In the European Union, the license is slightly more restrictive: it is licensed for use in combination with MTX in patients with severe active RA who have had an inadequate response to one or more anti-TNF therapy.There is some evidence for efficacy, but not necessarily safety, in a range of other autoimmune diseases, and rituximab is widely used off-label to treat difficult cases of multiple sclerosis, systemic lupus erythematosus, chronic inflammatory demyelinating polyneuropathy and autoimmune anemias. The most dangerous, although among the most rare, side effect is progressive multifocal leukoencephalopathy (PML) infection, which is usually fatal; however only a very small number of cases have been recorded occurring in autoimmune diseases.Other autoimmune diseases that have been treated with rituximab include autoimmune hemolytic anemia, pure red cell aplasia, thrombotic thrombocytopenic purpura (TTP), idiopathic thrombocytopenic purpura (ITP), Evans syndrome, vasculitis (e.g., granulomatosis with polyangiitis), bullous skin disorders (for example pemphigus, pemphigoid—with very encouraging results of approximately 85% rapid recovery in pemphigus, according to a 2006 study), type 1 diabetes mellitus, Sjögren syndrome, anti-NMDA receptor encephalitis and Devics disease, Graves ophthalmopathy, autoimmune pancreatitis, Opsoclonus myoclonus syndrome (OMS), and IgG4-related disease. There is some evidence that it is ineffective in treating IgA-mediated autoimmune diseases.
Nocturnal polyuria
Nocturnal polyuria is defined as an increase in urine production during the night but with a proportional decrease in daytime urine production that results in a normal 24-hour urine volume. With the 24-hour urine production within normal limits, nocturnal polyuria can be translated to having a nocturnal polyuria index (NPi) greater than 35% of the normal 24-hour urine volume. NPi is calculated simply by dividing NUV by the 24-hour urine volume. Similar to the inability of control urination, a disruption of arginine vasopressin (ADH) levels has been proposed for nocturia. Compared with the normal patients, nocturia patients have a nocturnal decrease in ADH level.Other causes of nocturnal polyuria include diseases such as

congestive heart failure
nephritic syndrome
liver failure
lifestyle patterns such as excessive nighttime drinking
sleep apnea increasing obstructive airway resistance. Obstructive sleep apnea sufferers have shown to have increases in renal sodium and water excretion that are mediated by elevated plasma atrial natriuretic hormone (ANH) levels. ANH is released by cardiac muscle cells in response to high blood volume. When activated, ANH releases water, subsequently increasing urine production. Bladder storage
Normal human bladder storage capacity varies from person to person and is considered 400 – 600 mL. A bladder storage disorder is any factor that increases the frequency of small volume voids. These factors are usually related to lower urinary tract symptoms that affect the capacity of the bladder. Some patients with nocturia have neither global nor nocturnal polyuria according to the above criteria.