Acute Kidney Injury and Clinical Outcomes

A paper in the Mayo Clinic Proceedings, Acute Kidney Injury Predicts Outcomes of Non–Critically Ill Patients, examines the effect of Acute Kidney Injury (AKI) on the clinical out comes almost 6000 patients at a community teaching hospital affiliated with Yale. AKI was deined as an increase in serum creatinine of at least 0.3mg/dL over 48 hours or less. 735 patients with AKI and 5089 controls were studied.

The study was a followup to the observations of Chertow, et al in 2005. They showed that “Modest changes in serum creatinine were significantly associated with mortality, length of hospitalization, and costs, even after adjustment for age, gender, admission International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis, severity of illness.” The hypothesis for the newer study “was that AKI similarly predicts in-hospital mortality, need for renal replacement therapy, and prolonged hospital stays of non–critically ill patients,” which is not much different from what Chertow, et al looked at, but it’s still worth revisiting

Not surprisingly outcomes were much worse in patients with AKI compared to those whose renal function remained intact.The table below shows that AKI group had a likelihood of death almost eight greater than patients without AKI. The other outcomes examined were similarly worse than controls.

Adverse outcomes

Several comments are appropriate. A rise in creatinine even when modest signals a breakdown in homeostasis which portends an ominous outcome. The kidney normally receives 20% of cardiac output. When volume regulation is impaired irrespective of cause renal blood flow falls. This has the effect of redirecting blood flow to vital organs that poorly tolerate decreased blood flow, eg the heart and brain.  Thus volume contraction, heart failure,  severe infection, liver disease, and on and on may cause reduced kidney perfusion and a rise in creatinine. The rise in creatinine indicates associated medical problems which are going to make life shorter, more unpleasant, or both for the patient. The clinician who encounters this situation must ensure that his diagnosis is complete and that treatment is inclusive.

The next issue is the term “AKI” itself. It’s relatively new and not an improvement on “acute renal failure” which it replaced. Kidney function commonly deteriorates without true tissue injury. The kidney has a great tolerance for underperfusion. The term “prerenal azotemia” describes reversible renal insufficiency due to underperfusion which does not cause significant (or any) tissue injury. Using the term “kidney injury” to denote a condition without kidney injury does not represent a nosological improvement.

Many of the patients whose creatinine jumps 0.3 mg/dL or more in the hospital don’t have kidney injury. Restore perfusion and renal function returns to what it was. Why the change in terminology? The same reason medical schools keep changing the curriculum. It’s about the only issue confronting a medical school that the school can do anything about; it’s powerless over everything else. We can change words much easier than substance.There’s also the hidden, but real, purpose of language – to confuse rather than communicate. Regardless. try to prevent your patient’s creatinine from rising, but if it does figure out why and fix things if you can. If you can’t alert the next of kin.

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