Cardiovascular diseases are the main causes of morbidity and mortality following renal transplantation. Atherosclerotic structural changes, which can be detected by high-resolution B-mode ultrasonography, begin before clinical findings. However, little is known about the extent of these abnormalities in children after renal transplantation. We aimed to determine early structural changes of large arteries in renal transplant recipients without cardiovascular disease and to evaluate the role of clinical and laboratory features on IMT of carotid arteries. IMT and hemoglobin, serum levels of creatinine, acute phase proteins, lipid profile, and homocysteine were examined in 24 asymptomatic renal transplant recipients (median age 16.5 yr; range 8-25), and 20 healthy controls (median age 16 yr; range 9-24). CCA and ICA were evaluated in patients and controls with a high-resolution B-mode ultrasonography in multiple projections to optimize detection of carotid IMT. Measurement of IMT of both CCA [0.36 mm (range 0.16-0.48) vs. 0.28 mm (range 0.21-0.35), p < 0.001] and ICA [0.27 mm (range 0.16-0.48) vs. 0.22 mm (range 0.1-0.26), p < 0.001] were significantly higher in renal recipients than in healthy controls. Among several parameters assessed, only significant correlations were found between duration of CRF, duration of dialysis prior to transplantation and ICA-IMT (p = 0.06 and p = 0.02, respectively) and between mean past serum calcium-phosphorus ion product and CCA-IMT (p = 0.002). In conclusion, our observations indicate that vascular changes begin early in the course of CRF and are directly related to time on CRF and dialysis. These changes can be detected by measuring CCA/ICA-IMT ultrasonographically. We suggest that early renal transplantation can potentially avoid long-term cardiovascular events in children with end stage kidney disease.
The authors present two cases of primary sclerosing epithelioid fibrosarcoma (SEF) of the kidney. Both patients had a mass in the upper part of the left kidney without any primary extrarenal neoplastic lesions. Grossly, the tumors were solid masses both measuring 7.5 cm in the greatest diameter. Histologically, one of the lesions exhibited a predominantly lobular growth of round or oval small uniform epithelioid cells in variable cellularity. Circular zones of crowded tumor cells alternating with hypocellular collagenous tissue in a concentric fashion around entrapped native renal tubules were distinctive. The second case was distinctive with significant cytological atypia in the neoplastic cells and prominent reactive proliferations in the trapped renal tubules. Immunohistochemically, vimentin, bcl-2 and MUC4 were diffusely positive in both. They were negative for S-100 protein, CD34, and desmin, whereas CD99 were positive in one lesion. Fluorescence in situ hybridization assay using dual staining probes detected EWSR1-CREB3L1 fusion in each lesion, which is characteristic molecular findings of SEF. One patient presented widespread distant metastases at the time of diagnosis. In the other, no tumor deposits were detected other than primary. Both patients have been alive with 30 and 10 month follow-ups, respectively. These tumors are 6th and 7th cases of primary renal SEF in the literature confirmed by FISH study, which exhibit unique and remarkable histomorphologic features.
Patients with endothelial dysfunction had significantly higher ambulatory blood pressure values and higher BPV. There was a significant negative correlation between endothelial function and BPV.
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