The International Journal of Romanian Society of Endocrinology / Registered in 1938

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  • Case Report

    Badiu C, Capatana C, Cristofor D, Mircescu G, Coculescu M

    Apparent mineralocorticoid excess in a case of lung paraneoplastic Cushing syndrome

    Acta Endo (Buc) 2005 1(1): 97-107 doi: 10.4183/aeb.2005.97

    Abstract References
    Severe hypokalemia is a life threatening event, which triggers a number of therapeutic and diagnostic attitudes. In this paper we present a case of 63 years old man, who presented with progressive lassitude, edema, weight loss. The mild hypertension and hyperglycaemia were treated with spironolactone and diet. Initial evaluation showed severe hypokalemia (1.7 mmol/l), hepatomegalia, hyperplasic/nodular adrenal masses; in addition, he has developed a right middle lobe pneumonia which improved with antibiotics. Referred for the suspicion of hyperaldosteronism, aldosterone values were normal (9.3-9.5 ?g/dl), but ACTH was high (725 pg/ml) and did not suppress (710.8 pg/ml) to high dose DXM, as well as cortisol: basal values 27.78 ug/dl, high dose DXM 35.06 ug/dl, showing an ACTH dependent Cushing syndrome despite lack of suggestive clinical signs. Tumor markers suggested a neuroendocrine neoplasia: carcinoembryonic antigen=101 ng/ml (normal values=0.52-6.3 ng/ml), CA 19-9= 155 ng/ml (N < 33 ng/ml). Further radiological evaluation showed a 3 cm right lobe lung tumour. Despite high potassium supplements and spironolactone, the hypokalemia remained around 3.2 mmol/l, characteristic for an apparent mineralocorticoid excess. Because of aggressive evolution of the lung tumour, he died three months after the initial admission into the hospital. Pathology report showed a lung carcinoma. ACTH immunostaining of the lung tumour was positive and revealed a paraneoplastic secretion.
    1. Martinez Maldonado Manuel. Approach to the patient with hypokalemia. In: Humes H.David, editor. Kelley?s Textbook of Internal Medicine. Lippincott Williams & Wilkins, 2000.
    2. Beuschlein F, Hammer GD. Ectopic pro-opiomelanocortin syndrome. Endocrinol Metab Clin North Am 2002; 31(1):191-234. [CrossRef]
    3. Schrier W Robert. The patient with hypokalemia or hyperkalemia. Manual of nephrology. Lippincott Williams& Wilkins, 2000.
    4. Davison M.Alex. Hypo-hyperkalemia. Oxford Textbook of Clinical Nephrology. Oxford University Press, 2003.
    5. Walker BR, Campbell JC, Fraser R, Stewart PM, Edwards CR. Mineralocorticoid excess and inhibition of 11 beta-hydroxysteroid dehydrogenase in patients with ectopic ACTH syndrome. Clin Endocrinol (Oxf) 1992; 37(6):483-492. [CrossRef]
    6. Campusano C, Arteaga E, Fardella C, Cardenas I, Martinez P. [Cushing syndrome by ectopic ACTH secretion: analysis of the physiopathologic mechanism of hypokalemia. Report of two cases]. Rev Med Chil 1999; 127(3):332-336.
    7. Torpy DJ, Mullen N, Ilias I, Nieman LK. Association of hypertension and hypokalemia with Cushing?s syndrome caused by ectopic ACTH secretion: a series of 58 cases. Ann N Y Acad Sci 2002; 970:134-144. [CrossRef]
