For my part, I would consign the label MSBP to the history books and however useful FII may apparently be to the child protection practitioner I would caution against its use other than as a factual description of a series of incidents or behaviors that should then be accurately set out (and even then only in the hands of the pediatrician or psychiatrist/psychologist). I cannot emphasis too strongly that my conclusion cannot be used as a reason to re-open the many cases where facts have been found against a carer and the label MSBP or FII has been attached to that carers behavior. What I seek to caution against is the use of the label as a substitute for factual analysis and risk assessment. In his book Playing Sick (2004), Marc Feldman notes that such findings have been in the minority among U.S. and even Australian courts. Pediatricians and other physicians have banded together to oppose limitations on child-abuse professionals whose work includes FII detection. The April 2007 issue of the journal Pediatrics specifically mentions Meadow as an individual who has been inappropriately maligned. In the context of child protection (a child being removed from the custody of a parent), the Australian state of New South Wales uses a "on the balance of probabilities" test, rather than a "beyond reasonable doubt" test.
Other types of genetic cystic kidney disease include juvenile nephronophthisis (JNPHP), medullary cystic kidney disease (MCKD), and glomerulocystic kidney disease (GCKD). Polycystic Kidney Disease
PKD causes numerous cysts to grow in the kidneys. These cysts are filled with fluid and if they grow excessively, changing the shape of them and making them larger, leading to kidney damage. Mutations in genes PKD1 and PKD2 are responsible for autosomal dominant polycystic kidney disease (ADPKD), which is typically diagnosed in adulthood. Those genes encode for polycystic proteins and mutations regarding those genes are inherited and responsible for the disorder of autosomal dominant cystic kidney disease. In the United States, more than half a million people have PKD, making it the fourth leading cause of kidney failure. PKD affects all races and genders equally and those with PKD have a possibility of developing cysts in other organs such as liver, pancreas, spleen, ovaries, and large bowel. Usually, these latter cysts do not impose a problem. Half of patients have no manifestation of symptoms, but symptoms may include: hematuria, back or abdominal pain, or the development of hypertension. The disease is usually manifested before age 30, and 45% develop kidney failure by age 60. Mutation in the HDK1 gene is currently thought to be responsible for autosomal recessive polycystic kidney disease (ARPKD), which can be diagnosed in the womb, shortly after birth, and usually before 15 years of age. Cause
The site of preference for cyst development is the renal tubule.