The boys were never able to sit up on their own, and none learned how to talk. They all had a characteristically aged appearance, earning them the family nickname of "little old men." Several of the boys had structural anomalies of their hearts including ventricular septal defect, atrial septal defect, and pulmonary artery stenosis. Events recorded on electrocardiogram before death included torsades de pointes, premature ventricular contraction (PVC), premature atrial contraction (PAC), supraventricular tachycardia (SVtach), and ventricular tachycardia (Vtach). Most of the children had inguinal hernias, and the majority had, at least, unilateral cryptorchidism. All had neonatal hypotonia progressing to hypertonia, and cerebral atrophy on MRI; several, but not all, had neurogenic scoliosis. Death occurred prior to two years in all cases and prior to one year in the majority. There are extensive clinical details for each child reported in the original publication

Biochemistry
Ogden syndrome is a lethal X-linked recessive condition. Because the affected gene is on the X-chromosome, it affects males far more severely due to the fact that males only carry one copy of the X chromosome so the mutation is in every cell but females carry two and therefore some cells may use the non mutated copy and others use the mutated copy. It was the first reported human genetic disorder linked with a mutation in an N-terminal acetyltransferase (NAT) gene. The original Ogden family males have the Ser37Pro (S37P) mutation in the gene encoding NAA10, the catalytic subunit of NatA, the major human enzyme heterodimer involved in the post-translational acetylation of proteins.
Retroperitoneal fibrosis or Ormonds disease is a disease featuring the proliferation of fibrous tissue in the retroperitoneum, the compartment of the body containing the kidneys, aorta, renal tract, and various other structures. It may present with lower back pain, kidney failure, hypertension, deep vein thrombosis, and other obstructive symptoms. It is named after John Kelso Ormond, who rediscovered the condition in 1948. Causes
The association of idiopathic retroperitoneal fibrosis with various immune-related conditions and response to immunosuppression led to a search for an autoimmune cause of idiopathic RPF. Many of these previously idiopathic cases can now be attributed to IgG4-related disease, an autoimmune disorder proposed in 2003. Otherwise, one-third of cases are secondary to malignancy, medication (methysergide, hydralazine, beta blockers), prior radiotherapy, or certain infections.Other associations include:

connective tissue disease
Riedels thyroiditis
sclerosing cholangitis
membranous nephropathy
ankylosing spondylitis
inflammatory bowel disease
ANCA-associated vasculitis
autoimmune pancreatitis
sarcoidosis
primary biliary cirrhosis
inflammatory abdominal aortic aneurysm

Diagnosis
The diagnosis of retroperitoneal fibrosis cannot be made on the basis of the results of laboratory studies. CT is the best diagnostic modality: a confluent mass surrounding the aorta and common iliac arteries can be seen. On MRI, it has low T1 signal intensity and variable T2 signal. Malignant retroperitoneal fibrosis usually gives uneven MRI signals, is bulky, extends above the origins of renal arteries, or displaces the aorta anteriorly.