    8. Torpy DJ, Mullen N, Ilias I, Nieman LK. Association of hypertension and hypokalemia with Cushing?s syndrome caused by ectopic ACTH secretion: a series of 58 cases. Ann N Y Acad Sci 2002; 970:134-144. [CrossRef]
    9. Newell-Price J, Trainer P, Besser M, Grossman A. The diagnosis and differential diagnosis of Cushing?s syndrome and pseudo-Cushing?s states. Endocr Rev 1998; 19(5):647-672. [CrossRef]
    10. Howlett TA, Drury PL, Perry L, Doniach I, Rees LH, Besser GM. Diagnosis and management of ACTH-dependent Cushing?s syndrome: comparison of the features in ectopic and pituitary ACTH production. Clin Endocrinol (Oxf) 1986; 24(6):699-713. [CrossRef]
    11. Schiller JH, Jones JC. Paraneoplastic syndromes associated with lung cancer. Curr Opin Oncol 1993; 5(2):335-342. [CrossRef]
    12. Crapo L. Cushing?s syndrome: a review of diagnostic tests. Metabolism 1979; 28(9):955-977. [CrossRef]
    13. White A, Clark AJ, Stewart MF. The synthesis of ACTH and related peptides by tumours. Baillieres Clin Endocrinol Metab 1990; 4(1):1-27. [CrossRef]
    14. Wajchenberg BL, Mendonca B, Liberman B, Adelaide M, Pereira A, Kirschner MA. Ectopic ACTH syndrome. J Steroid Biochem Mol Biol 1995; 53(1-6):139-151.
    15. Kraus J, Buchfelder M, Hollt V. Regulatory elements of the human proopiomelanocortin gene promoter. DNA Cell Biol 1993; 12(6):527-536. [CrossRef]
    16. Stewart PM, Gibson S, Crosby SR, Penn R, Holder R, Ferry D et al. ACTH precursors characterize the ectopic ACTH syndrome. Clin Endocrinol (Oxf) 1994; 40(2):199-204. [CrossRef]
    17. Wajchenberg BL, Mendonca B, Liberman B, Adelaide M, Pereira A, Kirschner MA. Ectopic ACTH syndrome. J Steroid Biochem Mol Biol 1995; 53(1-6):139-151.
    18. Kocijancic I, Vidmar K, Zwitter M, Snoj M. The significance of adrenal metastases from lung carcinoma. Eur J Surg Oncol 2003; 29(1):87-88. [CrossRef]
    19. Usalan C, Emri S. Membranoproliferative glomerulonephritis associated with small cell lung carcinoma. Int Urol Nephrol 1998; 30(2):209-213. [CrossRef]
    20. Norris SH. Paraneoplastic glomerulopathies. Semin Nephrol 1993; 13(3):258-272.
    21. Terzolo M, Reimondo G, Ali A, Bovio S, Daffara F, Paccotti P et al. Ectopic ACTH syndrome: molecular bases and clinical heterogeneity. Ann Oncol 2001; 12 Suppl 2:S83-S87. [CrossRef]
    22. Shepherd FA, Laskey J, Evans WK, Goss PE, Johansen E, Khamsi F. Cushing?s syndrome associated with ectopic corticotropin production and small-cell lung cancer. J Clin Oncol 1992; 10(1):21-27.
    23. Abeloff MD, Trump DL, Baylin SB. Ectopic adrenocorticotrophic (ACTH) syndrome and small cell carcinoma of the lung-assessment of clinical implications in patients on combination chemotherapy. Cancer 1981; 48(5):1082-1087. [CrossRef]
    24. Pastore V, Santini M, Vicidomini G, D?Aniello G, Fiorello A, Parascandolo V. [Role of the surgeon in the treatment of small cell lung carcinoma]. Minerva Endocrinol 2001; 26(4):263-267.
  • Endocrine Care

