MIBI scintigraphy, indicators of cell proliferation and histology of parathyroid glands in uraemic patients.

BACKGROUND: Although scintigraphy with (99m)Tc-sestamibi (MIBI) has been used to localize parathyroid glands prior to surgery for hyperparathyroidism, using it to evaluate parathyroid function remains controversial. The purpose of this study was to evaluate the possible association of MIBI uptake with gland weight, histological pattern and proliferative activity of parathyroid cells. METHODS: We studied 18 patients with secondary hyperparathyroidism (SHP); mean age 38+/-3 years, 55% female, mean time on haemodialysis 7.7+/-0.9 years. All patients had parathyroidectomy (PTx). The weights of the removed glands were estimated, and parathyroid hyperplasia was classified as diffuse (n = 28) or nodular (n = 29). The expression of proliferative cell nuclear antigen (PCNA) was evaluated by immunohistochemistry. Before PTx, all patients underwent MIBI evaluation and were categorized using a 0-3 uptake scoring system. Low uptake (scores of 0 and 1) was seen in 39 glands and high uptake (scores of 2 and 3) in 18. RESULTS: Estimated gland weights, percentage of nodular hyperplasia and PCNA expression were greater in glands with high MIBI scores than in those with low scores (P<0.01). In glands with nodular hyperplasia, PCNA expression was higher (318+/-66 cells/mm2) than in those with diffuse hyperplasia (104+/-16 cells/mm2; P<0.001). CONCLUSIONS: High MIBI scores were associated with high estimated gland weight, degree of cell proliferation and presence of nodular hyperplasia. MIBI scintigraphy is useful in clinical practice for localizing parathyroid glands, and it could guide the management of SHP by indicating the degree of its severity.

Apoptosis in kidney and pancreas allograft biopsies.

BACKGROUND: Apoptosis is a particular form of cell death involved in the elimination of somatic cells. In this study, the occurrence of apoptotic cells in kidney and pancreas allograft biopsies was analyzed and correlated with the number of infiltrating macrophages and lymphocytes and granzyme B expression. METHODS: Kidney and pancreas biopsies from patients submitted to simultaneous pancreas-kidney transplantation were classified into three groups: acute rejection, chronic rejection, and transplant cases without evidence of rejection. Formalin-fixed paraffin biopsies were used to identify apoptosis by the terminal deoxynucleotidyl transferase [TdT]-mediated dUTP nick end labeling (TUNEL) method. RESULTS: In normal kidney, only few apoptotic cells were observed. In contrast, in kidney-allograft biopsies, the TUNEL signal was detected in the nuclei of tubular epithelial cells and also in mononuclear cells scattered in the interstitium. In pancreas biopsies, numerous apoptotic cells were detected in acinar cells, in ducts, and occasionally in islets. The number of apoptotic cells in acute pancreas rejection was significantly higher compared with acute rejection of kidney grafts (50+/-14 vs. 21+/-4 cells/mm2; P<0.05). In kidney biopsies, there was a positive correlation between apoptosis and macrophages (r=0.51; P<0.005), and apoptosis versus T lymphocytes (r=0.45; P<0.05). In pancreas biopsies, the number of apoptotic cells correlated only with the number of macrophages (r=0.41; P<0.05). CONCLUSIONS: Apoptosis occurs in kidney and pancreas allograft biopsies, markedly in acute rejection in pancreas biopsies. Although apoptosis may reflect a mechanism of down-regulation of the allograft immune response by eliminating infiltrating cells, the elimination of graft cells may result in graft damage, particularly in pancreas transplantation.