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Am J Kidney Dis. 2003 Mar;41(3 Suppl 1):S52-6.
Are advanced glycation end products cardiovascular risk factors in patients with CRF?

Stein G, Busch M, Muller A, Wendt T, Franke C, Niwa T, Franke S.

Department of Internal Medicine IV, University of Jena, Germany; and Nagoya University Hospital, Nagoya, Japan.

BACKGROUND: Chronic renal failure (CRF) is characterized by enhanced formation and accumulation of advanced glycation end products (AGEs), which are involved in the pathogenesis of vascular damage. Their role as risk factors for cardiovascular complications is still unknown. This study aims to investigate whether elevated serum levels of the AGEs pentosidine, N(epsilon)-carboxymethyllysine (CML), and the 3-deoxyglucosone-derived imidazolone involve a greater risk for cardiovascular events (CVEs) and left ventricular hypertrophy (LVH). Methods: Patients with CRF (n = 99), on maintenance hemodialysis (HD) therapy (n = 84), and renal transplant recipients (RTRs; n = 50) were included. Pentosidine was measured by high-performance liquid chromatography, and CML and imidazolone, by enzyme-linked immunosorbent assays. Statistical analyses were performed using Mann-Whitney U test, logistic regression analysis, and Cox proportional hazards model. Results: At baseline in all investigated groups, patients with a history of CVEs or LVH showed greater mean serum AGE levels. By retrospective data analysis, significant odds ratios for increases in CML and imidazolone levels were calculated for LVH in HD patients, as well as for increases in CML levels for CVEs in RTRs, respectively. By prospective data analysis, serum AGE levels could not be evaluated as independent risk factors for CVEs in all investigated groups. Conclusion: From these preliminary results, serum AGE levels could not be identified as independent risk factors for CVEs or LVH in patients with CRF. Prospective studies are needed to answer this question. Am J Kidney Dis 41(S1):S52-S56. 2003 by the National Kidney Foundation, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12751105&dopt=Abstract [PubMed - in process]

Am J Kidney Dis. 2003 Mar;41(3 Suppl 1):S96-9.
Vascular calcification in dialysis patients: Pathogenesis and consequences.

Reslerova M, Moe SM.

Department of Medicine, Indiana University School of Medicine; and Department of Medicine, Roudebush Veterans Affairs Medical Center, Indianapolis, IN.

BACKGROUND: Vascular calcification is believed to have a crucial role in the excess cardiovascular mortality and morbidity in patients with end-stage renal disease (ESRD). Methods and Results: Recent evidence suggests that uremic vascular calcification is an active cell-mediated process resembling osteogenesis in bone, rather than passive precipitation of calcium and phosphorus in the setting of deranged mineral metabolism. To date, several bone-associated proteins (osteopontin, bone sialoprotein, alkaline phosphatase, and type I collagen) have been shown in histological sections of vessels obtained from patients with ESRD or calcific uremic arteriolopathy. In in vitro experiments, the addition of uremic serum upregulates osteopontin expression by cultured vascular smooth muscle cells (VSMCs). Conclusion: We are only beginning to understand the process by which VSMCs transform into osteoblast-like cells, although phosphorus may have a key role. Additional factors mediating or modulating the development of vascular calcification in patients with ESRD remain to be identified. Further understanding of the pathophysiological state of uremic vascular calcification is needed to design effective therapeutic strategies to intervene with this devastating condition in the ESRD population. Am J Kidney Dis 41(S1):S96-S99. 2003 by the National Kidney Foundation, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12751114&dopt=Abstract [PubMed - in process]

Am J Kidney Dis. 2003 Mar;41(3 Suppl 1):S100-3.
New strategies for the treatment of secondary hyperparathyroidism.

Akizawa T, Shiizaki K, Hatamura I, Kamimura M, Mizobuchi M, Narukawa N, Sumikado S, Sakaguchi T, Negi S, Ogata H, Kinugasa E.

Center of Blood Purification Therapy; First Department of Pathology, Wakayama Medical University, Wakayama; and Internal Medicine, Showa University Northern Yokohama Hospital, Yokohama, Japan.

