P Martínez

Morphological findings in 70 kidneys of living donors for renal transplant

Seventy donor kidneys for transplant were studied with light microscopy (LM), electron microscopy (EM) and immunofluorescence (IM) for C3, C4, Clq, IgG, IgA, IgE, IgM, and antifibrin; the samples were taken just before transplanting the allograft kidney. Glomerular changes were found in 35.7% of apparently normal living donors: 9 cases showed relative glomerular ischemia with an irregular basal membrane (12.9%); 5 cases showed a diffusely widened basal membrane without antecedents of hyperglycemia (7.1%); in one case (1.4%) there was a lesion similar to type 1 mesangio-capillary glomerulonephritis with C3++, IgG++, IgA+, and IgM+; in another case (1.4%) there were scant isolated C3 glomerular, subepithelial deposits with indentation of the basement membrane of the immunocomplex type with a microhematuria which was demonstrated only after donation, and in 9 cases (among them two pairs of siblings) there were mesangial IgA and mesangial electron-dense deposits compatible with Bergers disease (12.9%). None of these glomerulopathies were evident under LM.

Association of adrenal medullar and cortical nodular hyperplasia: a report of two cases with clinical and morpho-functional considerations.

Arterial hypertension of adrenal etiology is mainly attributed to primary hyperaldosteronism. However, subtle expressions of hyperadrenergic or glucocorticoid excess can also generate arterial hypertension. The present report describes two hypertensive patients cataloged as resistant essential hypertensives, in whom adrenal masses were found incidentally, who highlight the need to recognize these tenuous clinical or laboratory presentations. Case 1 was a 50-yr-old female with hyperadrenergic hypertension associated to a left adrenal node, normal cortisol and aldosterone:renin ratio, marginally increased urinary normetanephrine, and a positive 131I MIBG radioisotope scan. Adrenalectomy normalized blood pressure and urinary metanephrines. Pathology showed a hyperplastic adrenal medulla associated to a multinodular cortical hyperplasia. Case 2 was a 62-yr-old female with progressive hypertension, a slight Cushing phenotype, non-suppressible hypercortisolism, normal urinary metanephrines, and bilateral adrenal nodes. Bilateral adrenalectomy and subsequent replacement normalized blood pressure and phenotypic stigmata. Pathology demonstrated bilateral cortical multinodular hyperplasia and medullary hyperplasia. The clinical study in both patients was negative for MEN. The apparently rare association of cortical and medullary lesions presented by both patients is probably overlooked in routine pathology exams, but should be meticulously searched since the crosstalk between the adrenal cortex and medulla may prompt dual abnormalities.