- PROFESSOR | Medicine, Nephrology
- Hospital Affiliation
- The Mount Sinai Hospital
American Board of Internal Medicine
MD, University of Chile Medical School
Residency, Internal Medicine
The Brooklyn Hospital
Residency, Internal Medicine
Brooklyn Hospital-Caledonian Hosp.
Downstate Medical Center
Advanced glycoxidation end products as cardiovascular risk factors in renal failure
Serum levels of advanced glycoxidation end products (AGE) are elevated in diabetes, renal failure and advanced age and these compounds are thought to mediate, at least in part, many of the vascular complications associated with these conditions. AGEs are a heterogeneous group of compounds formed from the non-enzymatic reaction of reducing sugars with the free amino groups of proteins. It had been assumed that circulating AGE originate exclusively from endogenous sources but now it has become clear that foods contain a variable amount of pre-formed AGE and AGE-precursors that contribute to the body AGE pool.We have recently demonstrated that serum AGE levels correlate with dietary AGE content in ESRD patients on dialysis. When a subgroup of these patients was randomized to follow a diet low in AGE content for 4 weeks, we observed 30% of decrease of serum AGE levels and parallel changes in CRP levels. These studies suggest that dietary AGEs play an important role in determining the body AGE pool and that dietary AGE modulation is a feasible, safe and effective way to decrease body AGE pool. Our working hypothesis is that AGEs represent independent risk factors for cardiovascular disease in renal failure patients. Our next research phase will try to demonstrate in a larger number of patients that low AGE diet can reduce serum AGE levels and at the same time improve the direct markers of vascular structure and function: brachial artery dilatation in response to hyperemia and arterial stiffness.
Other areas of research interest include:
Uribarri J, Buquing J, Oh MS. Acid-base balance in chronic peritoneal dialysis patients. Kidney Int 1995 Jan; 47(1): 269-273.
Uribarri J. Acid production in chronic hemodialysis patients. J Am Soc Nephrol 1998 Jan; 9(1): 114-120.
Uribarri J, Oh MS, Carroll HJ. D-lactic acidosis: a review of clinical presentation, biochemical features and pathophysiologic mechanisms. Medicine 1998 Mar; 77(2): 73-82.
Uribarri J, Levin NW, Delmez J, Depner TA, Ornt D, Owen W, Yan G. Association of acidosis and nutritional parameters in hemodialysis patients. Am J Kidney Dis 1999 Sep; 34(3): 493-499.
Uribarri J. Doqi guidelines for nutrition in long-term peritoneal dialysis patients: a dissenting view. Am J Kidney Dis 2001 Jun; 37(8): 1313-1318.
Sedlacek M, Teodorescu V, Falk A, Vassalotti JA, Uribarri J. Hemodialysis access placement with preoperative noninvasive vascular mapping: comparison between patients with and without diabetes. Am J Kidney Dis 2001 Sep; 38(3): 560-564.
Uribarri J, Peppa M, Cai W, Goldberg T, Lu M, Baliga S, Vassalotti JA, Vlassara H. Dietary glycotoxins correlate with circulating advanced glycation end product levels in renal failure patients. Am J Kid Dis 2003 Sep; 42(3): 532-538.
Uribarri J, Peppa M, Goldberg T, Cai W, Lu M, He C, Vlassara H. Restriction of dietary glycotoxins markedly reduces elevated advanced glycation end products in renal failure patients. J Am Soc Nephrol 2003; 14: 728-731.
Caplin N, Sedlacek M, Teodorescu V, Falk A, Uribarri J. Venous access: women are equal. Am J Kidney Dis 2003 Feb; 41(2): 429-432.
Peppa M, Uribarri J, Cai W, Lu M, Vlassara H. Glycoxidation and inflammation in renal failure patients. Am J Kidney Dis 2004 Apr; 43(4): 690-695.
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Below are financial relationships with industry reported by Dr. Uribarri during 2016 and/or 2017. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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