Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
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Target Concepts:
Gene/Protein
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Query: EC:4.1.1.6 (
CAD
)
4,420
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Histopathological findings of 13 LRD and 17
CAD
renal allografts of paediatric recipients were prospectively semiquantitatively scored and correlated with clinical and functional parameters 18 and 36 months after transplantation. The most common findings at 18 months were diffuse interstitial fibrosis (incidence 57%), glomerular mesangial matrix increase (91%), arteriolar intimal proliferation (70%), and tubular atrophy (83%). Most changes were mild and most biopsies were scored normal or borderline (Banff classification). At 18 and at 36 months 30% of grafts showed mild chronic rejection (CR). Only two grafts showed grade II CR at 18 months and one graft grade III CR at 36 months. Progressive CR was not seen. Donor source or recipient age had no effect on graft histology. Vascular-interstitial cyclosporin (CsA) nephrotoxicity was not found. On the contrary, cumulative CsA dose (mg/kg/day) showed an inverse correlation with arteriolar intimal proliferation (P < 0.001). 51Cr-EDTA and lithium clearances showed inverse correlations with diffuse interstitial fibrosis and lymphocytosis. PAH clearance did not correlate with interstitial or vascular changes. The results indicate good prognosis in children on triple immunosuppression (with CsA administered in three doses/day to pre school children) regardless of donor source.
Nephrol
Dial
Transplant 1995
PMID:Renal allograft histology and correlation with function in children on triple therapy. 772 39
All uremic patients have multiple risk factors for
CAD
including in many, the conditions that caused their ESRD--for example, diabetes and hypertension. conventional risk factors--for example, dyslipidemia and hyperhomocysteinemia. risk factors that are unique to uremia--for example, calcium and phosphate abnormalities. PD patients have particular risk with respect to their lipid status and hyperinsulinemia. Many of these risks are potentially modifiable, but evidence does not exist to assess the impact of treatment on clinical outcomes. Therefore, current decisions for therapy directed at risk factor modification must be made on an individual basis.
Perit
Dial
Int 2000
PMID:Major and minor risk factors for cardiovascular disease in peritoneal dialysis. 1091 62
Chronic kidney disease (CKD) has become a major health-care problem of global proportions. Progression to end-stage renal disease (ESRD), the need for renal replacement therapy, and the high annual death rate of dialysis patients are the most noticeable outcomes of CKD. Less appreciated, however, is the fact that most patients with CKD actually die mainly from cardiovascular disease, rather than progress to ESRD. Coronary artery calcification (CAC), a surrogate marker of atherosclerosis, is common in dialysis and CKD patients. Coronary artery calcium scores, as measured by ultrafast computed tomography, is an independent predictor of future cardiac events. Using this technique, several studies have documented extensive calcification in dialysis patients, a subject of several exhaustive reviews. Unfortunately, much less attention has been paid to calcification in nondialyzed patients with CKD. In this review, I will emphasize the fact that CVC is common in patients with CKD not yet on dialysis, develops early in the course of CKD, and worsens with the decline in renal function particularly among diabetics who progressed to ESRD. I will also discuss the pathogenesis of CVC in CKD patients and highlight the lack of a major role for abnormalities of mineral metabolism in the pathogenesis of calcification in CKD patients. In addition to the high prevalence of traditional risk factors for
CAD
, the presence of proteinuria, reduced renal function, diabetic nephropathy, and the rate of progression to ESRD may represent the main uremia-related factors that increase the risk for calcification in CKD. Finally, I will review the protective role of inhibitors of calcification in CKD.
Semin
Dial
PMID:Cardiovascular calcification in nondialyzed patients with chronic kidney disease. 1737 87