After growth of a few millimeters has occurred, the cysts detach from the parent tubule, this detachment induced by excessive proliferation of tubular epithelium or excessive fluid secretions. Diagnosis
Diagnosis includes imaging with ultrasound, CT and/or MRI. The least expensive, non-invasive, and most reliable method is ultrasonography but smaller cysts may escape detection, while the resolution of CT and MRI will enable smaller cysts to be captured. However, the increased complexity and expense of CT and MRI is usually reserved for higher risk situations. MRI can be used to monitor the development of cysts and growth of kidneys.Genetic test can be applicable to those who have a family history of PKD but is expensive and fails to detect PKD in 15% of cases where it is present. Antenatal scans
Many forms of cystic kidney disease can be detected in children prior to birth. Abnormalities which only affect one kidney are unlikely to cause a problem with the healthy arrival of a baby. Abnormalities which affect both kidneys can have an effect on the babys amniotic fluid volume which can in turn lead to problems with lung development. Some forms of obstruction can be very hard to differentiate from cystic renal disease on early scans. Treatment
The goal of treatment is to manage the disease and its symptoms, and to avoid or delay complications. Options include pain medication (except ibuprofen and other ‘non-steroidal anti-inflammatory agents (NSAID’s)’ which may worsen kidney function), low protein and sodium diet, diuretics, antibiotics to treat urinary tract infection, or interventions to drain cysts.
Activated FVII binds to endothelial protein C receptor (EPCR), which enhances hemostasis.14 One study showed that eptacog beta binds to EPCR with 25% to 30% more affinity than eptacog alfa, displacing protein C from EPCR binding sites and downregulating activated protein C generation, contributing to its hemostatic effect. Physiology
The main role of factor VII (FVII) is to initiate the process of coagulation in conjunction with tissue factor (TF/factor III). Tissue factor is found on the outside of blood vessels - normally not exposed to the bloodstream. Upon vessel injury, tissue factor is exposed to the blood and circulating factor VII. Once bound to TF, FVII is activated to FVIIa by different proteases, among which are thrombin (factor IIa), factor Xa, IXa, XIIa, and the FVIIa-TF complex itself. The complex of factor VIIa with TF catalyzes the conversion of factor IX and factor X into the active proteases, factor IXa and factor Xa, respectively.The action of the factor is impeded by tissue factor pathway inhibitor (TFPI), which is released almost immediately after initiation of coagulation. Factor VII, which was discovered around 1950, is vitamin K-dependent and produced in the liver. Use of warfarin or similar anticoagulants decreases hepatic synthesis of FVII. Structure
Factor VII shares a common domain architecture with factors IX and X.

Genetics
The gene for factor VII is located on chromosome 13 (13q34). Role in disease
Factor VII deficiency (congenital proconvertin deficiency) is rare and inherited recessively. It presents as a hemophilia-like bleeding disorder. It is treated with recombinant factor VIIa (NovoSeven or AryoSeven).