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The aim of the present study was to determine urinary potassium (K) loss (as measured by fractional excretion of KFEK and transtubular Kgradient TTKG) in children with acute liver failure (ALF) and acute viral hepatitis (AVH) at the time of presentation to the hospital and day 45 of follow-up.

The aim of the present study was to determine urinary potassium (K+) loss (as measured by fractional excretion of K+[FEK] and transtubular K+gradient [TTKG]) in children with acute liver failure (ALF) and acute viral hepatitis (AVH) at the time of presentation to the hospital and day 45 of follow-up. Twenty-five patients with ALF and 84 patients with AVH were worked up for clinical features, liver function tests, and hepatitis viral infections and monitored for outcome. All of the patients with ALF were hospitalized. FEK and TTKG were estimated on the day patients were first seen in the hospital or hospitalized and later on day 45 of follow-up. Sixty percent (15/25) of patients with ALF were hypokalemic (serum K+<3.5 mEq/L) as compared with only 12% (10/84) in the AVH group (P= 0.000) at the time of presentation in the hospital. Inappropriate kaliuresis was present in 80% to 100% of hypokalemic children compared with 0% to 30% of normokalemic individuals at the time of first contact in either the ALF or AVH group. Inappropriate urinary K+loss and serum K+ levels in the hypokalemic individuals improved as the hepatic functions recovered by day 45 of follow-up (P= 0.014–0.000). No significant change in kaliuresis was observed among normokalemic subjects between first contact and later on day 45 of follow-up (P= 0.991–0.228). Despite different physiologic mechanisms, appropriateness of kaliuresis measured by FEK and TTKG showed results in the same direction. Hypokalemia and inappropriate kaliuresis observed during the acute phase of ALF and AVH reversed with clinical and biochemical recovery. In the absence of major gastrointestinal losses and renal abnormalities, there is need to investigate the contributory role of factors like hyperaldosteronism and food intake, which may have therapeutic implications.

The successful development of pediatric liver transplantation (LT) over the past four decades has dramatically changed the prognosis for children dying of acute and end-stage liver failure. Over the past two decades survival post transplantation has improved because of better preoperative management, optimal nutritional support, innovative surgical techniques, and improvements in immunosuppressive medications. The ensuing improvement in survival rate has extended the range of indications for LT in children to include transplantation for metabolic liver disease and unresectable hepatic tumors.

Chronic hepatitis B infection remains a significant global health problem. Acquisition during infancy or childhood causes many of the chronic infections that are responsible for the morbidity associated with this disease. Some children with chronic hepatitis B are candidates for treatment based on the viral load and presence of transaminitis. Three medications are currently licensed for use in children, and it is anticipated that others will be available in the next several years. This article reviews the current knowledge regarding the natural history and treatment of chronic hepatitis B in children.

Pediatric Liver Transplant (LT) is now an established procedure for End Stage Liver Disease (ESLD) with biliary atresia being the commonest indication. Intensive pre-transplant evaluation, nutritional buildup and immunization are the fundamental pre-requisites of a successful LT. With improvement in surgical micro-anastomotic techniques and superior immunosuppressive regimens the success rate of pediatric LT is in excess of 90%. Most of the transplants in our country however are Living related, due to which a fairly large number of children expire awaiting a donor liver. There should be a concerted effort to evolve the cadaveric donation program, so that majority of the children are benefitted.