Reply to: “To close the stable door before the horse has bolted”
Authors: Salvatore Piano, Filippo Morando, Paolo Angeli
Journal: Journal of Hepatology (2013)

Evaluation of the Acute Kidney Injury Network criteria in hospitalized patients with cirrhosis and ascitesJournal of HepatologyVol. 59Issue 3PreviewFor several years hepatologists have defined acute renal failure in patients with cirrhosis as an increase in serum creatinine (sCr) ⩾50% to a final value of sCr >1.5 mg/dl (conventional criterion). Recently, the Acute Kidney Injury Network (AKIN) defined acute renal failure as acute kidney injury (AKI) on the basis of an absolute increase in sCr of 0.3 mg/dl or a percentage increase in sCr ⩾50% providing also a staging from 1 to 3. AKIN stage 1 was defined as an increase in sCr ⩾0.3 mg/dl or increase in sCr ⩾1.5-fold to 2-fold from baseline. Full-Text PDF To close the stable door before the horse has boltedJournal of HepatologyVol. 60Issue 3PreviewWe read with interest the studies by Fagundes and colleagues [1], Piano and colleagues [2] and the accompanying editorial [3]. Full-Text PDF Open AccessA modified acute kidney injury classification for diagnosis and risk stratification of impairment of kidney function in cirrhosisJournal of HepatologyVol. 59Issue 3PreviewThe Acute Kidney Injury Network (AKIN) criteria are widely used in nephrology, but information on cirrhosis is limited. We aimed at evaluating the AKIN criteria and their relationship with the cause of kidney impairment and survival. Full-Text PDF To the Editor: We want to thank Thalheimer et al. for their interest in our study and the Fagundes study recently published in Journal of Hepatology regarding the application of acute kidney injury network (AKIN) criteria in the diagnosis of acute kidney injury (AKI) in patients with cirrhosis and ascites [1Piano S. Rosi S. Maresio G. Fasolato S. Cavallin M. Romano A. et al.Evaluation of the acute kidney injury network criteria in hospitalized patients with cirrhosis and ascites.J Hepatol. 2013; 59: 482-489Abstract Full Text Full Text PDF PubMed Scopus (208) Google Scholar, 2Fagundes C. Barreto R. Guevara M. Garcia E. Sola E. Rodriguez E. et al.A modified acute kidney injury classification for diagnosis and risk stratification of impairment of kidney function in cirrhosis.J Hepatol. 2013; 59: 474-481Abstract Full Text Full Text PDF PubMed Scopus (218) Google Scholar]. In their letter Thalheimer et al. highlighted that although patients with stage 1 AKI and serum creatinine (sCr) <1.5 mg/dl did not show a higher mortality rate with respect to patients without AKI, stage 1 AKI with a sCr <1.5 mg/dl should not be considered a benign condition [[3]Thalheimer U, Burrhougs AK. To close the stable door before the horse has bolted. J Hepatol 2014;60:678–679.Google Scholar]. We are in agreement with Thalheimer et al. and we did not define it as a benign condition. Currently, there is no evidence that AKI stage 1 with a final value lower than 1.5 mg/dl is associated with a higher hospital and or 90-day mortality rate in patients with cirrhosis [1Piano S. Rosi S. Maresio G. Fasolato S. Cavallin M. Romano A. et al.Evaluation of the acute kidney injury network criteria in hospitalized patients with cirrhosis and ascites.J Hepatol. 2013; 59: 482-489Abstract Full Text Full Text PDF PubMed Scopus (208) Google Scholar, 2Fagundes C. Barreto R. Guevara M. Garcia E. Sola E. Rodriguez E. et al.A modified acute kidney injury classification for diagnosis and risk stratification of impairment of kidney function in cirrhosis.J Hepatol. 2013; 59: 474-481Abstract Full Text Full Text PDF PubMed Scopus (218) Google Scholar, 4Bucsics T. Schwabl P. Soucek K. Mandorfer M. Ferlitsch A. Peck-Radosavljevic M. et al.Is acute kidney injury stage 1 (AKI 1) according to modified AKIN criteria associated with higher mortality in cirrhotic patients with ascites?.Hepatology. 2013; 58 ([abstract]): 864AGoogle Scholar]. Furthermore, in our study, patients with AKI stage 1 and sCr <1.5 mg/dl had a low rate of progression of AKI stage and a high rate of resolution of AKI. Nevertheless, an AKI with these features is associated with an increase in the medium-term mortality [[5]Tsien C.D. Rabie R. Wong F. Acute kidney injury in decompensated cirrhosis.Gut. 2013; 62: 131-137Crossref PubMed Scopus (188) Google Scholar]. Therefore, the question is not if to treat or not to treat AKI stage 1 with sCr <1.5 mg/dl, but how to treat it in order to prevent a further renal impairment and thereby avoid an unjustified early use of some therapeutic resources, which are expensive and/or may induce severe adverse effects, such as vasoconstrictors. Regarding this last point, we should recognize that both in our study and in Fagundes’s study, almost all patients with AKI and sCr <1.5 mg/dl were effectively treated with simple measures: tapering or withdrawal of diuretics, withdrawal of nephrotoxic drugs, vasodilators or non-steroidal anti-inflammatory drugs (NSAIDs), plasma volume expansion in case of dehydration, the treatment of any bacterial infections when diagnosed. In our opinion, these measures should be applied soon to all patients with AKI. This is the reason why these measures were suggested in the algorithm for the management of AKI in patients with cirrhosis and ascites, which we recently proposed [[1]Piano S. Rosi S. Maresio G. Fasolato S. Cavallin M. Romano A. et al.Evaluation of the acute kidney injury network criteria in hospitalized patients with cirrhosis and ascites.J Hepatol. 2013; 59: 482-489Abstract Full Text Full Text PDF PubMed Scopus (208) Google Scholar]. More in detail, patients with cirrhosis and ascites with initial AKIN stage 1 without progression and with a sCr <1.5 mg/dl should be treated as soon as possible by the therapeutic approach previously discussed. Plasma volume expansion with albumin was proposed in patients with initial AKIN stage higher than 1 and in those with initial AKIN stage 1 and sCr ⩾1.5 mg/dl or with progression towards a higher stage in spite of the therapeutic measures previously suggested. The further treatment of patients who do not respond to the withdrawal of diuretics and plasma volume expansion will depend, of course, on the final diagnosis of the AKI phenotype. Therefore, summing up, this algorithm implies the following:•The acceptance of the main point that derived from the application of AKIN criteria that is to focus attention on and to manage promptly even small increases in sCr.•The maintenance of a sCr cut off value (1.5 mg/dl) not to define AKI, but to titrate its treatment.•A more rational application of the therapeutic resources (avoiding the potentially dangerous consequences of an overtreatment of AKI as a consequence of an uncritical application of the AKIN criteria).•A clear distinction between AKI and HRS, since HRS is only one among the possible phenotypes of AKI.•The definitive removal of any cut off of sCr from the criteria for diagnosis of HRS in the setting of AKI. This algorithm is a simple working hypothesis and large perspective interventional studies are needed to validate it. Nevertheless, it appears a step forward in the management of AKI in these patients. The authors who have taken part in this study declared that they do not have anything to disclose regarding funding or conflicts of interest with respect to this manuscript.