Encouraging a child with separation anxiety disorder to feel competent and empowered, as well as to discuss feelings associated with anxiety-provoking events promotes recovery. Children with separation anxiety disorder often respond negatively to perceived anxiety in their caretakers, in that parents and caregivers who also have anxiety disorders may unwittingly confirm a childs unrealistic fears that something terrible may happen if they are separated from each other. Thus, it is critical that parents and caretakers become aware of their own feelings and communicate a sense of safety and confidence about separation. Longitudinal effects
Several studies aim to understand the long-term mental health consequences of SAD. SAD contributed to vulnerability and acted as a strong risk factor for developing other mental disorders in people aged 19–30. Specifically disorders including panic disorder and depressive disorders were more likely to occur. Other sources also support the increased likelihood of displaying either of the two psychopathologies with previous history of childhood SAD.Studies show that children who have separation anxiety at younger ages have more complex fear acquisition. This means that there is likely an interplay between associative and non-associative processes concerning fear and anxiety later in life. Epidemiology
Anxiety disorders are the most common type of psychopathology to occur in todays youth, affecting from 5–25% of children worldwide. Of these anxiety disorders, SAD accounts for a large proportion of diagnoses. SAD may account for up to 50% of the anxiety disorders as recorded in referrals for mental health treatment. SAD is noted as one of the earliest-occurring of all anxiety disorders.
Mutations in the genes AGXT  and GRHPR cause PH1 and PH2, respectively, through decreased production or activity of the proteins they make, which stops the normal breakdown of glyoxylate. Similarly, mutations in the gene HOGA1 cause PH3 due to loss-of-function mutations resulting in impaired protein function.PH1 is considered to be the most common and rapidly progressing form, accounting for about 80% of all currently diagnosed cases and PH2 and PH3 accounting for approximately 10% each of the current cases. However, recent evidence has suggested that PH2 and PH3 are not as benign as previously thought, with up to 50% of patients with PH2 developing kidney failure (chronic kidney disease [CKD] stage 5). While current estimates indicate that kidney failure is rarer in patients with PH3 compared to PH1 and PH2, CKD has been reported in patients with PH3. Moreover, the genetic prevalence based on known PH3 variants is much higher than the diagnosed prevalence of the disease, which could mean either incomplete penetrance (i.e. variant present with no clinical symptoms) or underdiagnosis (i.e. variant present with clinical symptoms but not diagnosed). Treatment
Increased water intake and alkalinization of urine is advised to prevent oxalate precipitation in urinary tract. In addition, Vitamin B6 (pyridoxine) is used to treat PH1 because alanine glyoxylate transaminase requires pyridoxine as cofactor. In approximately one third of patients with PH1, pyridoxine treatment decreases oxalate excretion and prevent kidney stone formation.