Pyelonephritis  is inflammation of the kidney, typically due to a bacterial infection. Symptoms most often include fever and flank tenderness. Other symptoms may include nausea, burning with urination, and frequent urination. Complications may include pus around the kidney, sepsis, or kidney failure.It is typically due to a bacterial infection, most commonly Escherichia coli. Risk factors include sexual intercourse, prior urinary tract infections, diabetes, structural problems of the urinary tract, and spermicide use. The mechanism of infection is usually spread up the urinary tract. Less often infection occurs through the bloodstream. Diagnosis is typically based on symptoms and supported by urinalysis. If there is no improvement with treatment, medical imaging may be recommended.Pyelonephritis may be preventable by urination after sex and drinking sufficient fluids. Once present it is generally treated with antibiotics, such as ciprofloxacin or ceftriaxone. Those with severe disease may require treatment in hospital. In those with certain structural problems of the urinary tract or kidney stones, surgery may be required.Pyelonephritis affects about 1 to 2 per 1,000 women each year and just under 0.5 per 1,000 males. Young adult females are most often affected, followed by the very young and old. With treatment, outcomes are generally good in young adults. Among people over the age of 65 the risk of death is about 40%. Signs and symptoms
Signs and symptoms of acute pyelonephritis generally develop rapidly over a few hours or a day. It can cause high fever, pain on passing urine, and abdominal pain that radiates along the flank towards the back.
Causes
DEB is caused by genetic defects (or mutations) within the human COL7A1 gene encoding the protein type VII collagen (collagen VII). DEB-causing mutations can be either dominant or recessive. Most families with family members with this condition have distinct mutations.Collagen VII is a very large molecule (300 kDa) that dimerizes to form a semicircular looping structure: the anchoring fibril. Anchoring fibrils are thought to form a structural link between the epidermal basement membrane and the fibrillar collagens in the upper dermis. Pathophysiology
In the absence of mutations of the COL7A1 gene, an autoimmune response against type VII collagen can result in an acquired form of epidermolysis bullosa called epidermolysis bullosa acquisita.There exist other types of inherited epidermolysis bullosa, junctional epidermolysis bullosa and epidermolysis bullosa simplex, which are not related to type VII collagen deficiency. These arise from mutations in the genes encoding other proteins of the epidermis or the basement membrane at the junction between the epidermis and the dermis. Diagnosis
Classification
See also
Epidermolysis bullosa

References
Sources
Freedberg, Irwin M.; Eisen, Arthur Z.; Wolff, Klauss; Austen, K. Frank; Goldsmith, Lowell A.; Katz, Stephen I., eds. (2003). Fitzpatricks Dermatology in General Medicine (6th ed.). McGraw-Hill. ISBN 978-0-07-138076-8. James, William; Berger, Timothy; Elston, Dirk (2005). Andrews Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. ISBN 978-0-7216-2921-6. Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 978-1-4160-2999-1. External links

ebd at NIH/UW GeneTests