    Mircescu G, Capusa C, Andreiana I

    The management of secondary hyperparathyroidism in chronic kidney disease

    Acta Endo (Buc) 2005 1(2): 181-200 doi: 10.4183/aeb.2005.181

    Abstract References
    Secondary hyperparathyroidism, i.e. increased synthesis and secretion of parathyroid hormone and gland hyperplasia, is commonly found in chronic kidney disease. Although it is, at first, an adaptive response to the loss of renal functions in order to maintain the calcium/phosphate homeostasis and normal bone turnover, it is also an important cause of increased morbidity in this clinical setting by leading to renal osteodystrophy and cardiovascular complications. Recent advances in the knowledge on the pathogenesis of parathyroid-related complications in renal failure allowed for new therapeutic approaches. However, many problems remain to be solved in the future. This paper briefly presents the current understanding of pathogenic mechanisms of hyperparathyroidism, bone disease and vascular calcification during chronic kidney disease. In addition, it summarizes the main therapeutic methods available today for controlling secondary hyperparathyroidism and the challenges of practitioners concerning this issue. Finally, the current status of secondary hyperparathyroidism management is analyzed, with emphasis on the Romanian experience.
    1. K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. Am J Kidney Dis, 42(4, suppl 3):S1-S201, 2003. [CrossRef]
    2. Hsu C-Y, Chertow GM. Chronic renal confusion: Insufficiency, failure, dysfunction, or disease. Am J Kidney Dis, 36(2):415-418, 2000. [CrossRef]
    3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification, Am J Kidney Dis, 39(suppl 1):S1-S92, 2002.
    4. Mircescu G, Capusa C. Chronic kidney disease: A useful concept for integrated approach of chronic renal failure (Part I). Medicina Interna, 1(4):17-28, 2004.
    5. Fournier A, Oprisiu R, Hottelart C et al. Renal osteodystrophy in dialysis patients: Diagnosis and treatment. Artif Org, 22(7):530-557, 1998. [CrossRef]
    6. Elder J. Pathogenesis and management of hyperparathyroidism in end-stage renal disease and after renal transplantation. Nephrology, 6:155-160, 2001. [CrossRef]
    7. Cozzolino M, Brancaccio D, Gallieni M, Galasi A, Slatopolsky E, Dusso A. Pathogenesis of parathyroid hyperplasia in renal failure. J Nephrol, 18(1):5-8, 2005.
    8. Dusso AS, Thadhani R, Slatopolsky E. Vitamin D receptor and analogs. Sem Nephrol, 24(1):10-16, 2004. [CrossRef]
    9. Dusso AS. Vitamin D receptor: Mechanisms for vitamin D resistance in renal failure. Kidney Int, 63(suppl 85):S6-S9, 2003. [CrossRef]
    10. Urena P, Frazao JM. Calcimimetic agents: Review and perspectives. Kidney Int, 63(suppl 85): S91- S96, 2003. [CrossRef]
    11. Slatopolsky E, Dusso A, Brown AJ. Control of uremic bone disease: Role of vitamin D analogs. Kidney Int, 61(suppl 80):S143-S148, 2002. [CrossRef]
    12. Fatica RA, Dennis VW. Cardiovascular mortality in chronic renal failure: hyperphosphatemia, coronary calcification, and the role of phosphate binders. Cleve Clinic J Med, 69(suppl 3):S21-S27, 2002. [CrossRef]
    13. Hruska KA, Saab G, Chaudhary LR, Quinn CO, Lund RJ, Surendran K. Kidney-bone, bone-kidney, and cell-cell communications in renal osteodystrophy. Semin Nephrol, 24(1):25-38, 2004. [CrossRef]
    14. Hercz G. Regulation of bone remodeling: Impact of novel therapies. Semin Dialysis, 14(1):55-60, 2001. [CrossRef]
    15. Malluche HH, Langub MC, Monier-Faugere M-C. The role of bone biopsy in clinical practice and research. Kidney Int, 56(suppl 73): S20-S25, 1999. [CrossRef]
    16. Couttenye MM, D?Haese PC, Verschoren WJ, Behets GJ, Schrooten I, De Broe ME. Low bone turnover in patients with renal failure. Kidney Int, 56(suppl 73): S70-S76, 1999. [CrossRef]
    17. Ganesh SK, Stack AG, Levin NW, Hulbert-Shearon TE, Port FK. Association of elevated serum PO4, Ca ? PO4 product and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol, 12(10):2131-2138, 2001.
    18. Giachelli CM, Jono S, Shioi A, Nishizawa Y, Mori K, Morii H. Vascular calcification and inorganic phosphate. Am J Kidney Dis, 38(suppl 1):S34-S37, 2001. [CrossRef]
    19. Wilmer WA, Magro CM. Calciphylaxis: Emerging concepts in prevention, diagnosis, and treatment. Semin Dialysis, 15(3):172-186, 2002. [CrossRef]
    20. Shanahan C. Bone turnover and extraosseous calcifications: Is there a relationship? Presentation at the ASN Renal Week, San Diego, Nov 2003,
    21. Block G, Port FH. Calcium phosphate metabolism and cardiovascular disease in patients with chronic kidney disease. Semin Dialysis, 16(2):140-147, 2003. [CrossRef]
    22. Elder GJ. Targets for phosphate control in chronic kidney disease. Nephrology, 9:2-6, 2004. [CrossRef]
    23. Block GA, Martin KJ, de Francisco AM et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med, 350:1516-1525, 2004. [CrossRef]
    24. De Francisco AM, Ellis HA, Owen JP et al. Parathyroidectomy in chronic renal failure. Q J Med, 55(218):289-315, 1985.
    25. Malberti F, Marcelli D, Conte F, Limido A, Spotti D, Locatelli F. Parathyroidectomy in patients on renal replacement therapy: An epidemiologic study. J Am Soc Nephrol, 12:1242-1248, 2001.
    26. TominagaY, Uchida K, Haba T et al. More than 1000 cases of total parathyroidectomy with forearm autograft for renal hyperparathyroidism. Am J Kidney Dis, 38(4, suppl 1):S168-S171, 2001. [CrossRef]
    27. Mircescu G, C?pu?? C. Guidelines for surgical management of secondary hyperparathyroidism in dialysis patients. Nefrologia, 9(23-24):51-56, 2004.
    28. De Francisco AM, Fresnedo GF, Rodrigo E, Pinera C, Amado JA, Arias M. Parathyroidectomy in dialysis patients. Kidney Int, 61(suppl 80): S161-S166, 2002. [CrossRef]
    29. The CARI Guidelines (Caring for Australians with Renal Impairment) for bone disease, calcium, phosphate and parathyroid hormone. / Australian Kidney Foundation and Australia New Zealand Society of Nephrology
    30. Mircescu G et al, on behalf of the Romanian Society of Nephrology. Guidelines for best medical practice: Secondary hyperparathyroidism in chronic kidney disease, Ed. InfoMedica, Bucharest, 2005.
    31. Kim J, Pisoni RL, Danese MD et al. Achievement of proposed NKF-K/DOQI bone metabolism and disease guidelines : Results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Abstract for ASN Annual Meeting - San Diego, J Am Soc Nephrol (Nov), 1
  • General Endocrinology

