All people with "diabetes mellitus" are at riskthose with Type I diabetes and those with Type II diabetes. The longer a person has diabetes, the higher their risk of developing some ocular problem. Between 40 and 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. After 20 years of diabetes, nearly all patients with Type I diabetes and >60% of patients with Type II diabetes have some degree of retinopathy; however, these statistics were published in 2002 using data from four years earlier, limiting the usefulness of the research. The subjects would have been diagnosed with diabetes in the late 1970s, before modern fast acting insulin and home glucose testing.

Prior studies had also assumed a clear glycemic threshold between people at high and low risk of diabetic retinopathy.

However, it has been shown that the widely accepted WHO and American Diabetes Association diagnostic cutoff for diabetes of a fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) does not accurately identify diabetic retinopathy among patients. The cohort study included a multi-ethnic, cross-sectional adult population sample in the US, as well as two cross-sectional adult populations in Australia. For the US-based component of the study, the sensitivity was 34.7% and specificity was 86.6%. For patients at similar risk to those in this study (15.8% had diabetic retinopathy), this leads to a positive predictive value of 32.7% and negative predictive value of 87.6%.

Published rates vary between trials, the proposed explanation being differences in study methods and reporting of prevalence rather than incidence values.

During pregnancy, diabetic retinopathy may also be a problem for women with diabetes.

It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to protect their vision.

People with Down's syndrome, who have extra chromosome 21 material, almost never acquire diabetic retinopathy. This protection appears to be due to the elevated levels of endostatin, an anti-angiogenic protein, derived from collagen XVIII. The collagen XVIII gene is located on chromosome 21.

In the UK, screening for diabetic retinopathy is part of the standard of care for people with diabetes. After one normal screening in people with diabetes, further screening is recommended every two years. Teleophthalmology has been employed in these programs.

The two most common causes of retinopathy include diabetic retinopathy and retinopathy of prematurity. Diabetic retinopathy affects about 5 million people and retinopathy of prematurity affect about 50,000 premature infants each year worldwide. Hypertensive retinopathy is the next most common cause affecting anywhere from 3 to 14% of all non-diabetic adults.

Genetic mutations are rare causes of certain retinopathies and are usually X-linked including "NDP" family of genes causing Norrie Disease, FEVR, and Coats disease among others. There is emerging evidence that there may be a genetic predisposition in patients who develop retinopathy of prematurity and diabetic retinopathy. Trauma, especially to the head, and several diseases may cause Purtscher's retinopathy.

A 1988 study over 41 months found that improved glucose control led to initial "worsening of complications" but was not followed by the expected improvement in complications. In 1993 it was discovered that the serum of diabetics with neuropathy is toxic to nerves, even if its blood sugar content is normal.

Research from 1995 also challenged the theory of hyperglycemia as the cause of diabetic complications. The fact that 40% of diabetics who carefully controlled their blood sugar nevertheless developed neuropathy made clear other factors were involved.

In a 2013 meta-analysis of 6 randomized controlled trials involving 27,654 patients, tight blood glucose control reduced the risk for some macrovascular and microvascular events but without effect on all-cause mortality and cardiovascular mortality.

Research from 2007 suggested that in type 1 diabetics, the continuing autoimmune disease which initially destroyed the beta cells of the pancreas may also cause retinopathy, neuropathy, and nephropathy.

In 2008 it was even suggested to treat retinopathy with drugs to suppress the abnormal immune response rather than by blood sugar control.

Several other diseases can result in retinopathy that can be confused with hypertensive retinopathy. These include diabetic retinopathy, retinopathy due to autoimmune disease, anemia, radiation retinopathy, and central retinal vein occlusion.

Signs of damage to the retina caused by hypertension include:

- Arteriolar changes, such as generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, changes in the arteriolar wall (arteriosclerosis) and abnormalities at points where arterioles and venules cross. Manifestations of these changes include "Copper wire arterioles" where the central light reflex occupies most of the width of the arteriole and "Silver wire arterioles" where the central light reflex occupies all of the width of the arteriole, and "arterio-venular (AV) nicking" or "AV nipping", due to venous constriction and banking.

