title: Dramatic worsening of vascular calcifications after kidney transplantation in spite of early parathyroidectomy.
abstract: Vascular calcification is a common feature in chronic dialysis patients, but their clinical significance is debated and the role of kidney transplantation (TP) in the natural history of their development has received scanty attention. We will describe a case of dramatic worsening of vascular calcifications during TP in a young patient in spite of early and successful parathyroidectomy (PTX), and will discuss other causes which might be putatively linked to vascular damage during the time of TP. A 37-year-old man on regular dialytic treatment (RDT) for 11 years, received his first cadaveric transplantation in January 1993. He underwent PTX 6 months after TP because of the lack of decreasing in parathyroid hormone values despite normal graft function. Although PTX was effective, a dramatic worsening was evident in large as well as in medium and small-sized arteries during the following three years of TP. In February 1997, few months after starting dialysis again because of the recurrence of his primary membranoproliferative glomerulonephritis (MPGN), the patient experienced myocardial infarction followed by aorto-coronary bypass (right coronary artery and anterior descending coronary artery) and leg "claudicatio". Though a role for parathyroid hormone in vascular disease has been commonly accepted, the case here reported clearly shows that blunting parathyroid gland activity may be unable to avoid the worsening of a process of vascular disease during the time of TP. Many other factors--linked to the time of TP--may be involved in vascular diseases, such as nephrotic syndrome, dyslipidemia, hypertension and drugs. In the case of our patient, a clear cut risk factor for his progressive atherosclerosis can be designated hyperlipidema and other disturbancies secondary to a nephrotic syndrome due to relapse of MPGN, together with persistent hypertension. This is the first case report in the English literature which clearly demonstrates that TP may add fuel to the fire of vascular disease also in young people and even in the absence of parathyroid hyperactivity, perhaps on the basis of a favorable genetic background. Furthermore, the history of our patient demonstrates that vascular calcifcation heralds major cardiovascular diseases.
authors.affiliation: Department of Internal Medicine of the University of Torino, S. Giovanni-Molinette Hospital, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Canavese
authors.forename: F
authors.initials: F
authors.lastname: Cesarani
authors.forename: C
authors.initials: C
authors.lastname: Stratta
authors.forename: E
authors.initials: E
authors.lastname: Maddalena
authors.forename: M
authors.initials: M
authors.lastname: Messina
authors.forename: D
authors.initials: D
authors.lastname: Hamido
authors.forename: D S
authors.initials: DS
authors.lastname: Bianchi
authors.forename: G P
authors.initials: GP
authors.lastname: Segoloni
mesh_terms: D000328:Adult; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000209:etiology*; D015432:Glomerulonephritis, Membranoproliferative / Q000150:complications / Q000601:surgery*; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D016105:Parathyroidectomy; D011859:Radiography; D006435:Renal Dialysis / Q000379:methods; D012720:Severity of Illness Index; D014652:Vascular Diseases / Q000000981:diagnostic imaging / Q000209:etiology*