    Capusa C, Chirculescu B, Vladu I, Viasu L, Lipan M, Mota E, , Mircescu G

    The Prevalence of Biochemical Abnormalities of Chronic Kidney Disease. Mineral and Bone Disorders in Untreated Non-dialysis Patients – A Multicenter Study

    Acta Endo (Buc) 2016 12(3): 282-290 doi: 10.4183/aeb.2016.282

    Background. There are scarce data about prevalence of mineral metabolism (MM) disorders in Romanian predialysis patients, so we assessed their occurrence and relationships in mild to severe chronic kidney disease (CKD). Methods. One hundred fifteen non-dialysis CKD (eGFR 31, 95% CI 29-35mL/min) and 33 matched non-CKD subjects entered this multicentric, cross-sectional study. Serum 25-hydroxyvitamin D (25OHD), intact parathyroid hormone (iPTH), phosphate (PO4), total calcium (tCa) and alkaline phosphatase (AP) were measured, along with demographic and past medical history data. Results. Hypovitaminosis D was equally prevalent in Controls and CKD (91% vs. 96% had 25OHD<30ng/mL). Increasing proportions of hyperparathyroidism (33% - stage 2 to 100% - stage 5; p<0.001) and hyperphosphatemia (2% - stage 3 to 38% - stage 5; p<0.001) were found. Hypocalcemia was more prevalent in stage 5 (25% vs. 6% in stage 4, none in stage 3 and Controls, p<0.001). Mineral metabolism parameters correlated with eGFR. In addition, iPTH was directly associated with PO4, AP, and urinary albumin-tocreatinine ratio (ACR), but inversely with tCa and 25OHD, while negative correlation of 25OHD with age, AP, ACR, and C-reactive protein emerged. In multiple regression, eGFR was the only predictor of iPTH (Beta -0.68, 95%CI -1.35 to -0.90, R2 0.46, p<0.001), whereas age and ACR were the determinants of 25OHD (a model which explained 14% of its variation). Conclusions. Hypovitaminosis D was very common irrespective of CKD presence and severity, and it seems worsened by older age and higher albuminuria. Hyperparathyroidism preceded hyperphosphatemia and hypocalcemia, and it seems mostly dependent on kidney function decline
  • Editorial

