William “Kegley” Hubbard was born August 16^th 2003.

    Kegley had a typical birth without complications, and developed into an extremely happy and hyper toddler with typical milestones – crawling, running, and especially jumping from chair to couch and back. No ear infections, stomach viruses, strep throat or any typical childhood illnesses ever seemed to affect him.

     In March 2005 Kegley complained of feeling tired and went to bed early – he slept most of the weekend and on Monday we took him to his pediatrician. At that time it was thought he had the flu, but his white count was not elevated. The PA in his office requested a CBC and, after testing, it was noted that his platelets seemed low but not so low as to be concerned. A hematologist was consulted and he agreed. Over the course of the next three days, further tests were completed on an outpatient basis. Kegley’s urine had turned from yellow to neon green to black and by Wednesday he was admitted to the pediatric ICU in order to be tested for leukemia, lupus, and various other diseases. At this point Kegley had stopped producing urine and had frighteningly low platelets and red blood cells. The cause of these symptoms was unknown and the treatment protocol fluctuated between the use of IVIg, steroids to depress his immune system and the suggestion of chemotherapy drugs. Kidney failure was imminent. Treatment became supportive. Strangely, by Thursday and Friday his condition began to improve. Late Friday his system had returned to normal and he was discharged from the hospital on Saturday.  At that time we had not received a diagnosis – just the supposition from the hematologist that his immune system was immature and he would probably grow out of it.  Kegley continued to grow and remain healthy over the course of two years.

      The last Friday of February 2007 Kegley again went to bed early and slept most of the weekend. By Monday his urine was black and again his platelets and red blood cells were low. Kegley progressed into renal failure and  was transferred to Egleston as an inpatient. The same medications were used again on a trial basis with no idea as to whether they would be effective. Fortunately, Kegley’s symptoms progressed as before and he was better by Saturday. Kegley was diagnosed with AHUS at Egleston – however, the underlying genetic mutation was not identified until August 2007.

     At this time we do not know what triggers AHUS in Kegley. We do not have an effective treatment once he becomes ill. Due to Kegley’s particular genetic mutation, plasma pheresis and various other treatments would be ineffective. Research into better diagnostics, preventative measures, and effective medications is the key to healthy futures for Kegley, Hyde, Bryan, and other children affected by AHUS.