Chronic exposure to abnormally high blood sugar levels and hypertension doesn’t just damage the kidneys. In other parts of the body, organs and blood vessels are also affected. When microalbuminuria appears as a sign of the onset of kidney failure, it is high time to check for other complications.

Patients with diabetes and microalbuminuria frequently show changes to the back of the eye, socalled ‘retinopathy’, as well as signs of cardiovascular disease and problems with the circulation to the brain or the legs. People with diabetes should undergo an eye examination at least once a year.

This does not just look at vision and the blood pressure in the eye, but also examines the retina at the back of the eye, paying close attention to the capillaries. If these tiny blood vessels become damaged by the blood pressure being too high, your visual ability may be seriously compromised.

This is because the image seen by the eye falls onto the retina, where it is converted by special cells into nerve impulses that travel along the optic nerve to the brain. In the worst cases, diabetes can cause total blindness. Just like nephropathy, diabetes-associated damage to the eye, known as retinopathy, does not develop overnight but gradually over years.

This means that with early diagnosis, we can use this time to halt the progress of the retinopathy by giving the appropriate therapy and prevent the onset of blindness. At first, diabetic retinopathy does not produce any symptoms. Only an ophthalmologist or optician can detect small swellings in the capillaries, called microaneurysms, during a routine examination.

The first minor haemorrhages (bleeding) in the capillaries in the retina may even occur without affecting the vision. These early changes are known as non-proliferative diabetic retinopathy and can be reversed by good management of blood sugar levels and blood pressure.

But if these two factors cannot be controlled, they may lead to damage and destruction of the capillaries and from there to major bleeding in the retina. The eye tries to combat this by growing new capillaries to deliver blood to its cells correctly. This stage is called proliferative retinopathy.

The new capillaries, however, are brittle and bleed easily. Once the majority of the retina is covered with blood from this bleeding, there is acute loss of vision. Bleeding in the vitreous humour is particularly damaging. The vitreous humour is a clear, gelatinous mass that fills most of the eye and helps it to maintain its shape.

The blood that leaks from the capillaries is broken down but leaves fragments and scars that seriously impair vision. In people with diabetes, kidney and eye damage often develop in parallel.

For both these complications, the blood sugar level plays a decisive role: the lower the blood sugar, the less likely is the development of retinopathy or nephropathy. The blood pressure has a similar effect – and in this case, low values can protect against ongoing damage, as shown by the major trials in people with Type 1 and Type 2 diabetes (DCCT and UKPDS).

Sadly, blindness and dialysis used to be a common fate for people with diabetes. Today, this is not the case. By intensive management of the blood sugar level and blood pressure, we can delay or prevent the onset and further progression of retinopathy in patients with nephropathy, as shown in the large Swedish study.

As with nephropathy, the ACE inhibitors have a significant beneficial effect on retinopathy. It is important that patients with kidney failure, who are therefore at high risk of damage to their vision, have their eyes examined by an ophthalmologist at least every six months and eventually even more frequently.

Fortunately, the treatment of diabetic retinopathy has made great progress in recent years. Laser therapy and surgical treatment of the retina and vitreous humour can often prevent the worse case scenario, blindness. The prospects, as with diabetic nephropathy, are better when the damage is detected early and the blood sugar level and blood pressure are reduced.