    Mircescu G

    Oxidative stress of chronic kidney disease

    Acta Endo (Buc) 2008 4(4): 433-446 doi: 10.4183/aeb.2008.433

    Oxidative stress is defined as a rupture in the prooxidant-antioxidant balance in favor of\r\nthe former, leading to characteristic changes in biomolecules of all types, and to tissue damage.\r\nIt was implied in ageing-related processes, both by direct actions of various oxidative adducts\r\nand by its cardiovascular consequences. In the latest years, it has become evident that chronic\r\nkidney disease (CKD) is itself a condition characterized by oxidative stress. Although\r\nconflictual results were reported in non-dialysis CKD patients, there is an increasing trend in\r\noxidative stress markers and a decreasing one in antioxidative activity along with progressive\r\nreduction in glomerular filtration rate. A combination of inflammation, abnormal nutrition,\r\ndisturbed metabolism by the uremic milieu and defective renal clearance seems to be the cause.\r\nClearly, longitudinal studies with larger participation are necessary to define the precise\r\ncontribution of each element and the relationships between oxidative stress and CKD\r\nprogression. In dialysis CKD patients, bioincompatibility reactions during HD sessions\r\n(dialyzor membrane, dialysis solution), anemia and its therapy (iv iron) come into play. The\r\nclinical consequences of oxidative stress are difficult to ascertain, because oxidative stress,\r\ninflammation and malnutrition were found to be, in various proportion, strong predictors of\r\noutcome in CKD patients, but the precise contribution of each factor is difficult to elucidate for\r\nthe moment.
  • Endocrine Care

    Stancu S, Chiriac C, Maria DT, Mota E, Mircescu G, Capusa C

    Nutritional or Active Vitamin D for the Correction of Mineral Metabolism Abnormalities in Non-Dialysis Chronic Kidney Disease Patients?

    Acta Endo (Buc) 2018 14(4): 505-513 doi: 10.4183/aeb.2018.505

    Context. Benefits of vitamin D therapies in chronic kidney disease (CKD) are debated. Objective. To compare the effects of medium-term native (VitD) and active (VDRA) vitamin D on parameters of mineral metabolism and arterial function in non-dialysis CKD. Design. Open-label, active comparator, randomized study. Subjects and Methods. Forty-eight adult patients, vitamin D naïve, CKD stage 3 to 5 with increased parathyroid hormone (iPTH) were randomized to receive either oral cholecalciferol 1000UI/day (n=24) or paricalcitol 1mcg/day (n=24) for 6 months. Median changes at end of study vs. baseline in serum calcidiol, iPTH, total alkaline phosphatase (ALP), and cardio-ankle vascular index (CAVI) were the efficacy parameters. Results. Higher increase in calcidiol (15.5 [95%CI 13.3; 17.2] vs. 0.4 [95%CI −6.1; 3.7]ng/mL, p<0.001) were found in VitD group. Conversely, the decline of iPTH (−35.2 [95%CI −83; 9] vs. 13.3 [95%CI −8.1; 35]pg/mL, p=0.008) and ALP (−34 [95%CI −58; −11] vs. −10 [95%CI −23; −2] U/L, p=0.02) were greater after paricalcitol. More subjects experienced iPTH decrease in VDRA group (71% vs. 39%, p=0.03). The variation in CAVI and the incidence of hypercalcemia and hyperphosphatemia were similar. Conclusions. It seems that secondary hyperparathyroidism was more efficiently treated by VDRA, whereas cholecalciferol better corrected the calcidiol deficiency in non-dialysis CKD.
  • Notes & Comments

    Mircescu G, Stanescu B

    Surgical or medical therapy for severe hyperparathyroidism or chronic kidney disease? An appraisal of current practice guidelines

    Acta Endo (Buc) 2010 6(4): 541-576 doi: 10.4183/aeb.2010.541

    Long lasting hypocalcemia, hyperphosphatemia, low calcitriol and high fibroblast growth factor 23 could result in progressive parathyroid gland hyperplasia with high, uncontrolled, parathormone production, e.g. severe secondary hyperparathyroidism (sHPT), in 10% of dialysis patients. Parathyroidectomy (PTX) could be a solution, but has inherent (low) surgical risks and although dramatically decreases parathormone levels, could induce hypoparathyroidism (50-66%) and low turnover bone disease. Moreover, the rate of recurrences is 15-20% at 10 years. Total and subtotal PTX with autografting are equally safe and effective with similar recurrences rates. Calcimimetics are efficient drugs, but with limited effectiveness in sHPT, as only 25% of patients responded to cinacalcet. In the USA, they are more cost-effective than PTX only in patients with >2 years expected dialysis duration. As there are not randomized studies to compare surgical to medical therapy, the strength of evidence allows only for suggestions in guidelines. In countries like Romania, where dialysis vintage is high because of the low transplantation rate and calcimimetics are costly, PTX seems a better solution when parathyroid glands are large (diameter >1cm or\r\ntotal mass >500mg), parathormone levels >800pg/mL, in patients who are not candidates for renal transplantation or are anticipated to stay >2 years on dialysis.