Back اعتلال الكلى السكري Arabic Nefropatia diabètica Catalan Diabetická nefropatie Czech Diabetische Nephropathie German ހަކުރު ބަލީގައި ގުރުދާ ފޭލްވުން DV Nefropatía diabética Spanish نفروپاتی دیابتی Persian Diabeettinen nefropatia Finnish Néphropathie diabétique French Nefropatía diabética Galician

Diabetic nephropathy

Diabetic nephropathy
Other namesDiabetic kidney disease
Two glomeruli in diabetic nephropathy: the acellular light purple areas within the capillary tufts are the destructive mesangial matrix deposits.
SpecialtyNephrology, endocrinology Edit this on Wikidata
SymptomsAlbuminuria,[1] peripheral edema,[1] high blood pressure,[1] tiredness[2]
Risk factorsHigh blood pressure, tobacco smoking,[1] unstable blood glucose[2]
Diagnostic methodAbnormal levels of urinary albumin[3]
PreventionSmoking cessation[1]
TreatmentACE inhibitors[4]

Diabetic nephropathy, also known as diabetic kidney disease,[5] is the chronic loss of kidney function occurring in those with diabetes mellitus. Diabetic nephropathy is the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. The triad of protein leaking into the urine (proteinuria or albuminuria), rising blood pressure with hypertension and then falling renal function is common to many forms of CKD. Protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called nephrotic syndrome. Likewise, the estimated glomerular filtration rate (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage renal disease.[6] It usually is slowly progressive over years.[7]

Pathophysiologic abnormalities in diabetic nephropathy usually begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the nephrons. (There are normally about 750,000–1.5 million nephrons in each adult kidney).[8] Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration particularly as nephrons become obsolescent and the adaption of hyperfiltration paradoxically causes further shear stress related damage to the delicate glomerular capillaries, further proteinuria, rising blood pressure and a vicious circle of additional nephron damage and decline in overall renal function.[9][10] Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.[11]

The status of diabetic nephropathy may be monitored by measuring two values: the amount of protein in the urine - proteinuria; and a blood test called the serum creatinine. The amount of the proteinuria reflects the degree of damage to any still-functioning glomeruli. The value of the serum creatinine can be used to calculate the estimated glomerular filtration rate (eGFR), which reflects the percentage of glomeruli which are no longer filtering the blood. [citation needed] Treatment with an angiotensin converting enzyme inhibitor or angiotensin receptor blocker, which dilates the arteriole exiting the glomerulus, thus reducing the blood pressure within the glomerular capillaries, may slow (but not stop) progression of the disease. Three classes of diabetes medications – GLP-1 agonists, DPP-4 inhibitors, and SGLT2 inhibitors– are also thought to slow the progression of diabetic nephropathy.[12]

Diabetic nephropathy is the most common cause of end-stage renal disease and is a serious complication that affects approximately one quarter of adults with diabetes in the United States.[13][14] Affected individuals with end-stage kidney disease often require hemodialysis and eventually kidney transplantation to replace the failed kidney function.[15] Diabetic nephropathy is associated with an increased risk of death in general, particularly from cardiovascular disease.[13][16]

  1. ^ a b c d e Alamo, A.; Campagna, D.; Di Pino, A.; Russo, C.; Calogero, A. E.; Polosa, R.; Purrello, F. (October 2019). "Smoking and diabetes: dangerous liaisons and confusing relationships" (PDF). Diabetology & Metabolic Syndrome. 11 (85). BioMed Central: 85. doi:10.1186/s13098-019-0482-2. ISSN 1758-5996. PMC 6813988. PMID 31666811. S2CID 204882089. Retrieved 20 August 2021.
  2. ^ a b Cite error: The named reference nih22 was invoked but never defined (see the help page).
  3. ^ Lewis G, Maxwell AP (February 2014). "Risk factor control is key in diabetic nephropathy". The Practitioner. 258 (1768): 13–7, 2. PMID 24689163.
  4. ^ Lim AK (2014). "Diabetic nephropathy – complications and treatment". International Journal of Nephrology and Renovascular Disease. 7: 361–81. doi:10.2147/IJNRD.S40172. PMC 4206379. PMID 25342915.
  5. ^ Kittell F (2012). "Diabetes Management". In Thomas LK, Othersen JB (eds.). Nutrition Therapy for Chronic Kidney Disease. CRC Press. p. 198. ISBN 9781439849491.
  6. ^ Longo D, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J (2013). Harrison's manual of medicine (18th ed.). New York: McGraw-Hill Medical. p. 2982. ISBN 978-0-07-174519-2.
  7. ^ Afkarian M, Zelnick LR, Hall YN, Heagerty PJ, Tuttle K, Weiss NS, de Boer IH (August 2016). "Clinical Manifestations of Kidney Disease Among US Adults With Diabetes, 1988–2014". JAMA. 316 (6): 602–10. doi:10.1001/jama.2016.10924. PMC 5444809. PMID 27532915.
  8. ^ Hall J, Guyton A (2005). Textbook of Medical Physiology (11th ed.). Philadelphia: W.B. Saunders. p. 310. ISBN 978-0-7216-0240-0.
  9. ^ Hostetter, T. H.; Olson, J. L.; Rennke, H. G.; Venkatachalam, M. A.; Brenner, B. M. (July 1981). "Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation". The American Journal of Physiology. 241 (1): F85–93. doi:10.1152/ajprenal.1981.241.1.F85. ISSN 0002-9513. PMID 7246778. S2CID 1553863.
  10. ^ "diabetic nephropathy". Retrieved 2015-06-27.
  11. ^ Schlöndorff D, Banas B (June 2009). "The mesangial cell revisited: no cell is an island". Journal of the American Society of Nephrology. 20 (6): 1179–87. doi:10.1681/ASN.2008050549. PMID 19470685.
  12. ^ de Boer IH (August 2017). "A New Chapter for Diabetic Kidney Disease". The New England Journal of Medicine. 377 (9): 885–887. doi:10.1056/nejme1708949. PMID 28854097.
  13. ^ a b Mora-Fernández C, Domínguez-Pimentel V, de Fuentes MM, Górriz JL, Martínez-Castelao A, Navarro-González JF (September 2014). "Diabetic kidney disease: from physiology to therapeutics". The Journal of Physiology. 592 (18): 3997–4012. doi:10.1113/jphysiol.2014.272328. PMC 4198010. PMID 24907306.
  14. ^ Ding Y, Choi ME (January 2015). "Autophagy in diabetic nephropathy". The Journal of Endocrinology. 224 (1): R15–30. doi:10.1530/JOE-14-0437. PMC 4238413. PMID 25349246.
  15. ^ Lizicarova D, Krahulec B, Hirnerova E, Gaspar L, Celecova Z (2014). "Risk factors in diabetic nephropathy progression at present". Bratislavske Lekarske Listy. 115 (8): 517–21. doi:10.4149/BLL_2014_101. PMID 25246291.
  16. ^ Pálsson R, Patel UD (May 2014). "Cardiovascular complications of diabetic kidney disease". Advances in Chronic Kidney Disease. 21 (3): 273–80. doi:10.1053/j.ackd.2014.03.003. PMC 4045477. PMID 24780455.

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