- advanced retinopathy lesions, such as microaneurysms, blot hemorrhages and/or flame hemorrhages, ischemic changes (e.g. "cotton wool spots"), hard exudates and in severe cases swelling of the optic disc (optic disc edema), a ring of exudates around the retina called a "macular star" and visual acuity loss, typically due to macular involvement.

Mild signs of hypertensive retinopathy can be seen quite frequently in normal people (3–14% of adult individuals aged ≥40 years), even without hypertension. Hypertensive retinopathy is commonly considered a diagnostic feature of a hypertensive emergency although it is not invariably present.

Diabetes mellitus is the most common cause of adult kidney failure worldwide. It also the most common cause of amputation in the US, usually toes and feet, often as a result of gangrene, and almost always as a result of peripheral vascular disease. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US.

As insulin is required for glucose uptake, hyperglycemia in diabetes mellitus does not result in a net increase in intracellular glucose in most cells. However, chronic dysregulated blood glucose in diabetes is toxic to cells of the vascular endothelium which passively assimilate glucose. That is, cells in which insulin is not required for intercellular transport of glucose, most-notably the pericytes of the microvasculature. In addition to direct glucose-induced damage by (e.g.) glycation, pericytes express enzymes which convert glucose into osmologically-active metabolites such as sorbitol leading to hypertonic cell lysis.

Over time, pericyte death may result in reduced capillary integrity; subsequently, there is leaking of albumin and other proteins into fluid compartments. The glomeruli of the kidneys are especially sensitive – see diabetic nephropathy – where protein leakage caused by late-stage angiopathy results in diagnostic proteinuria and eventually renal failure. In diabetic retinopathy the end-result is often blindness due to irreversible retinal damage.

Diabetic nephropathy in type 2 diabetes can be more difficult to predict because the onset of diabetes is not usually well established. Without intervention, 20-40 percent of patients with type 2 diabetes/microalbuminuria, will evolve to macroalbuminuria.

Diabetic nephropathy is the most common cause of end-stage kidney disease, which may require hemodialysis or even kidney transplantation. It is associated with an increased risk of death in general, particularly from cardiovascular disease.

The causes of macular edema are numerous and different causes may be inter-related.

- It is commonly associated with diabetes. Chronic or uncontrolled diabetes type 2 can affect peripheral blood vessels including those of the retina which may leak fluid, blood and occasionally fats into the retina causing it to swell.

- Age-related macular degeneration may cause macular edema. As individuals age there may be a natural deterioration in the macula which can lead to the depositing of drusen under the retina sometimes with the formation of abnormal blood vessels.

- Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) also known as Irvine-Gass syndrome The surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. Less common today with modern lens replacement techniques.

- Chronic uveitis and intermediate uveitis can be a cause.

- Blockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina. The blockage may be caused, among other things, by atherosclerosis, high blood pressure and glaucoma.

- A number of drugs can cause changes in the retina that can lead to macular edema. The effect of each drug is variable and some drugs have a lesser role in causation. The principal medication known to affect the retina are:- latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others.

- A few congenital diseases are known to be associated with macular edema for example retinitis pigmentosa and retinoschisis.

Macular edema occurs when fluid and protein deposits collect on or under the macula of the eye (a yellow central area of the retina) and causes it to thicken and swell (edema). The swelling may distort a person's central vision, because the macula holds tightly packed cones that provide sharp, clear, central vision to enable a person to see detail, form, and color that is directly in the centre of the field of view.

The incidence of diabetic nephropathy is higher in diabetics with one or more of the following conditions:

- Poor control of blood glucose

- Uncontrolled High blood pressure

- Type 1 diabetes mellitus, with onset before age 20

- Past or current cigarette use

- A family history of diabetic nephropathy

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.

The mechanisms of diabetic neuropathy are poorly understood. At present, treatment alleviates pain and can control some associated symptoms, but the process is generally progressive.

As a complication, there is an increased risk of injury to the feet because of loss of sensation (see diabetic foot). Small infections can progress to ulceration and this may require amputation.

Purtscher's retinopathy can lead to loss of vision, and recovery of vision may occur very little. However, vision recovery does occur in some cases, and reports have varied on the long-term prognosis.

