Anaemia in chronic kidney disease- new treatment options

2018 ◽  
Vol 8 (2) ◽  
pp. 210-214
Author(s):  
M. Żórawski ◽  
B. Musiałowska ◽  
M. Rudzińska ◽  
E. Koc-Żórawska ◽  
J.S. Małyszko
Keyword(s):  
Chronic Kidney Disease ◽  
Bone Marrow ◽  
Kidney Disease ◽  
Treatment Options ◽  
Nutritional Deficiencies ◽  
Renal Anaemia ◽  
Disease Pathogenesis ◽  
Multiple Factors ◽  
Erythrocyte Survival ◽  
New Treatment

In recent years anaemia has been recognized as one of the most specific and evident manifestations of chronic renal failure. In the majority of cases, renal anaemia is normocytic and normochromic with normal cellularity of bone marrow. Multiple factors contribute to the molecular origins of the anaemia of chronic kidney disease. Within those factors, the disturbances in the production of erythropoietin have the greatest impact on the disease pathogenesis. However, other components such as shortened erythrocyte survival, blood loss, iron or other nutritional deficiencies, hemolysis, the presence of uremic inhibitors of erythropoiesis among others can also significantly contribute to the occurrence of anaemia.

Clinical aspects and overview of renal anaemia

2015 ◽  
Author(s):  
Iain C. Macdougall
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Intravenous Iron ◽  
Severe Anaemia ◽  
Adverse Outcomes ◽  
Clinical Aspects ◽  
Red Cell ◽  
Renal Anaemia

Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.

scholarly journals Chronic Hyperkalemia in Cardiorenal Patients: Risk Factors, Diagnosis, and New Treatment Options

2018 ◽  
Vol 9 (1) ◽  
pp. 8-21 ◽  
Author(s):  
Luca Di Lullo ◽  
Claudio Ronco ◽  
Antonio Granata ◽  
Ernesto Paoletti ◽  
Vincenzo Barbera ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Medical Condition ◽  
Treatment Options ◽  
Correct Diagnosis ◽  
New Treatment ◽  
Poor Outcomes ◽  
Careful Management

Chronic hyperkalemia (HK) is a serious medical condition that often manifests in patients with chronic kidney disease (CKD) and heart failure (HF) leading to poor outcomes and necessitating careful management by cardionephrologists. CKD, HF, diabetes, and renin-angiotensin-aldosterone system inhibitors use is known to induce HK. Current therapeutic options are not optimal, as pointed out by a large number of CKD and HF patients with HK. The following review will focus on the main risk factors for developing HK and also aims to provide a guide for a correct diagnosis and present new approaches to therapy.

scholarly journals New Treatment Options for Hyperkalemia in Patients with Chronic Kidney Disease

2020 ◽  
Vol 9 (8) ◽  
pp. 2337 ◽  
Author(s):  
Pasquale Esposito ◽  
Novella Evelina Conti ◽  
Valeria Falqui ◽  
Leda Cipriani ◽  
Daniela Picciotto ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Therapeutic Option ◽  
Treatment Options ◽  
New Drugs ◽  
Sodium Polystyrene Sulfonate ◽  
Sodium Zirconium ◽  
Life Threatening ◽  
New Treatment ◽  
Sodium Zirconium Cyclosilicate

Hyperkalemia may cause life-threatening cardiac and neuromuscular alterations, and it is associated with high mortality rates. Its treatment includes a multifaceted approach, guided by potassium levels and clinical presentation. In general, treatment of hyperkalemia may be directed towards stabilizing cell membrane potential, promoting transcellular potassium shift and lowering total K+ body content. The latter can be obtained by dialysis, or by increasing potassium elimination by urine or the gastrointestinal tract. Until recently, the only therapeutic option for increasing fecal K+ excretion was represented by the cation-exchanging resin sodium polystyrene sulfonate. However, despite its common use, the efficacy of this drug has been poorly studied in controlled studies, and concerns about its safety have been reported. Interestingly, new drugs, namely patiromer and sodium zirconium cyclosilicate, have been developed to treat hyperkalemia by increasing gastrointestinal potassium elimination. These medications have proved their efficacy and safety in large clinical trials, involving subjects at high risk of hyperkalemia, such as patients with heart failure and chronic kidney disease. In this review, we discuss the mechanisms of action and the updated data of patiromer and sodium zirconium cyclosilicate, considering that the availability of these new treatment options offers the possibility of improving the management of both acute and chronic hyperkalemia.

scholarly journals Efficacy and safety of gout flare prophylaxis and therapy use in people with chronic kidney disease: a Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN)-initiated literature review

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Huai Leng Pisaniello ◽  
Mark C. Fisher ◽  
Hamish Farquhar ◽  
Ana Beatriz Vargas-Santos ◽  
Catherine L. Hill ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Literature Review ◽  
Interleukin 1 ◽  
Treatment Options ◽  
Cochrane Library ◽  
Efficacy And Safety ◽  
Clinical Trial Results ◽  
Gout Flare

AbstractGout flare prophylaxis and therapy use in people with underlying chronic kidney disease (CKD) is challenging, given limited treatment options and risk of worsening renal function with inappropriate treatment dosing. This literature review aimed to describe the current literature on the efficacy and safety of gout flare prophylaxis and therapy use in people with CKD stages 3–5. A literature search via PubMed, the Cochrane Library, and EMBASE was performed from 1 January 1959 to 31 January 2018. Inclusion criteria were studies with people with gout and renal impairment (i.e. estimated glomerular filtration rate (eGFR) or creatinine clearance (CrCl) < 60 ml/min/1.73 m2), and with exposure to colchicine, interleukin-1 inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), and glucocorticoids. All study designs were included. A total of 33 studies with efficacy and/or safety analysis stratified by renal function were reviewed—colchicine (n = 20), anakinra (n = 7), canakinumab (n = 1), NSAIDs (n = 3), and glucocorticoids (n = 2). A total of 58 studies reported these primary outcomes without renal function stratification—colchicine (n = 29), anakinra (n = 10), canakinumab (n = 6), rilonacept (n = 2), NSAIDs (n = 1), and glucocorticoids (n = 10). Most clinical trials excluded study participants with severe CKD (i.e. eGFR or CrCl of < 30 mL/min/1.73 m2). Information on the efficacy and safety outcomes of gout flare prophylaxis and therapy use stratified by renal function is lacking. Clinical trial results cannot be extrapolated for those with advanced CKD. Where possible, current and future gout flare studies should include patients with CKD and with study outcomes reported based on renal function and using standardised gout flare definition.

scholarly journals Sympathetic hyperactivity in chronic kidney disease: Pathogenesis, clinical relevance, and treatment

2004 ◽  
Vol 65 (5) ◽  
pp. 1568-1576 ◽  
Author(s):  
Jutta Neumann ◽  
Gerry Ligtenberg ◽  
Inge I. Klein ◽  
Hein A. Koomans ◽  
Peter J. Blankestijn
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Relevance ◽  
Disease Pathogenesis ◽  
Sympathetic Hyperactivity
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