Growth failure is a clinically important issue in children with chronic kidney disease (CKD) and is associated with significant morbidity and mortality. Many factors contribute to impaired growth in these children, including abnormalities in the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis, malnutrition, acidosis, and renal bone disease. The management of growth failure in children with CKD is complicated by the presence of other disease-related complications requiring medical intervention. Despite evidence of GH efficacy and safety in this population, some practitioners and families have been reluctant to institute GH therapy, citing an unwillingness to comply with daily injections, reimbursement difficulties, or impending renal transplantation. Suboptimal attention to growth failure management may be further compounded by a lack of clinical guidelines for the appropriate assessment and treatment of growth failure in these children. This review of growth failure in children with CKD concludes with an algorithm developed by members of the consensus committee, outlining their recommendations for appropriate steps to improve growth and overall health outcomes in children with CKD.

The impact of FSGS on graft survival in children is greatest in LD transplants, resulting in loss of expected LD graft survival advantage. The rationale for LD grafts in children with FSGS should be based on factors other than better outcomes typically associated with LD transplantation.

The hemolytic uremic syndrome (HUS) is most commonly associated with Escherichia coli, but has been associated with other infections such as Streptococcus pneumoniae. Pneumococcus-induced HUS carries an increased risk of mortality and renal morbidity compared with E. coli-induced HUS. The pneumococcal organism produces an enzyme, which can expose an antigen (T-antigen) present on erythrocytes, platelets, and glomeruli. Antibodies to the T-antigen, normally found in human serum, bind the exposed T-antigen, and the resultant antigen-antibody reaction (T-activation) can lead to HUS and anemia. Clinicians need to be aware to request specific testing when pneumococcus-induced HUS/anemia is suspected, as current blood banking techniques do not routinely test for the presence of the T-antigen. Once this association is documented, washing all blood products and avoiding plasma products, if possible, is recommended. Plasmapheresis can be considered for the more critically ill patient. The incidence of pneumococcus-induced HUS may be increasing. We report six cases of pneumococcus-induced HUS/anemia presenting at our hospital.

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A 14-month-old girl with chronic renal insufficiency received a massive overdose of vancomycin, resulting in worsened renal failure and ototoxicity. We report the use of combined charcoal hemoperfusion and dialysis to accelerate vancomycin removal in this patient.

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