Anaemia and Mineral Bone Disorder in Chronic Kidney Disease: A Review of the Current Literature and Implications for Clinical Nursing Practice

Limrick, Claire; McNichols-Thomas, Coral

doi:10.1111/j.1755-6686.2009.00062.x

Cited by 5 publications

(5 citation statements)

References 30 publications

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“…When interpreting the serum ferritin concentrations, it should be remembered that SF concentrations are increased independently of the amount of iron stores in some conditions, particularly in manifest and latent infections, liver diseases, or malignant tumors 38,39 . For completeness of the present overview of methods, it should be noted that determination of the urinary excretion of iron after the administration of desferioxamine or determination of the 59 …”

Section: Iron Metabolism Disordersmentioning

confidence: 99%

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Pathophysiology of anemia in chronic kidney diseases: A review

Zadrazil¹,

Horák²

2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Backgroud. Anemia is one of the laboratory and clinical findings of chronic kidney diseases (CKD). The presence of anemia in patients with CKD has a wide range of clinically important consequences. Some of the symptoms that were previously attributed to reduced renal function are, in fact, a consequence of anemia. Anemia contributes to increased cardiac output, the development of left ventricular hypertrophy, angina, and congestive heart failure. According to current knowledge, anemia also contributes to the progression of CKD and is one of the factors that contribute to the high morbidity and mortality in patients with chronic renal failure and their reduced survival. Methods. MEDLINE search was performed to collect both original and review articles addressing anemia in CKD, pathophysiology of renal anemia, erythropoiesis, erythropoietin, iron metabolism, inflammation, malnutrition, drugs, renal replacement therapy and anemia management Conclusion. The present review summarized current knowledge in the field of the pathophysiology of renel anemia. Understanding the pathophysiology of anemia in CKD is crucial for the optimal treatment of anemia according to recent clinical practice guidelines and recommendation, and correct recognition of causes of resistence to treatment of erythropoietin stimulating agents (ESA).

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Section: Iron Metabolism Disordersmentioning

confidence: 99%

“…Excessive parathormone levels are known to reduce EPO production, increase hemolysis, and suppress stem cells of the red blood cell line in the bone marrow 59 . Anemia may be further aggravated by drugs, particularly by ACE inhibitors.…”

mentioning

confidence: 99%

Pathophysiology of anemia in chronic kidney diseases: A review

Zadrazil¹,

Horák²

2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Anaemia management strategies, and the optimisation of Hb and iron status, constitute an essential element of quality patient care. Nurse management includes ensuring patients are aware of the medications required, are fully educated into administration of erythropoietin therapy and that we ensure blood results are reviewed, and any abnormalities reported appropriately, with particularly reference to iron deficiency, infection, inadequate dialysis, malnutrition and secondary hyperparathyroidism as these can all cause a suboptimal response to erythropoietin therapy (Limrick & McNichols‐Thomas 2009).…”

Section: Anaemiamentioning

confidence: 99%

“…Emotional support and follow‐up care is needed, we need to ensure that patients participate in the decision‐making process and encourage them to continue with their activities of daily living within the physical and psychological limitations that they have. It is imperative that nurses work in partnership with patients to encourage adherence to their therapy and its encompassing areas (Limrick & McNichols‐Thomas 2009).…”

Section: Renal Osteodystrophy (Ro) and Secondary Hyperparathyroidismmentioning

confidence: 99%

CE: Continuing Education Article MANAGEMENT OF CO‐MORBID DISEASES IN A PATIENT WITH ESTABLISHED RENAL FAILURE

Chamney

Pugh-Clarke

Kafkia

2009

Journal of Renal Care

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This follows on from an article relating to chronic kidney disease (CKD) and co-morbidities. Not only do these co-morbid diseases cause problems to patients with CKD, they continue to impact upon them when they develop established renal failure (ERF). Various co-morbid conditions can affect the patient including diabetes, hypertension, anaemia and cardiovascular issues. As nephrology nurses we play a fundamental role in patient education, monitoring and management of these factors.

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“…When diffuse hyperplasia develops into a nodular type of hyperplasia, sHPT might be refractory to medical treatment as adenomas (1,7,8,11). Serious complications, such as calciphylaxis, bone fractures, brown tumors, vascular calcifications, anemia, peptic ulcers, and cholelithiasis might develop in patients with long-term highconcentration serum PTH levels (10,(13)(14)(15)(16)(17). Detecting the subgroup of patients with nodular hyperplasia might be useful for selecting patients for early parathyroidectomy to prevent serious complications from developing.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Proliferative Activity in Parathyroid Glands in Primary and Secondary Hyperparahyroidism

Demıralay¹

2011

Acta Endo (Buc)

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Objective.Parathyroid gland hyperplasia is diffuse or nodular in secondary hyperparathyroidism (sHPT) in patients with renal failure. Whether the nodular growth starts from the beginning or is the transformation of a diffusely-growing gland into nodular hyperplasia in parallel with increases in the severity of the disease is unknown. The disease might be unresponsive to medical treatment when nodular hyperplasia develops. This study aims to differentiate the characteristics of the parathyroid glands with and without nodular hyperplasia in sHPT, and to investigate if there is any similarity between the nodular hyperplastic glands of sHPT and the parathyroid adenomas of primary hyperparathyroidism.Materials and Methods. Hyperplasia types (nodular or diffuse) and parathyroid cell types, and the expression of proliferating cell nuclear antigen (PCNA) and Ki-67 in parathyroid tissue were investigated histopathologically and immunohistochemically in 94 parathyroid glands of 42 patients with hyperparathyroidism. Results andDiscussion. 63 glands showed nodular hyperplasia and 16 diffuse hyperplasia in sHPT. Chief cells predominated across the whole series. Vacuolated chief cells most frequently accompanied chief cells in both nodular hyperplasia (28.6%) and adenomas (53%). The median ratio of PCNA LI (labelling index) was 30/10³ (min: 4-max: 720) cells in nodular hyperplasia, 16/10³ (min: 2-max: 180) cells in diffuse hyperplasia and 30/10³ (min: 10-max: 707) cells in adenomas (p>0.05). The highest PCNA LI according to all the cell types in the series was in chief cell and vacuolated chief cell combinations (53/10³, p=0.04). These findings suggest that parathyroid adenoma and nodular hyperplasia have histopathologically-and i m m u n o h i s t o c h e m i c a l l y -s i m i l a r characteristics suggesting that both have aggressive cell proliferation.

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Anaemia and Mineral Bone Disorder in Chronic Kidney Disease: A Review of the Current Literature and Implications for Clinical Nursing Practice

Cited by 5 publications

References 30 publications

Pathophysiology of anemia in chronic kidney diseases: A review

Pathophysiology of anemia in chronic kidney diseases: A review

CE: Continuing Education Article MANAGEMENT OF CO‐MORBID DISEASES IN A PATIENT WITH ESTABLISHED RENAL FAILURE

Comparison of Proliferative Activity in Parathyroid Glands in Primary and Secondary Hyperparahyroidism

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