Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired autoimmune disease of the peripheral nervous system characterized by progressive weakness and impaired sensory function in the legs and arms. The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy (because it involves the nerve roots). CIDP is closely related to Guillain–Barré syndrome and it is considered the chronic counterpart of that acute disease. Its symptoms are also similar to progressive inflammatory neuropathy. It is one of several types of neuropathy. Types
Several variants have been reported. Specially important are:

An asymmetrical variant of CIDP is known as Lewis-Sumner Syndrome. or MADSAM (multifocal acquired demyelinating sensory and motor neuropathy)
A variant with CNS involvement named combined central and peripheral demyelination (CCPD)Currently there is one special variant in which the CNS is also affected. It is termed "combined central and peripheral demyelination" (CCPD) and is special because it belongs at the same time to the CDIP syndrome and to the multiple sclerosis spectrum. These cases seem to be related to the presence of anti-neurofascin autoantibodies. Causes
Chronic inflammatory demyelinating polyneuropathy (or polyradiculoneuropathy) is considered an autoimmune disorder destroying myelin, the protective covering of the nerves. Typical early symptoms are "tingling" (sort of electrified vibration or paresthesia) or numbness in the extremities, frequent (night) leg cramps, loss of reflexes (in knees), muscle fasciculations, "vibration" feelings, loss of balance, general muscle cramping and nerve pain.
Other ANCA small-vessel vasculitides - The conditions included in this category are eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis, and granulomatosis with polyangiitis. Pathophysiology
The pathophysiology of nephritic syndrome is dependent on the underlying disease process, which can vary depending on what condition the nephritic syndrome is secondary to. More specifically, different diseases (many of which are mentioned above in the Causes section) affect different segments of the glomerulus and cause disease-specific segments of the glomerulus to become inflamed. Most often, it is dependent on what part of the glomerulus is damaged by antibody-antigen complex (immune complex) deposition. In all cases, however, the inflammatory processes in the glomerulus cause the capillaries to swell and the pores between podocytes become large enough that inappropriate contents in the blood plasma (i.e. red blood cells, protein, etc.) will begin to spill into the urine. This causes a decrease in glomerular filtration rate (GFR) and, if left untreated over time, will eventually produce uremic symptoms and retention of sodium and water in the body, leading to both edema and hypertension. Diagnosis
The diagnostic approach to nephritic syndrome includes evaluating the patient for any suspected underlying pathology that could cause a nephritic syndrome. Physical examination
If the person in the office is being examined by a physician, some physical exam findings consistent with nephritic syndrome include the following:

Edema - This could present as generalized edema (anasarca) or specific swelling of the hands, feet, and/or face.