Predisposing factors for Postoperative PVR are preoperative PVR, aphakia, high levels of vitreous proteins, duration of retinal detachment before corrective surgery, the size of the retinal hole or tear, intra-ocular inflammation, vitreous hemorrhage, and trauma to the eye. An equation to calculate the patient's risk for acquiring PVR is:

1 is added if the risk factor is present and 0 if the risk factor is absent. A patient is at a high risk for developing PVR is the PVR score is >6.33.

Globally diabetic neuropathy affects approximately 132 million people as of 2010 (1.9% of the population).

Diabetes is the leading known cause of neuropathy in developed countries, and neuropathy is the most common complication and greatest source of morbidity and mortality in diabetes. It is estimated that neuropathy affects 25% of people with diabetes. Diabetic neuropathy is implicated in 50–75% of nontraumatic amputations.

The main risk factor for diabetic neuropathy is hyperglycemia. In the DCCT (Diabetes Control and Complications Trial, 1995) study, the annual incidence of neuropathy was 2% per year but dropped to 0.56% with intensive treatment of Type 1 diabetics. The progression of neuropathy is dependent on the degree of glycemic control in both Type 1 and Type 2 diabetes. Duration of diabetes, age, cigarette smoking, hypertension, height, and hyperlipidemia are also risk factors for diabetic neuropathy.

Familial transmission is now recognized in a small proportion of people with MacTel type 2; however, the nature of any related genetic defect or defects remains elusive. The MacTel genetic study team hopes that exome analysis in the affected population and relatives may be more successful in identifying related variants.

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 VEGF. These factors stimulate the formation of new blood vessels (angiogenesis). Unfortunately, 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.

Although a variety of complex classification schemes are described in the literature, there are essentially two forms of macular telangiectasia: type 1 and type 2. Type 1 is typically unilateral and occurs almost exclusively in males after the age of 40.

Type 2 is mostly bilateral, occurs equally in males and females.

The pathogenesis of this disease is unclear. Arteriosclerosis obliterans has been postulated as the cause, along with errors of the clotting and fibrinolytic pathways such as antiphospholipid syndrome.

ROP prevalence varies, from 5–8% in developed countries with adequate neonatological facilities, to up to 30% in middle-income developing countries.

There is increasing evidence that ROP and blindness due to ROP are now public health problems in the middle income countries of Latin America, Eastern Europe and the more advanced economies in South East Asia and the Middle east region. In these countries ROP is often the most common cause of blindness in children. ROP is highly likely to become an increasing problem in India, China and other countries in Asia as these countries expand the provision of services for premature infants.

There is also evidence that the population of premature infants at risk of severe ROP varies depending on the level of neonatal intensive care being provided. In countries with high development indices and very low neonatal mortality rates (e.g. North America, western Europe), severe ROP is generally limited to extremely preterm infants i.e. those weighing less than 1 kg (2.2 lbs) at birth. At the other end of the development spectrum, countries with very low development indices and very high neonatal mortality rates (e.g. much of subSaharan Africa) ROP is rare as most premature babies do not have access to neonatal intensive care and so do not survive. Countries with moderate development indices are improving access to neonatal intensive care, and in these settings bigger, more mature babies are also at risk of severe ROP as neonatal care may be suboptimal i.e. those weighing 1.5–2 kg (3.3-4.4 lbs) at birth. These findings have two main implications: firstly, much can be done in countries with moderate development indices to improve neonatal care, to reduce the risk of severe ROP in bigger babies and increase survival of extremely preterm infants, and secondly, in these settings bigger more mature babies need to be included in ROP programs and examined regularly so as to detect those babies developing ROP requiring treatment.

In 2012, the World Health Organization published data on rates of preterm birth and the number of premature babies born in different regions of the world. This report contained three main findings:

- Premature birth has many different causes, and prevention is challenging,

- Prematurity is the most common cause of neonatal death in many countries, totaling as many as 1 million infants annually due to complications of preterm birth, and

- the number of preterm births is currently estimated to be 15 million, and increasing.

It may be treated with triamcinolone in some cases. However, in general, there are no treatments for Purtscher's retinopathy. If it is caused by a systemic disease or emboli, then those conditions should be treated.