even if subsequent renal decline is slow (pink dashed line).…”
The extent to which renal progression after acute kidney injury (AKI) arises from an initial step drop in kidney function (incomplete recovery), or from a long-term trajectory of subsequent decline, is unclear. This makes it challenging to plan or time post-discharge follow-up. This study of 14651 hospital survivors in 2003 (1966 with AKI, 12685 no AKI) separates incomplete recovery from subsequent renal decline by using the post-discharge estimated glomerular filtration rate (eGFR) rather than the pre-admission as a new reference point for determining subsequent renal outcomes. Outcomes were sustained 30% renal decline and de novo CKD stage 4, followed from 2003-2013. Death was a competing risk. Overall, death was more common than subsequent renal decline (37.5% vs 11.3%) and CKD stage 4 (4.5%). Overall, 25.7% of AKI patients had non-recovery. Subsequent renal decline was greater after AKI (vs no AKI) (14.8% vs 10.8%). Renal decline after AKI (vs no AKI) was greatest among those with higher post-discharge eGFRs with multivariable hazard ratios of 2.29 (1.88-2.78); 1.50 (1.13-2.00); 0.94 (0.68-1.32) and 0.95 (0.64-1.41) at eGFRs of 60 or more; 45-59; 30-44 and under 30, respectively. The excess risk after AKI persisted over ten years of study, irrespective of AKI severity, or post-episode proteinuria. Thus, even if post-discharge kidney function returns to normal, hospital admission with AKI is associated with increased renal progression that persists for up to ten years. Follow-up plans should avoid false reassurance when eGFR after AKI returns to normal.
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