Sympathetic Hyperactivity in Chronic Kidney Disease: Pathophysiology and (New) Treatment Options

2013 ◽  
Vol 15 (2) ◽  
pp. 95-101 ◽  
Author(s):  
Eva E. Vink ◽  
Rosa L. de Jager ◽  
Peter J. Blankestijn
2018 ◽  
Vol 9 (1) ◽  
pp. 8-21 ◽  
Author(s):  
Luca Di Lullo ◽  
Claudio Ronco ◽  
Antonio Granata ◽  
Ernesto Paoletti ◽  
Vincenzo Barbera ◽  
...  

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.


2018 ◽  
Vol 8 (2) ◽  
pp. 210-214
Author(s):  
M. Żórawski ◽  
B. Musiałowska ◽  
M. Rudzińska ◽  
E. Koc-Żórawska ◽  
J.S. Małyszko

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.


2020 ◽  
Vol 9 (8) ◽  
pp. 2337 ◽  
Author(s):  
Pasquale Esposito ◽  
Novella Evelina Conti ◽  
Valeria Falqui ◽  
Leda Cipriani ◽  
Daniela Picciotto ◽  
...  

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.


2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Huai Leng Pisaniello ◽  
Mark C. Fisher ◽  
Hamish Farquhar ◽  
Ana Beatriz Vargas-Santos ◽  
Catherine L. Hill ◽  
...  

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.


2007 ◽  
Vol 27 (2_suppl) ◽  
pp. 293-297
Author(s):  
Peter J. Blankestijn

Chronic kidney disease is often characterized by the presence of sympathetic hyperactivity. The aim of this brief review is to summarize available knowledge on the pathogenesis of sympathetic hyperactivity and to discuss its clinical relevance, the consequences of this knowledge for the choice of treatment, and the yet unresolved issues.


2004 ◽  
Vol 65 (5) ◽  
pp. 1568-1576 ◽  
Author(s):  
Jutta Neumann ◽  
Gerry Ligtenberg ◽  
Inge I. Klein ◽  
Hein A. Koomans ◽  
Peter J. Blankestijn

Hypertension ◽  
2007 ◽  
Vol 49 (5) ◽  
Author(s):  
Jutta Neumann ◽  
Gerry Ligtenberg ◽  
Inge H.T. Klein ◽  
Peter Boer ◽  
P. Liam Oey ◽  
...  

2021 ◽  
Vol 49 (10) ◽  
pp. 030006052110532
Author(s):  
Zhe Feng ◽  
Ting Wang ◽  
Sheng Dong ◽  
Hongli Jiang ◽  
Jianzhong Zhang ◽  
...  

Chronic kidney disease (CKD) is a serious non-communicable disease that poses a significant burden on healthcare and society. It is essential to devise new strategies to better treat patients with CKD. Research has illustrated that gut dysbiosis, describing an abnormal intestinal ecology, is closely associated with CKD. In this narrative review, we summarized the evidence of their mutual relationship and discussed the potential treatment options to correct gut dysbiosis in patients with CKD. Gut dysbiosis significantly increases the risk of CKD, especially in the older population. Gut dysbiosis also plays a role in CKD complications, such as hypertension, cardiovascular events, and cognitive dysfunction. The relationship between gut dysbiosis and CKD is bidirectional, and CKD itself can lead to changes in gut microecology. The usual therapies for CKD can also increase the incidence of gut dysbiosis. Meanwhile, probiotics and antibiotics are generally used to correct gut dysbiosis. Further studies are required to elaborate the association between gut dysbiosis and CKD, and more treatment options should be explored to prevent CKD in patients with gut dysbiosis.


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