Acute kidney injury (AKI) is increasingly common [1] and is associated with negative short-term outcome partly as consequences of distant organ–kidney interactions [2]. More strikingly, even mild AKI is related… Click to show full abstract
Acute kidney injury (AKI) is increasingly common [1] and is associated with negative short-term outcome partly as consequences of distant organ–kidney interactions [2]. More strikingly, even mild AKI is related to long-term mortality in ICU survivors [3], increased risk of chronic and end-stage kidney diseases [4], and increased risk of major cardiovascular events [5]. Although risk seems to be correlated with severity and duration of AKI, even mild and transient AKI is associated with higher mortality and morbidity [3, 6]. Data from ICU survivors suggest that nephron loss occurs following AKI, leading to long-term renal dysfunction: the more severe the AKI is, the more severe the renal sequela is [7]. In this regard, the risk of chronic kidney disease (CKD) and end-stage CKD has been described to be increased by ninefold and fourfold, respectively [4]. Despite the increasing number of studies in this field, the exact epidemiology of renal function following ICU stay remains blurry mainly as a result of the unavoidable number of patients with unknown baseline renal function, the lack of consensus to define renal recovery, and time-dependency of the renal recovery or progression toward CKD [8]. Patients who died will never develop CKD, a limitation not often taken into account in available reports [8]. Furthermore, renal function as assessed by serum creatinine at ICU discharge is unreliable and impaired by sarcopenia [9]. Finally, the impact of subclinical AKI on subsequent nephron loss and risk of CKD is unknown and frequently unmentioned. In view of this evidence, and to adequately assess renal history and deal with remaining uncertainties, a systematic follow-up by a nephrologist with adequate renal function assessment may be required. Beyond research, early and prolonged follow-up by a nephrologist in ICU patients with AKI is mostly theoretical or supported by evidence with a high risk of bias. Although the bulk of ICU-acquired AKI is believed to be multifactorial, specific causes of AKI are often seen in ICU patients and may require specific diagnostic testing or management. Some of these aetiologies, such as postinfectious glomerulonephritis or acute interstitial nephritis, are probably underestimated, and assistance from a nephrologist should be sought more frequently. The benefit from such early nephrologist involvement has been suggested by low level evidence studies [10]. In some countries, their help might also be required to select an adequate renal replacement modality and run intermittent haemodialysis, the latter limiting need for anticoagulation, limiting costs and performing better in subgroups of patients without shock [11, 12]. Finally, they may participate in ICU multidisciplinary daily rounds, increasing quality and safety as suggested by guidelines from the European Society of Intensive Care Medicine [13]. Later during the ICU stay, at the time of ICU or hospital discharge, their help might be required in assessing residual function, identifying high-risk patients and selecting subgroups of patients in whom renal recovery might deserve to be more clearly assessed. Finally, a nephrologist will obviously be the best-suited clinician to arrange for a proper follow-up, most conveniently through an outpatient nephrology clinic. Although input of a nephrologist is to a large extent speculative, there is some evidence that suggests an improved survival rate associated with de novo follow-up by a nephrologist in survivors of AKI [14]. *Correspondence: [email protected] 1 General ICU, KSK Haukeland University Hospital and Department of Clinical Medicine, University of Bergen, Bergen, Norway Full author information is available at the end of the article
               
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