given to prevent possible new extramedullary haemopoiesis. Pier Paolo Piccaluga, Carlo Finelli, Ernesto Vigna, Claudio Agostinelli, Francesco Bacci, Stefania Padini, Cristina Papayannidis, Claudio Laterza, Giovanni Martinelli, Stefano A Pileri, Michele Baccarani Institute of Haematology and Medical Oncology ‘‘L and A Sera ` gnoli’’, University of Bologna, Bologna, Italy Correspondence to: Dr Pier Paolo Piccaluga, Institute of Haematology and Medical Oncology ‘‘L and A Sera ` gnoli’’, S Orsola Malpighi Hospital, University of Bologna, Via Massarenti, 9-40138 Bologna, Italy; ppicca@med.unibo.it doi: 10.1136/jcp.2006.039149 Obesity-related glomerulopathy: another nail in the coffin of the epidemic of end-stage renal disease The clustering of insulin resistance, dysglycae- mia, dyslipidaemia, hypertension and central obesity represents the major features of meta- bolic syndrome. These clusters of factors may share common aetiology, each of which is a risk factor for cardiovascular disease. The metabolic syndrome seems to affect between 10% and 25% of adult populations worldwide. Several studies have described the association between metabolic syndrome, and diabetes and cardiovascular disease. 1 Although obesity is often associated with diabetes and hyperten- sion, which are two of the most common risk factors for the development of end-stage renal disease (ESRD), it has been suggested that obesity in itself is an independent risk factor. The prevalence of obesity-related glomerulo- pathy (ORG), which may lead to end-stage renal disease, has increased 10-fold over the past 15 years as a consequence of the spread of the obesity epidemic. The increasing prevalence of ESRD, with its associated high annual mortality and rates of cardiovascular complications, is a worldwide problem. 2 In the US alone, the prevalence of ESRD has more than doubled in the past decade and the population living with ESRD is projected to increase to 650 000 persons by the year 2010, with associated Medicare expenditures of $28 billion. 3 Identifying new and potentially modifiable risk factors for ESRD is critical in order to devise effective, population- based preventive strategies. Massive obesity has been shown to produce nephrotic syndrome, and it has been reported that proteinuria and segmental glomerulo- sclerosis can be present in obese patients, even in the absence of diabetes. 2 In addition, a large- scale study including 6818 renal biopsies from 1986 to 2000 showed a 10-fold increase in renal lesion, such as glomerulomegaly and focal segmental glomerulosclerosis, which were asso- ciated with obesity. 2 ORG was recently defined morphologically as glomerulomegaly with or without focal segmental glomerulosclerosis. The syndrome constitutes the triad of morbid obesity, marked proteinuria without oedema and normal serum albumin concentration. It can occur in any degree of obesity but is more common in the morbidly obese group—that is, body mass index .40 kg/m 2 . It often presents as proteinuria on urinary dipsticks, followed by the confirmation of gross proteinuria of up to 32 g/dl. ORG should be diagnosed by excluding the presence of hypertension or undetected type 2 diabetic renal diseases. 2 The pathogenesis is unknown (thought to be due to low renal nitric oxide production) and most of the available information comes from studies in Zucker fa/fa rats which often die from ESRD. These rats are a genetic model of obesity that results from a mutation in the leptin receptor gene. 4 Homozygous Zucker fa/fa rats exhibit most of the metabolic picture seen in human obesity, including hypercholesterolaemia, hypertrigly- ceridaemia, hyperinsulinaemia and proteinuria. Although the condition is said to be benign, a small proportion of patients will progress towards end-stage renal failure requiring replacement therapy, a further addition to the cost. The condition is readily reversible and ameliorated with weight loss, an important consideration in the management of this condition. In association with increasing pre- valence of chronic kidney disease, this will inevitably result in increasing proportions of deaths from cardiovascular disease as well as increased prevalence and associated conse- quences of other complications of chronic kidney disease. A concerted, global initiative is required to deal with the ORG epidemic. Mohamed H Ahmed Department of Chemical Pathology, Southampton General Hospital, Southampton, UK Atif A Khalil Department of Nephrology, Royal Liverpool University Hospital, Liverpool, UK Correspondence to: Dr M H Ahmed, Department of Chemical Pathology, Mail point 6, Level D South Academic Block, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK; elziber@yahoo.com doi: 10.1136/jcp.2006.040410 References 1 Wild SH, Byrne CD. The global burden of the metabolic syndrome and its consequences for diabetes and cardiovascular disease. In: Byrne CD, Wild SH, eds. Metabolic syndrome. Chichester: Wiley & Sons, 2005:1–32. 