Myelofibrosis-Induced Erythropoietin-Resistant Anemia Due to Severe Refractory Hyperparathyroidism

Sethi, Sidharth Kumar; Bansal, Shyam Bihari; Wadhwani, Nikita; Makasana, Mayur; Nandwani, Ashish; Kher, Vijay; Raina, Rupesh

doi:10.1016/j.ekir.2018.04.003

Cited by 8 publications

(8 citation statements)

References 23 publications

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“…Since the parathyroid glands of our patient showed diffuse hyperplasia and was <1 cm in diameter (data not shown), this might be a reason for successful pharmacological treatment for secondary HPT. Furthermore, the PTH level was relatively lower (585 pg/ml) in our patient than in those patients who needed parathyroidectomy (≥3000 pg/ml) ( Table 1 ) ( 13 , 14 ). PTH levels may also potentially identify patients who will benefit from pharmacological treatment.…”

Section: Discussionmentioning

confidence: 53%

“…Parathyroidectomy ameliorates anemia and reduces the requirement of postoperative erythropoiesis-stimulating agents ( 17 ). There have been reports of patients with myelofibrosis caused by secondary HPT, who were successfully treated using a parathyroidectomy ( 13 , 14 , 18 ). However, cinacalcet has been effective even in patients with marked parathyroid hyperplasia, suggesting that it may serve as an alternative to parathyroidectomy for treatment of severe secondary HPT ( 15 ).…”

Section: Discussionmentioning

confidence: 99%

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Case Report: Effects of Secondary Hyperparathyroidism Treatment on Improvement of Juvenile Nephronophthisis-Induced Pancytopenia and Myelofibrosis

et al. 2021

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Secondary hyperparathyroidism (HPT) is a common complication of end-stage renal disease (ESRD) and may be an important precipitating factor for the development of myelofibrosis. However, there have been only a few reports on myelofibrosis caused by secondary HPT in children. We describe a case of a 15-year-old boy with myelofibrosis due to secondary HPT who was successfully treated with hemodialysis, erythropoietin, phosphate binders, and activated vitamin D agents. The patient had no past medical history and had been admitted to the hospital for abdominal pain. Routine blood examination revealed pancytopenia combined with renal impairment. Hyperphosphatemia, decreased 1,25-dehydroxyvitamin D, decreased serum calcium, and increased parathyroid hormone (PTH) levels were observed. Bone marrow biopsy confirmed myelofibrosis and renal biopsy revealed nephronophthisis (NPHP). The possibility of renal osteodystrophy and myelofibrosis due to secondary HPT was considered. Hemodialysis and erythropoietin were initiated and combined therapy with a phosphate binder and an active vitamin D agent achieved greater reduction of PTH levels, along with improvement of pancytopenia. As medical treatment for secondary HPT can lead to a reversal of myelofibrosis and avoid parathyroidectomy in children, prompt recognition of this condition has major implications for treatment. Therefore, despite its rarity, pediatricians should consider myelofibrosis due to secondary HPT as a cause of pancytopenia in patients with chronic kidney disease.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Case Report: Effects of Secondary Hyperparathyroidism Treatment on Improvement of Juvenile Nephronophthisis-Induced Pancytopenia and Myelofibrosis

et al. 2021

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“…Studies have demonstrated that RBC lifespan is reduced in patients with CKD [22]. Uremic RBCs have been reported to become more fragile in response to osmotic stimuli and oxidative stress [23,24]. Moreover, blood loss in patients with CKD is common due to dialysis and coagulopathy associated with CKD, which causes iron loss in these patients.…”

Section: Shortened Rbc Lifespan and Increased Blood Lossmentioning

confidence: 99%

Iron Therapy in Chronic Kidney Disease: Days of Future Past

Lee

Tarng

2021

IJMS

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Anemia affects millions of patients with chronic kidney disease (CKD) and prompt iron supplementation can lead to reductions in the required dose of erythropoiesis-stimulating agents, thereby reducing medical costs. Oral and intravenous (IV) traditional iron preparations are considered far from ideal, primarily due to gastrointestinal intolerability and the potential risk of infusion reactions, respectively. Fortunately, the emergence of novel iron replacement therapies has engendered a paradigm shift in the treatment of iron deficiency anemia in patients with CKD. For example, oral ferric citrate is an efficacious and safe phosphate binder that increases iron stores to maintain hemoglobin levels. Additional benefits include reductions in fibroblast growth factor 23 levels and the activation of 1,25 dihydroxyvitamin D. The new-generation IV iron preparations ferumoxytol, iron isomaltoside 1000, and ferric carboxymaltose are characterized by a reduced risk of infusion reactions and are clinically well tolerated as a rapid high-dose infusion. In patients undergoing hemodialysis (HD), ferric pyrophosphate citrate (FPC) administered through dialysate enables the replacement of ongoing uremic and HD-related iron loss. FPC transports iron directly to transferrin, bypassing the reticuloendothelial system and avoiding iron sequestration. Moreover, this paper summarizes recent advancements of hypoxia-inducible factor prolyl hydroxylase inhibitors and future perspectives in renal anemia management.

