Rubeosis iridis is a medical condition of the iris of the eye in which new abnormal blood vessels (formed by neovascularization) are found on the surface of the iris. Causes
This condition is often associated with diabetes in advanced proliferative diabetic retinopathy. Other conditions causing rubeosis iridis include central retinal vein occlusion, ocular ischemic syndrome, and chronic retinal detachment. Pathophysiology
It is usually associated with disease processes in the retina, which involve the retina becoming starved of oxygen (ischaemic). The ischemic retina releases a variety of factors, the most important of which is vascular endothelial growth factor (VEGF). These factors stimulate the formation of new blood vessels (angiogenesis). These new vessels do not have the same characteristics as the blood vessels originally formed in the eye. In addition, new blood vessels can form in areas that do not have them. Specifically, new blood vessels can be observed on the iris. In addition to the blood vessels in the iris, they can grow into the angle of the eye. These blood vessels eventually go through a process called fibrosis which closes the normal physiologic anatomy of the angle. The closing of the angle prevents fluid from leaving the eye resulting in an increase in intraocular pressure. This is called neovascular glaucoma. Treatment
If caught early, the neovascularization can be reversed with prompt panretinal photocoagulation (PRP), or injection of anti-VEGF medications with subsequent PRP. The injection blocks the direct effect of VEGF and acts more quickly but will wear off in about six weeks.
Complement fixation causes the generation of additional inflammatory mediators.Complement activation is very important in acute proliferative glomerulonephritis. Apparently immunoglobulin (Ig)-binding proteins bind C4BP. Complement regulatory proteins (FH and FHL-1), may be removed by SpeB, and therefore restrain FH and FHL-1 recruitment in the process of infection. Diagnosis
The following diagnostic methods can be used for acute proliferative glomerulonephritis:
Kidney biopsy
Complement profile
Imaging studies
Blood chemistry studiesClinically, acute proliferative glomerulonephritis is diagnosed following a differential diagnosis between (and, ultimately, diagnosis of) staphylococcal and streptococcal impetigo. Serologically, diagnostic markers can be tested; specifically, the streptozyme test is used and measures multiple streptococcal antibodies: antistreptolysin, antihyaluronidase, antistreptokinase, antinicotinamide-adenine dinucleotidase, and anti-DNAse B antibodies. Differential diagnosis
The differential diagnosis of acute proliferative glomerulonephritisis is based on the following:

Prevention
It is unclear whether or not acute proliferative glomerulonephritis (i.e., poststreptococcal glomerulonephritis) can be prevented with early prophylactic antibiotic therapy, with some authorities arguing that antibiotics can prevent development of acute proliferative glomerulonephritis

Treatment
Acute management of acute proliferative glomerulonephritis mainly consists of blood pressure (BP) control. A low-sodium diet may be instituted when hypertension is present. In individuals with oliguric acute kidney injury, the potassium level should be controlled. Thiazide or loop diuretics can be used to simultaneously reduce edema and control hypertension; however electrolytes such as potassium must be monitored. Beta-blockers, calcium channel blockers, and/or ACE inhibitors may be added if blood pressure is not effectively controlled through diureses alone. Epidemiology
Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.