Initial workup can include a urinalysis, kidney function tests, serum albumin level and a lipid panel. Microscopic amounts of blood are present in the urine of 10-30% adults with MCD.As MCD is the most common type of nephrotic syndrome in children, renal biopsy is not usually done in children under the age of 10 unless there are concerning features that are unusual for the disease (high blood pressure, bloody urine, renal dysfunction) and if they fail to respond to corticosteroid therapy. These would suggest that it may not be minimal change disease. In adults, a renal biopsy is required as there is a much wider differential for nephrotic syndrome. As the name suggests, the renal biopsy of a patient with minimal change disease would show minimal or no evidence of disease in light microscopy, which is unique among the causes of nephrotic syndrome. Treatment
Children
The first line therapy to minimal change disease is corticosteroids T.Prednisolone 60mg/sq.m/day or 2mg/kg/day. For those are who are unable to tolerate corticosteroid treatment, cyclosporine is an alternative; other immunosuppressants have also been used such as calcineurin inhibitor, mycophenolate mofetil, rituximab though studies on their effectiveness is fairly limited. There is no common consensus on how long the corticosteroid therapy should be, with treatment length ranging from 4–12 weeks. Along with corticosteroid therapy, acute symptomatic management involves salt and fluid restriction to control the swelling.For children who do not respond to corticosteroids (usually after a trial of 8 weeks), cyclosporine can be tried.
Birth trauma or intrauterine malposition is considered to be the cause of damage to the sternocleidomastoid muscle in the neck. Other alterations to the muscle tissue arise from repetitive microtrauma within the womb or a sudden change in the calcium concentration in the body which causes a prolonged period of muscle contraction.Any of these mechanisms can result in a shortening or excessive contraction of the sternocleidomastoid muscle, which curtails its range of motion in both rotation and lateral bending. The head typically is tilted in lateral bending toward the affected muscle and rotated toward the opposite side. In other words,  the head itself is tilted in the direction towards the shortened muscle with the chin tilted in the opposite direction.Congenital Torticollis is presented at 1–4 weeks of age, and a hard mass usually develops. It is normally diagnosed using ultrasonography and a colour histogram or clinically through evaluating the infants passive cervical range of motion.Congenital torticollis constitutes the majority of cases seen in clinical practice. The reported incidence of congenital torticollis is 0.3-2.0%. Sometimes a mass, such as a sternocleidomastoid tumor, is noted in the affected muscle. Torticollis does not resolve on its own and may result in plagiocephaly. Acquired torticollis
Noncongenital muscular torticollis may result from scarring or disease of cervical vertebrae, adenitis, tonsillitis, rheumatism, enlarged cervical glands, retropharyngeal abscess, or cerebellar tumors. It may be spasmodic (clonic) or permanent (tonic). The latter type may be due to Potts Disease (tuberculosis of the spine).