Acute Kidney Injury May Not Be As Uncommon As Believed in Children With Advanced Chronic Liver Diseases.

Abstract

The article by Berg et al is interesting, where they have directly measured the glomerular filtration rate (GFR) in children with chronic liver disease (CLD) and showed that many of these children had hyperfiltration (1). A novel, though unexplainable finding is the increased GFR and effective renal plasma flow in children with higher international normalized ratio, aspartate aminotransferase to platelet ratio index, high bile acid concentration, and lower albumin (1). A cross-sectional design is not an ideal choice for studying renal involvement in CLD, as acute kidney injury (AKI) can occur at various time points in the natural course, especially when the patient decompensates. In the present study, hypofiltration was present in 15.2% of children with CLD and only 1.5% of the control population. As the current definitions of AKI are based on an interval decrease in GFR, we can assume that the prevalence of renal dysfunction in this study was 15.2%. AKI had been shown to be present in 22.6% of children admitted with acute-on-chronic liver failure, 10.6% children with decompensated CLD and only 1.33% of children with compensated CLD (2). The frequency of AKI was 14.3% in children with CLD undergoing liver transplant (3). In addition, we have shown that presence of AKI leads to 7.7-fold higher risk of short-term mortality in advanced CLD (2). Hence, the conclusion by Berg et al that most children with CLD have well preserved renal functions may bring in a “false sense of security” to the readers and may delay the diagnosis as well as interventions. We believe that a high index of suspicion should be maintained for AKI, especially in decompensated CLD and an aggressive approach should be employed. It would be more informative if the authors could specify the percentage of patients with hyperfiltration/hypofiltration who fulfilled the current criteria for AKI/chronic kidney disease. Inclusion of heterogenous etiological groups and a fair number of noncirrhotic patients like glycogen storage disease who had high GFR could have decreased the significance of difference in GFR between CLD and controls. The authors have also included diseases like tyrosinemia and alagille's known to have primary renal involvement, which could lead to bias. The current emphasis while defining AKI in children as well as adults with CLD is on progressive rise in serum creatinine (4,5). In this study, eGFR overestimated lower mGFR and underestimated elevated mGFR. As lower body surface area in children leads to overestimation of GFR, absolute GFR gains significance. In fact, absolute mGFR correlated well with absolute eGFR (r = 0.82) in the present study (1). In current scenario, interval change in eGFR is easy and quick method to detect renal dysfunction and is best calculated by equations that employ a combination of creatinine, cystatin C, and growth parameters (6). With increasing evidence that hyperfiltration precedes end-stage kidney disease by several years, it would be interesting if the authors could monitor long-term renal functions of those who had initial hyperfiltration (7). To conclude, we need more studies in homogenous population to determine the true prevalence of AKI in CLD, but till then we need to maintain a high index of suspicion for early recognition of AKI as almost all modalities of treatment for AKI in CLD are effective if initiated early.