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“…Сохранение потребности в продолжении лечения рчЭПО, по данным литературы, может быть ассоциировано с вкладом вторичного гиперпаратиреоза в состояние чувствительности рецепторных структур костного мозга. Обнаруженные нами статистически значимые корреляции ЭПО с уровнем кальция, скорректированнного на альбумин, а также с TBS, указывают на вероятность влияния минеральных и костных нарушений при ХБП на кроветворную активность ростковых зон кости (фиброз костного мозга приводит к снижению ответа на ЭПО) [23]. Известно, что отсроченная функция трансплантата почки может быть ассоциирована с замедленным восстановлением уровня ЭПО и выступить причиной замедленной нормализации уровня гемоглобина -в нашей работе одному из двоих пациентов с отсроченной функцией аллотрансплантата почки потребовалось назначение терапии рчЭПО в раннем послеоперационном периоде.…”

Section: параметрыunclassified

Сhronic kidney disease complications in patients with type 1 diabetes mellitus after simultaneous pancreas-kidney transplantation – potential role of oxidative stress and glycation end products

Larina¹,

Severina²,

Шамхалова³

et al. 2020

Diabetes mellitus

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BACKGROUND: Normoglycaemia in patients with diabetes mellitus type 1 (T1DM) after simultaneous pancreas-kidney transplantation (SPKT) is very interesting in regards to chronic kidney disease (CKD) complications dynamics depending of posttransplantation period and possible targets of potential treatment from the point of view metabolic memory AIM: To evaluate the relationship between oxidative stress indicators and advanced glycation end products and complications of end-stage renal disease (ESRD) in patients with T1DM аnd a long-term history of diabetes decompensation, who reached stable euglycemia after SPKT. MATERIALS AND METHODS: The study included 20 patients with compensation of carbohydrate metabolism after SPKT performed from November 2011 to September 2018. Assessment included examination of complications of ESRD (arterial hypertension, dyslipidemia, anemia, mineral and bone disorder) and analysis of "metabolic memory" markers: 3-nitrothyrosine (3-NT), superoxide dismutase (SOD), advanced glycation end products (AGE) and AGE receptor (RAGE). We performed follow-up examination of patients included in the early postoperative period (1st day/week) in 6-12 months after SPKT. RESULTS: All patients with DM1 duration for 22 [19; 28] years, diabetic nephropathy (DN) 8 [6; 14] years and duration of renal replacement therapy (dialysis) for 3 [1.5; 4] years reached euglycemia (HbA1c 5,5 [5,1; 5,8] %; С-peptide 3,2 [2,45; 3,63] ng/ml) after 6 month of surgical treatment. Despite of stable graft function (estimated glomerular filtration rate (eGFR) CKD-EPI 84 [69; 95] ml/min/1.73m2) 35% of patients still needed antihypertensive therapy, 40% needed treatment with recombinant human erythropoietin (RHuEPO) and 15% ferrotherapy. With vitamin D deficiency, observed in 80% of cases (13.3 [9.3; 18.5] ng/ml), 55% of patients had secondary hyperparathyroidism, 45% osteoporosis. The results of the correlation analysis revealed the association of the state of ESRD target organs with the studied "metabolic memory" markers: oxidative stress and AGE-RAGE system. CONCLUSIONS: SPKT as the way to achieve compensation of carbohydrate metabolism and uremia does not provide regress of diabetes and complications of ESRD. Analysis of "metabolic memory" markers indicate their direct contribution to the persistence of metabolic consequences of diabetic nephropathy (DN). Found trends need more long-lasting observation and enlargement of study groups.

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Myelofibrosis-Induced Erythropoietin-Resistant Anemia Due to Severe Refractory Hyperparathyroidism

Cited by 8 publications

References 23 publications

Case Report: Effects of Secondary Hyperparathyroidism Treatment on Improvement of Juvenile Nephronophthisis-Induced Pancytopenia and Myelofibrosis

Case Report: Effects of Secondary Hyperparathyroidism Treatment on Improvement of Juvenile Nephronophthisis-Induced Pancytopenia and Myelofibrosis

Iron Therapy in Chronic Kidney Disease: Days of Future Past

Сhronic kidney disease complications in patients with type 1 diabetes mellitus after simultaneous pancreas-kidney transplantation – potential role of oxidative stress and glycation end products

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