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.
Pantothenate kinase-associated neurodegeneration (PKAN), formerly called Hallervorden–Spatz syndrome, is a genetic degenerative disease of the brain that can lead to parkinsonism, dystonia, dementia, and ultimately death. Neurodegeneration in PKAN is accompanied by an excess of iron that progressively builds up in the brain. PKAN is caused by loss of function of the enzyme PANK2, due to bi-allelic genetic mutations. It follows autosomal recessive inheritance. This enzyme is the first step in the pathway converting vitamin B5 into coenzyme A. There are currently no treatments that modify disease progress, though there are a number of medications and therapies that can help improve symptoms and there is active research into treatments. Signs and symptoms
Symptoms typically begin in childhood and are progressive, often resulting in death by early adulthood. Symptoms of PKAN begin before middle childhood, and most often are noticed before ten years of age. Symptoms include:
dystonia (repetitive uncontrollable muscle contractions that may cause jerking or twisting of certain muscle groups)
dysphagia & dysarthria due to muscle groups involved in speech being involved
rigidity/stiffness of limbs
tremor
writhing movements
dementia
spasticity
weakness
seizures (rare)
toe walking
retinitis pigmentosa, another degenerative disease that affects the individuals retina, often causing alteration of retinal color and progressive deterioration of the retina at first causing night blindness and later resulting in a complete loss of vision.25% of individuals experience an uncharacteristic form of PKAN that develops post-10 years of age and follows a slower, more gradual pace of deterioration than those pre-10 years of age.