Classic pathogeneses of secondary hyperparathyroidism (2HPT), hyperphosphatemia, vitamin D deficiency, and hypocalcemia, have been treated by the administration of phosphorus binders and vitamin D derivatives. However, these therapies have not brought about a successful result. The main reason could be attributed to hypercalcemia resulting from the administration of calcium salts as a phosphorus binder and the calcemic action of vitamin D. To prevent hypercalcemia, non-calcium-containing phosphorus binders and vitamin D analogues, which suppress parathyroid hormone (PTH) secretion with minimum calcemic action, have been developed. Furthermore, calcimimetics that stimulate the calcium-sensing receptor of parathyroid cells and suppress PTH secretion are now under clinical trial. Direct injection therapy of vitamin D analogues or calcimimetics into the parathyroid gland also has been reported. These new strategies are expected to effectively and safely suppress 2HPT, which has been resistant to conventional medical treatments. Am J Kidney Dis 41(S1):S100-S103. 2003 by the National Kidney Foundation, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12751115&dopt=Abstract [PubMed - in process]

Int J Neurosci. 2003 Feb;113(2):235-58.
Hypothalamic digoxin, cerebral chemical dominance, and pathogenesis of pulmonary diseases.

Kurup RK, Kurup PA.

Department of Medicine, Medical College Hospital, Trivandrum, Kerala, India.

The isoprenoid pathway is a key regulatory pathway in the cell. It synthesizes digoxin, an endogenous membrane Na(+)-K+ ATPase inhibitor and modulator of synaptic transmission. The role of the isoprenoid pathway in lung diseases and its relation to hemispheric dominance was assessed in this study. The following parameters were measured in patients with (i) bronchial asthma, (ii) chronic bronchitis emphysemia, (iii) idiopathic pulmonary fibrosis, (iv) sarcoidosis, and (v) in individuals with right hemispheric, left hemispheric and bihemispheric dominance: 1. plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels, 2. tryptophan, tyrosine catabolic patterns, 3. free radical metabolism, 4. glycoconjugate metabolism, and 5. membrane composition. In patients with lung disease there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels, and low ubiquinone and elevated free radical levels. The RBC membrane Na(+)-K+ ATPase activity and serum magnesium were decreased. There was also an increase in tryptophan catabolites and reduction in tyrosine catabolites in the serum. There was an increase in cholesterol:phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in these patients. The same biochemical patterns were obtained in individuals with right hemispheric chemical dominance. An upregulated isoprenoid pathway and hyperdigoxinemia are characteristic of lung disease and right hemispheric chemical dominance. Right hemispheric chemical dominance is important in deciding the predisposition to lung disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12751434&dopt=Abstract

Afr J Med Med Sci. 2002 Sep;31(3):219-22.
Oxygenation of blood in varicose veins.

Wali MA.

Department of Surgery, College of Medicine and Medical Sciences, King Khalid University, Abha, Saudi Arabia. mahmoudwalahoo.com

The aim of this prospective, controlled study is to compare the oxygen tension of blood from varicose veins with that from both the antecubital vein of the same patients and the normal long saphenous vein of normal controls at high altitude in Abha (8,000 feet above sea level), Saudi Arabia. Forty-two subjects (21 normal controls and 21 with uncomplicated primary varicose veins) had blood samples taken from 41 normal long saphenous veins and 35 varicose veins near the ankle, respectively (a total of 76 lower limbs). Samples were also taken simultaneously from the right antecubital vein in all the subjects. There was no difference in either oxygen tension (pO2) or saturation (sO2) between blood from varicose veins and blood from normal long saphenous veins. However, in patients with varicose veins, both pO2 and sO2 of varicose veins blood were significantly higher than those of arm venous blood (P = 0.009 and P = 0.018, respectively). In normal subjects, blood from normal long saphenous veins had also significantly higher sO2 (P = 0.001) than that from arm veins, but pO2 was not higher. In conclusion, the theory of arteriovenous communication is poorly founded. There must be other more important explanations for the pathogenesis of varicose veins.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12751560&dopt=Abstract

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