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"Sugary Urine" the subtle killer-

Devastating Complications of Diabetes Mellitus

Dr Sampurna Roy MD


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Diabetes mellitus is a global health problem that results in multiorgan complications leading to high morbidity and mortality.

It is regarded as one of the most serious pandemics affecting all societies today.

Some of the major long term complications have been discussed in this post.

Newborn Pancreas:

Infiltration of eosinophils and some lymphocytes within and around the islets and in the interstitial tissue of the pancreas is observed in approximately 25% of infants who are born to diabetic mothers and who die within 1 to 2 weeks after birth.

This eosinophil infiltration is associated with hypertrophy and hyperplasia of the islets and is diagnostic of diabetes mellitus in the mother.

A severe diabetic state is produced and an infiltration of eosinophils and lymphocytes is present in  interstitial tissue and peri-insular areas of the pancreas.

It appears that the hyperplasia and hypertrophy of the B-cells is attributable to the hyperglycemia.

However, the lymphocytic and eosinophil infiltration may be caused by another factor involving an  infectious agent or the transfer of specific antibodies to the fetus.


Peripheral Nerves in Diabetes

Peripheral neuropathy occurs in diabetic patients, with approximately 30% to 50% of the patients showing minor reflex changes, pain in the extremities, and delayed conduction times of the peripheral nerves.

The basic pathologic change in the peripheral nerves is a segmental demyelination.

The elevated blood glucose in the diabetic state apparently activates the aldose reductase pathway for glucose metabolism resulting in the formation of sorbitol and fructose, which may in turn affect the  structure and function of Schwann cells.

The autonomic nervous system may also be involved in diabetic patients with resultant development of severe diarrhea and abdominal pain as well as impaired catecholamine release. 

Control of the diabetic state by islet transplantation results in either prevention or disappearance of these degenerative lesions in the autonomic nerves.   


Eye in Diabetes.

Diabetic retinopathy showing microaneurysms, edema, hemorrhage abnormal growth of blood vessels

Diabetic retinopathy is a common cause of blindness.

The sequence of events in the development of this lesion is changes in the pattern of blood flow through the retina with resultant areas of ischemia, occurrence of microaneurysms in the retinal capillaries, new formation of capillaries within the retina, hemorrhage from these newly formed capillaries into the vitreous, and finally formation of granulation tissue.

Development of these lesions requires many years with a varying degree of severity in individual patients and long periods of remission with no further impairment of vision.

The earliest anatomic change observed in the retina of diabetic patients is the loss of mural cells in the capillaries.

Ghostlike remnants of these cells persist for long periods of time.

Presumably the loss of these cells affects the capillary tone and leads in some way to the changes in the pattern of blood flow through the retina and the subsequent development of microaneurysms of the retina.

The earliest clinical change in the eyes of diabetic patients is an increase in permeability of retinal capillaries, which can be demonstrated by quantitative measurements of fluorescein leakage into the anterior chamber and vitreous of the eye.


Diabetic microangiopathy:

Pathologic changes in the small blood vessels and capillaries of the eye and kidney are responsible for the development of diabetic retinopathy and the Kimmelstiel-Wilson syndrome in patients with diabetes mellitus.

The important pathologic change is the prominent accumulation of basement membrane-like material around the vessels.

Electron microscopy studies have shown that this basement membrane change is not limited to only the  eye and kidney but occurs also in capillaries of the muscle and skin of diabetic patients.

In nondiabetic persons, thickening of muscle capillary basement membranes occurs in a linear fashion in males with increasing age, where as in females the basement membrane thickness increases until about 40 to 50 years of age, reaches a plateau, and increases again between 60 and 70 years of age.

Clinical evidence indicates that diabetic microangiopathy is a complication of the diabetic state and is not attributable to a separate genetic defect.

It would appear that the changes are caused by the inability of maintaining the blood glucose within normal limits at all times with insulin therapy.

These findings are of great importance, since they provide hope that if the diabetic state could be reverted to normal by new therapeutic means the early stage of the complications could be reverted and further progression of these lesions could be halted.

Kidney in diabetes:

Nodular lesions of the glomeruli and thickening of basement membrane

The nodular lesions of the glomeruli described by Kimmelstiel and Wilson are characteristic pathologic changes found in the kidney in diabetes mellitus.

This lesion is the result of focal thickening of the basement membrane.

Electron microscopic studies of the glomeruli in diabetic patients have demonstrated that the earliest  change occurs in the mesangial area of the glomerulus. 

Initially there is a thickening of the basement membrane in this area and an increase in the number of mesangial cells.

Serial renal biopsies on these diabetic patients over a period of years have shown that the amount of basement membrane in the kidney gradually increases and results in the formation of the nodular lesions.

These findings clearly indicate that the basement membrane changes result from the diabetic process.

Vacuolization of the cells of proximal convoluted tubules at the corticomedullary junction may be observed in patients dying of uncontrolled diabetes and severe hyperglycemia.

These sub-nuclear vacuoles have been reported to represent areas of glycogen deposition within the tubules.

These vacuoles disappear when the hyperglycemia is maintained within normal limits. This condition is called the 'Armanni Ebstein lesion of the kidney'.

More recent studies show them to contain fat.

Necrotizing renal papillitis is a rare but serious complication of diabetes mellitus.

This condition is not limited to diabetic patients but can also occur in non-diabetic persons with obstructive lesions of the urinary tract.

The condition is characterized clinically in the diabetic patient by the rapid onset of uremia and subsequent death caused by infarction and sloughing of the renal papillae.




Coronary arteriosclerosis in Diabetes Mellitus


Gangrene and ulceration of the foot              

Diabetes mellitus accelerates the development of arteriosclerosis with the resultant earlier onset of  coronary arteriosclerosis and atherosclerosis in general.

The arteriosclerotic process also involves vessels to the lower extremity with resultant production of gangrene of the toes and feet.

The precipitating causes of gangrene of the lower extremities are usually mechanical, thermal, or chemical trauma resulting in ulceration, infection, and subsequent gangrene.

Comparison of dermal capillaries of the toes amputated from diabetic and nondiabetic persons indicates  that thickening of basement membrane of the capillaries is limited to the diabetic group.

Pronounced thickening in the basement membranes of the capillaries in diabetic patients may play some role in the complication of the vascular insufficiency of the lower extremities, possibly by interference with nutrition and response of tissues to injury. 

Visit: Pancreatic Pathology Online

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Dr  Sampurna Roy  MD

Consultant Histopathologist (Kolkata - India)







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