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Background: Patients of end stage renal disease (ESRD) have an increased risk of cardiovascular events. Arterial stiffness is an established independent predictor of cardiovascular morbidity and mortality in ESRD patients. Carotid femoral pulse wave velocity (c-f PWV) and augmentation index (AI) are the indices which are used for the noninvasive assessment of arterial stiffness. Renal transplantation (RT) as a treatment modality in ESRD patients is associated with improvement in cardiovascular survival. Whether this improvement is due to attenuation of arterial stiffness has been inadequately investigated. The present study was conducted in ESRD patients before and 3 months after RT to assess the reversibility of the abnormalities of vascular compliance that are known to be associated with adverse outcome. Methods: Arterial stiffness indices (c-f PWV and AI) were measured using the principle of applanation tonometry with a SphygmoCor CvMS system (Atcor Medicals, Australia) in 23 ESRD patients (age: 35.9 ± 9.3 years) before and 3 months after successful RT. Results: After transplantation, augmentation index values reduced significantly as compared to their pre-transplant values (27.7 ± 11.3 % vs. 17.1 ± 9.0 %; P < 0.0001), while the carotid femoral pulse wave velocity values did not differ significantly (8.7 ± 2.0 vs. 8.6 ± 3.2 m/s). The augmentation index was correlated with the biochemical parameters of serum creatinine (Pearson r = 0.3628; P = 0.0128) and calcium phosphate product (Pearson r = 0.3868; P = 0.0079). Conclusions: Restoration of renal function following successful RT is associated with differential effects on the two indices of arterial stiffness. The salient finding of our study is that 3 months after transplantation, functional changes in vasculature lead to a significant reduction in the augmentation index, while the pulse wave velocity may take longer to show an improvement. [ABSTRACT FROM AUTHOR]

With the increasing number of patients with end stage renal disease comes an increasingly urgent need for renal replacement therapy that is both clinically effective and cost effective. This article explores some of the advantages of nocturnal hemodialysis as well as some of the barriers to its use. [ABSTRACT FROM AUTHOR]

Calcium oxalate (CaOx), calcium phosphate (CaP), and uric acid or urate are the most common crystals seen in the kidneys. Most of the crystals evoke an inflammatory response leading to fibrosis, loss of nephrons, and eventually to chronic renal failure. Of the three, CaOx monohydrate is the most reactive, whereas some forms of CaP do not evoke any discernible response. Reactive oxygen species are produced during the interactions between the crystals and renal cells and are responsible for the various cellular responses. CaOx crystals generally form in the renal tubules. Exposure of renal epithelial cells to CaOx crystals results in the increased synthesis of osteopontin, bikunin, heparan sulfate, monocyte chemoattractant protein 1 (MCP-1), and prostaglandin (PG) E2, which are known to participate in inflammatory processes and in extracellular matrix production. CaOx crystal deposition in rat kidneys also activates the renin–angiotensin system. Both Ox and CaOx crystals selectively activate p38 mitogen-activated protein kinase (MAPK) in exposed tubular cells. CaP crystals can form in the tubular lumen, tubular cells, or tubular basement membrane. Renal epithelial cells exposed to brushite crystals produce MCP-1. Basic CaP and calcium pyrophosphate dihydrate induce mitogenesis in fibroblasts, stimulate production of PGE2, and up-regulate the synthesis of metalloproteinases (MMP) while down-regulating the production of inhibitors of MMPs through activation of p42/44 MAPK. Deposition of urate crystals in the kidneys becomes associated with renal tubular atrophy, interstitial fibrosis, and development of inflammatory infiltrate. Renal epithelial cells exposed to uric acid crystals synthesize MCP-1 as well as PGE2. Monocytes or neutrophils exposed to urate crystals produce tumor necrosis factor α, interleukin-1 (IL-1), IL-6, and IL-8. Expression of IL-8 is mediated through extracellular signal-regulated kinase 1 (ERK-1)/ERK-2 and nuclear transcription factors activated protein 1 and nuclear factor κβ. Urate crystals also stimulate the macrophages to produce MMPs. [ABSTRACT FROM AUTHOR]