Diabetic angiopathy is a form of angiopathy associated with diabetic complications.[1] While not exclusive, the two most common forms are diabetic retinopathy and diabetic nephropathy, whose pathophysiologies are largely identical. Other forms of diabetic angiopathy include diabetic neuropathy and diabetic cardiomyopathy.[2][3]
Diabetic angiopathy | |
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Specialty | Diabetology, angiology |
Presentation
editComplications
editDiabetes 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 artery disease. Retinal damage (from microangiopathy) makes it the most common cause of blindness among non-elderly adults in the US.[citation needed]
Pathophysiology
editAs 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,[4] pericytes, express enzymes which convert glucose into osmotically active metabolites such as sorbitol leading to hypertonic cell lysis.[5] The enzyme, namely aldose reductase, is also expressed in the endothelial and Schwann cells of the peripheral nervous system, contributing to diabetic neuropathy.[6]
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 kidney failure. In diabetic retinopathy the end-result is often blindness due to irreversible retinal damage.[7]
Diagnosis
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Treatment
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Prognosis
editPrognosis is generally poor for all forms of diabetic angiopathy, as symptomatology is tied to the advancement of the underlying pathology i.e. the early-stage patient displays either non-specific symptoms or none at all.[citation needed]
"Diabetic dermopathy" is a manifestation of diabetic angiopathy. It is often found on the shin.There is also neuropathy; also associated with diabetes mellitus; type 1 and 2.[citation needed]
References
edit- ^ Holt RI, Cockram C, Flyvbjerg A, Goldstein BJ (2016). Textbook of Diabetes. John Wiley & Sons. p. 543. ISBN 978-1-118-92487-7. Retrieved 19 October 2017.
- ^ Vinik, Aaron I.; Nevoret, Marie-Laure; Casellini, Carolina; Parson, Henri (2013). "Diabetic Neuropathy". Endocrinology and Metabolism Clinics of North America. Acute and Chronic Complications of Diabetes. 42 (4): 747–787. doi:10.1016/j.ecl.2013.06.001. ISSN 0889-8529. PMID 24286949.
- ^ Shi, Yi; Vanhoutte, Paul M. (2017). "Macro- and microvascular endothelial dysfunction in diabetes". Journal of Diabetes (in Chinese). 9 (5): 434–449. doi:10.1111/1753-0407.12521. ISSN 1753-0407. PMID 28044409. S2CID 37269743.
- ^ Calcutt NA (September 2020). "Diabetic neuropathy and neuropathic pain: a (con)fusion of pathogenic mechanisms?". Pain. 161 (Suppl 1): S65–S86. doi:10.1097/j.pain.0000000000001922. PMC 7521457. PMID 32999525.
- ^ Takamura Y, Tomomatsu T, Kubo E, Tsuzuki S, Akagi Y (July 2008). "Role of the polyol pathway in high glucose-induced apoptosis of retinal pericytes and proliferation of endothelial cells". Investigative Ophthalmology & Visual Science. 49 (7): 3216–3223. doi:10.1167/iovs.07-1643. PMID 18362110.
- ^ Calcutt NA (September 2020). "Diabetic neuropathy and neuropathic pain: a (con)fusion of pathogenic mechanisms?". Pain. 161 (Suppl 1): S65–S86. doi:10.1097/j.pain.0000000000001922. PMC 7521457. PMID 32999525.
- ^ Cole, Joanne B.; Florez, Jose C. (2020). "Genetics of diabetes mellitus and diabetes complications". Nature Reviews Nephrology. 16 (7): 377–390. doi:10.1038/s41581-020-0278-5. ISSN 1759-5061. PMC 9639302. PMID 32398868.