Cardiovascular disease (CVD) is the leading cause of death in dialysis patients and the most common cause of death and allograft loss among kidney transplant recipients. End-stage renal disease (ESRD) is associated with an increased incidence and prevalence of a wide range of CVDs including coronary artery disease, stroke, congestive heart failure, atrial fibrillation, sudden cardiac death, pulmonary hypertension, and valvular heart disease. CVD risk factors are very common in patients with ESRD, and most patients have multiple risk factors. Kidney transplantation is the treatment of choice for patients with ESRD, as a successful transplant improves longevity and quality of life, primarily by decreasing the incidence and severity of CVD. Correction of the uremic state and improved glomerular filtration rate seem to be the major mechanism of this benefit. Transplant candidates should undergo cardiovascular assessment, usually echocardiography and exercise stress testing, and may require formal cardiology consultation. Higher risk candidates, including those aged >50 years, hypertension, diabetes, established coronary artery disease or peripheral vascular disease, left ventricular hypertrophy, and dialysis duration >1 year, should have repeat cardiovascular assessment every 1-2 years. Transplant candidates and recipients should have individualized treatment for CVD and risk factors such as hypertension, diabetes, hyperlipidemia, and obesity. Special consideration should be given for statin therapy, as its use is associated with decreased cardiovascular death in dialysis and transplant patients. Prospective randomized, controlled trials are needed to determine the optimal approach to diagnosis and treat CVD in the transplant candidate and recipient population.
We are presenting a case of renal failure with anti-GBM and p-ANCA antibodies positive. Patients with dual antibodies are considered to be a vasculitis-variant of anti-GBM antibody nephritis. These patients may have atypical presentation and it may delay diagnosis and treatment. Recurrence rate is higher in these patients. We reviewed the literature of cases and studies on cresenteric glomerulonephritis with anti-GBM and p-ANCA positive patients. We recommend that patients suspected with pulmonary-renal syndrome should be checked for anti-GBM and p-ANCA antibodies, should undergo renal biopsy and should should have close long term follow up to watch for recurrence.
Our laboratory documented progressive developments in our understanding of the unknown biological action of several classes of acetoxycoumarins (AC). These studies could be considered as significant from the point of view of unraveling the biological activity of AC for the first time when there was explosion of knowledge on the parent polyphenols alone.1) Firstly, 7,8-diacetoxy-4-methylcoumarin (DAMC) was found to interact with free radical resulting in the removal of acetyl group as the acetyl radical (CH 3 CO ϩ ) and the formation of phenoxyl radical as confirmed by pulse radiolysis.2) This finding accounted for the antioxidant action of AC independent of the formation of parent polyphenol 7,8-dihydroxy-4-methylcoumarin (DHMC). The observation that microsomes acted upon AC and caused the irreversible inhibition of several enzymes such as cytochrome P-450-linked mixed function oxidases (MFO) and the activation of nicotinamide adenine dinucleotide reduced (NADPH) cytochrome c reductase, prompted us to investigate the mode of action of AC.3) Further, detailed studies revealed the role of a unique enzyme (Fig. 1) catalyzing the transfer of acetyl group from AC to receptor proteins. 4,5) This enzyme was termed Acetoxy Drug: Protein Transacetylase (TAase), since the acetoxy derivatives of several classes of polyphenols were found to be substrates for TAase. [5][6][7][8] TAase from microsomes of rat and bovine liver as well as from human placenta were purified to homogeneity and its identity with the endoplasmic reticulum luminal protein Calreticulin (CR) was established and TAase was termed Calreticulin Transacetylase (CRTAase).9,10) In our earlier work, we have focused our attention on the role of CRTAase mediated acetylation of certain protein targets by acetoxycoumarins in the blood lymphocytes of asthmatic patients. We have demonstrated the irreversible inhibition of human blood lymphocyte Protein Kinase C (PKC) by way of acetylation. These studies revealed that several AC inhibited PKC of asthmatic patients.11) Several respiratory diseases such as coronary obstructive pulmonary diseases (COPD) and asthma are associated with hyperplasia and hypertrophy of airway smooth muscle. NO is strongly implicated in the amelioration of pathologies associated with the proliferation of airway smooth muscle cells. 12) Hence, it was thought interesting to investigate the influence of AC on tracheal smooth muscle cell (TSMC) NOS, with a view to highlight the possible application of AC in the management of airway diseases. The Transacetylase function of Calreticulin (CR) catalyzing the transfer of acetyl groups from acetoxycoumarins (AC) to certain proteins was identified for the first time in our laboratory. Protein acetyltransferase action of CR was termed Calreticulin Transacetylase (CRTAase). In the present work, CRTAase of rat tracheal smooth muscle cells (TSMC) was characterized with respect to the specificity for various AC and its role in the activation of nitric oxide synthase (NOS). 7,8-Diacetoxy-4-methylcoumarin (DAMC...
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