Practicing nephrologists are frequently consulted to evaluate acute kidney injury (AKI) as inpatient cases. Some of these patients require temporary dialysis treatment during hospitalization, and some are discharged while dialysis therapy continues for a while.

Eventually, all such individuals should regain their baseline kidney function or we would call it chronic kidney disease (CKD) if the renal failure continues for more than three months. It appears that several conditions and medical interventions predispose patients to AKI, such as advanced age, diabetes, septicemia, intravenous (IV) contrast medium for imaging studies, and IV antibiotics. AKI does not develop in everybody who receives IV contrast, however. So, who are those unlucky patients who suffer kidney injury and who may not easily recover from it?

During our hospital rounds, I invariably tell our fellows and residents that in my opinion, all AKIs are “acute on chronic” (A-on-C) until proved otherwise. Whereas stating such a strong opinion may exhibit escalation of clinical naiveté, I have come to believe that more than 90% of all AKI cases would not have happened were it not for pre-existing CKD. Indeed, for me, the diagnosis of AKI serves as a marker of ongoing background CKD.

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Considering AKI as A-on-C has important clinical, medico-legal, and public health implications. Imagine an 82-year-old diabetic and sarcopenic woman who is admitted to the hospital with obstructive gallbladder disease presenting with febrile spikes, mild tachycardia, low blood pressure, right upper quadrant tenderness, and a serum creatinine level of 1.3 mg/dL.

Upon IV contrast and antibiotic administration, serum creatinine rises to above 5.0 mg/dL with oliguria, and the nephrologist starts dialysis or continuous renal replacement therapy. The patient is eventually discharged home while thrice-weekly hemodialysis continues for weeks to months, if not forever.

In this case, can care providers be blamed for having caused the “permanent damage” to the kidneys? Does a lawsuit have merit to this end? The literature is not clear about it, even though many clinicians would agree that the acute event was a mere precipitating factor to expose the underlying CKD, which is likely due to diabetic or ischemic nephropathy.

Some clinicians see a persistent disconnect between the AKI research and clinical practice. Although my opinion that all AKIs are A-on-C may be based on anecdotal and biased observations, AKI researchers need to understand the necessity of practice-based research so that the state of AKI as a marker of underlying CKD can be better examined and defined.

Kamyar Kalantar-Zadeh, MD, MPH, PhD, is Associate Professor of Medicine and Pediatrics, and Director, Dialysis Expansion & Epidemiology, Harbor-UCLA Division of Nephrology & Hypertension. He serves as Medical Director for Nephrolog atr Renal & Urology News.