2 Kambham N, Markowitz GS, Valeri AM, et al. Obesity-related glomerulopathy: an emerging epidemic. Kidney Int 2001;59:1498–509. 3 Xue JL, Ma JZ, Louis TA, et al. Forecast of the number of patients with end-stage renal disease in the United States to the year 2010. J Am Soc Nephrol 2001;12:2753–8. 4 Gades MD, Van Goor H, Kaysen GA, et al. Brief periods of hyperphagia cause renal injury in the obese Zucker rat. Kidney Int 1999;56:1779–87. Osseous metaplasia in ovarian tumours: a case with serous cystadenoma In a recent paper in the Journal of Clinical Pathology, Godbole et al 1 reported a case of osseous metaplasia in a benign ovarian cyst in association with cloacal anomaly. These authors stated that only four published cases with osseous metaplasia in ovarian tumours exist, three in the literature, 2–4 and the one they presented. The former three cases were asso- ciated with papillary serous carcinoma, the- coma and endometrioma in a supernumerary ovary, respectively. According to their data, Godbole et al concluded that osseous metapla- sia is more common in anatomically abnormal ovarian tissue in women of reproductive age. However, a thorough search we made in the literature revealed that to date, the total number of cases with osseous metaplasia in an ovarian tumour reported in the literature has reached 10, 1–10 (one of them 5 was actually added after the report of Godbole et al, whereas one more case is described herein). Our case concerns a 37-year-old woman who was subjected to hysterectomy with the right adnexa, owing to multiple leiomyomas. The right ovary measured 7 cm in diameter, and presented an osseous lesion that was hard in consistency and 3 cm in diameter. Histologic examination, after decalcification, showed a serous cystade- noma with extensive, circumferential osseous metaplasia of its wall (fig 1). The cyst wall was lined by a single layer of flattened or cuboidal cells, whereas the osseous tissue consisted of mature lamellar bone. The ovary was searched thoroughly to exclude the possibility of an underlying teratoma. The rest of the pathology of the present specimen revealed only the afore- mentioned uterine leiomyomas. This is the first reported case where osseous metaplasia has occurred in a benign ovarian serous cystadenoma. Bone formation in the ovary, with the exception of developing in the setting of a mature cystic teratoma or a heterologous mixed mesodermal tumour, is exceedingly uncommon. Excluding the previous cases, so far, the ovarian neoplasms most commonly associated with osseous metaplasia are muci- nous cystadenomas (three cases), 6–8 followed by serous cystadenocarcinomas (two cases). 29 A minority only seems to occur in anatomically abnormal ovaries (two cases). The most plau- sible explanation for bone formation in an ovarian neoplasm is a metaplastic process of the multipotential stromal cell. No prognostic significance has been attributed to this unusual phenomenon. D Miliaras Laboratory of Histology & Embryology, Medical School, Aristotle University of Thessaloniki, Greece M Ketikidou Department of Pathology, National Security Foundation (IKA), Thessaloniki, Greece Accepted 3 May 2006 Funding: This work was supported in part by COFIN 2002–2003 (MB), AIRC, AIL Bologna, Ateneo 60% (MB and SAP), and Fondazione del Monte di Bologna e Ravenna grants. PPP was supported by Italian– American Cancer Foundation and AIRC (Leonino Fontana e Maria Lionello fellowship). Competing interests: None declared. Competing interests: None declared. Figure 1 The cyst wall is lined a single layer of cells and contains abundant osseous tissue. Ovarian stroma is seen on the right part of the picture. Original magnification, 6 25. 582 PostScript www.jclinpath.com