Causes
Causes of Page kidney have appeared to change over time. Initially, the phenomena were most often caused by traumatic injuries, such as contact sports or motor vehicle collisions. More recently, the majority of cases are postprocedural or secondary to mass lesions. Several factors have been implicated as contributory to this change, namely: the more liberal use of high-quality imaging and the increased utilization of invasive procedures. Documented iatrogenic causes include: intra-abdominal surgery, lithotripsy, renal biopsy, and percutaneous endopyelotomy. The biggest shift in cause comes from kidney allograft biopsy, which now accounts for the majority of Page kidney cases. Pathophysiology
Although to date there have not been any studies specific to Page kidney in humans, two studies in animals and known renal physiology provide a likely mechanism. The elevated blood pressure seen in Page kidney is thought to be caused by the activation of the renin–angiotensin–aldosterone system (RAAS). Compression of the renal parenchyma alters intrarenal blood flow, resulting in a localized decrease in blood flow to the affected nephrons. This decrease in blood flow is recognized by the juxtaglomerular (JG) cells and promotes the cleavage of prorenin into renin. Each kidney is surrounded by two layers of connective tissue, the inner renal capsule and outer renal (Gerotas) fascia. These layers thus form two potential spaces where fluid can form, the small subcapsular space and the large perinephric space. The renal capsule is fibrous and does not easily expand. Thus, even a small collection of blood in the subcapsular space can cause mass effect on the renal parenchyma.
Although he postulated that a similar scenario could be produced clinically in humans due to a hematoma, it was not until 1955 that Page and his colleague William J. Engel published the first case report on Page kidney. == References ==