Individuals with conduct disorder are characterized as having reduced serotonin and cortisol levels (e.g., reduced hypothalamic-pituitary-adrenal (HPA) axis), as well as reduced autonomic nervous system (ANS) functioning. These reductions are associated with the inability to regulate mood and impulsive behaviors, weakened signals of anxiety and fear, and decreased self-esteem. Taken together, these findings may account for some of the variance in the psychological and behavioral patterns of youth with conduct disorder. Intra-individual factors
Aside from findings related to neurological and neurochemical profiles of youth with conduct disorder, intraindividual factors such as genetics may also be relevant. Having a sibling or parent with conduct disorder increases the likelihood of having the disorder, with a heritability rate of .53. There also tends to be a stronger genetic link for individuals with childhood-onset compared to adolescent onset. In addition, youth with conduct disorder also exhibit polymorphism in the monoamine oxidase A gene, low resting heart rates, and increased testosterone. Family and peer influences
Elements of the family and social environment may also play a role in the development and maintenance of conduct disorder. For instance, antisocial behavior suggestive of conduct disorder is associated with single parent status, parental divorce, large family size, and the young age of mothers. However, these factors are difficult to tease apart from other demographic variables that are known to be linked with conduct disorder, including poverty and low socioeconomic status.
The diagnosis can be made with many different imaging modalities such as ultrasound, intravenous pyelogram, CT, and MRI.Common features that can be found on imaging include:

Midline symmetrical fusion (present in 90% of cases) or lateral asymmetric fusion (present in 10% of cases) of the lower poles
Position of fused kidneys are lower than normal with incomplete medial rotation
Renal pelvis and ureters are positioned more anteriorly and ventrally cross the isthmus
Isthmus that may be positioned below the inferior mesenteric artery
Variant arterial supply that can originate from the abdominal aorta or common illiac arteries
Lower poles of kidney that extend ventromedially and may be poorly defined

Treatment
Symphysiotomy, which involves separating the fused isthmus in order to release the kidneys, used to be a recommended treatment for this condition but has fallen out of favor due to complications and minimal benefit. Furthermore, kidneys can remain in their original abnormal location after the surgery. Instead, management focuses on treating the sequelae should the patient become symptomatic.While treatment typically does not differ from that of patients with normal kidney anatomy, kidney stones can warrant a different approach. Extracorporeal shockwave lithotripsy, a possible treatment for kidney stones, can be less effective in patients with horseshoe kidneys due to the abnormal anatomy causing difficulties with localizing the energy to the stones. Also, due to the kidney obstruction that can commonly occur with this renal fusion, clearance of the resulting stone fragments can also be impaired.