Acute kidney injury is a risk factor for subsequent proteinuria

Abstract

Acute kidney injury (AKI) is associated with subsequent chronic kidney disease (CKD), but the mechanism is unclear. To clarify this, we examined the association of AKI and new-onset or worsening proteinuria during the 12 months following hospitalization in a national retrospective cohort of United States Veterans hospitalized between 2004-2012. Patients with and without AKI were matched using baseline demographics, comorbidities, proteinuria, estimated glomerular filtration rate, blood pressure, angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker (ACEI/ARB) use, and inpatient exposures linked to AKI. The distribution of proteinuria over one year post-discharge in the matched cohort was compared using inverse probability sampling weights. Subgroup analyses were based on diabetes, pre-admission ACEI/ARB use, and AKI severity. Among the 90,614 matched AKI and non-AKI pairs, the median estimated glomerular filtration rate was 62 mL/min/1.73m. The prevalence of diabetes and hypertension were 48% and 78%, respectively. The odds of having one plus or greater dipstick proteinuria was significantly higher during each month of follow-up in patients with AKI than in patients without AKI (odds ratio range 1.20-1.39). Odds were higher in patients with Stage II or III AKI (odds ratios 1.32-1.81) than in Stage I AKI (odds ratios 1.18-1.32), using non-AKI as the reference group. Results were consistent regardless of diabetes status or baseline ACEI/ARB use. Thus, AKI is a risk factor for incident or worsening proteinuria, suggesting a possible mechanism linking AKI and future CKD. The type of proteinuria, physiology, and clinical significance warrant further study as a potentially modifiable risk factor in the pathway from AKI to CKD.

Is the kidney a target of SARS-CoV-2?

“…Interestingly, patients with COVID-19 with elevated serum creatinine at admission exhibited a higher incidence of moderate proteinuria compared with those with normal serum creatinine (30.2% vs. 7.5%) (13). However, there is no evidence that this depends on a disturbed RAAS and actually relies on the proximal tubule cell response to injury, including the transient loss of polarity and cell death (7,54).…”

The Clinical Course of Acute Kidney Disease after Cardiac Surgery: A Retrospective Observational Study

“…However, the trajectory of AKD remains poorly elucidated.Cardiac surgery-associated AKI (CSA-AKI) is the second most common type of AKI (next to septic shock) and is associated with high in-hospital mortality 9,10 . In addition, CSA-AKI is proven to be a risk for CKD [11][12][13] . Among the characteristics of CSA-AKI are the various timings of occurrence (early or late phase after cardiac surgery) and the various clinical courses (transient or persistent renal dysfunction) due to the complex pathophysiology of CSA-AKI, which includes hemodynamic instability, mechanical stress such as cardiopulmonary bypass, inflammation, oxidative stress, neurohormonal factors, nephrotoxic agents and postoperative complications such as infections 14 .…”

Endogenous factors and mechanisms of renoprotection and renal repair

“…2 The phenotype of progression of CKD is usually described by two biomarkers: albuminuria and glomerular filtration rate (GFR). 8,9 With the rise of "omics" techniques, it has become evident that on a molecular level, CKD is even much more complex with multiple processes interacting. 3 Research typically focuses on specific factors and pathways that drive the progression of CKD with the ultimate aim to identify targets for intervention.…”

“…7 Research also identified acute kidney injury (AKI) as risk factor for the development of CKD, which also affects injury and repair mechanisms. 8,9 With the rise of "omics" techniques, it has become evident that on a molecular level, CKD is even much more complex with multiple processes interacting. 10 Furthermore, intrinsic protective pathways have been identified as well counterbalancing deleterious developments, and probably the rate of progression of CKD is ultimately determined by the balance between injury and repair.…”