scholarly journals Pseudohyperkalemia and the Need for Imperative Caution With the Newly Introduced Potent Potassium Binders: Two Cases

Cureus ◽  
2021 ◽  
Author(s):  
Macaulay A Onuigbo ◽  
Adam Ross
Keyword(s):  
2020 ◽  
Vol 14 (6) ◽  
pp. 592-594
Author(s):  
Dario Manley-Casco ◽  
Paul Berkowitz

Chronic kidney disease (CKD) is a major health problem with substantial morbidity and mortality. Plant-based diets decrease the incidence of CKD and progression of kidney disease and help prevent and treat the important comorbidities of obesity, type 2 diabetes, hypertension, and cardiovascular disease. However, in patients with CKD, there is concern that a plant-based diet may contribute to life-threatening hyperkalemia. We present a patient with CKD secondary to hypertensive glomerulosclerosis that worsened despite standard of care treatment. Shared decision making was used to initiate a whole food plant-based diet along with a potassium-binding resin (Patiromer) to control the potassium levels. The patient was able to be maintained on the whole food plant-based diet and an angiotensin-converting enzyme inhibitor without the development of hyperkalemia. This case shows that patients with CKD may be able to enjoy the benefits of a whole food plant-based diet while decreasing the risk of hyperkalemia by using the new potassium binders.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hima Reddy Ammana ◽  
Susan Yuditskaya

Abstract Introduction Following unilateral adrenalectomy, some patients experience persistent hyperkalemia. This has been attributed to hypoaldosteronism due to severe suppression of aldosterone synthesis in the contralateral adrenal gland. Additionally, excess aldosterone leads to glomerular hyperfiltration masking kidney dysfunction, which can then manifest after cure with CKD-related hyperkalemia. Case Presentation We report a case of 51-year-old male who was diagnosed with hypertension in his late 30s. He required a beta-blocker and calcium channel blocker (CCB) for 10 years, and eventually developed hypertensive nephropathy. With worsening lower extremity edema, he was switched from a CCB to an angiotensin receptor blocker. Soon afterwards, he presented with hypertensive emergency and was discovered to have significant hypokalemia (K 2.1 mmol/L), prompting work up for primary aldosteronism. Biochemical evaluation revealed an elevated aldosterone to renin ratio of 38 [(ng/dL)/(ng/mL/hr)] and adrenal protocol CT scan revealed a 1.9 cm left adrenal nodule with benign characteristics. Adrenal vein sampling showed marked lateralization of excess aldosterone to the left adrenal gland, with proper catheter placement demonstrated in each adrenal veins (5-fold cortisol gradient bilaterally). He was started on spironolactone and 6 weeks later, underwent an uncomplicated laparoscopic left adrenalectomy. Spironolactone was discontinued Serum K level was normal at 4.8 mmol/L immediately postoperatively. Ten hours later, his K went up to 6.6 mmol/L which was confirmed by repeat blood work, accompanied by worsened renal function (Cr 2.5 mg/dL up from a of baseline 2.0). His hyperkalemia persisted in the 5.0 – 6.0 range despite IV Calcium Gluconate, Insulin and D50. Oral potassium binders were avoided due to concerns about ileus. Upon recognition of the possibility of hypoaldosteronism, we recommended a NaHCO3 gtt, with subsequent normalization of serum K. We avoided initiating fludrocortisone in the short term, due to uncertainty about duration of hypoaldosteronism, & because he was still requiring two antihypertensive agents. Plasma aldosterone 2 wks after surgery was fully suppressed, confirming suspicion of hypoaldosteronism. He has been managed successfully with oral sodium bicarbonate tablets, remaining normokalemic at 3 weeks post-surgery. Conclusion: Here we present a case of persistent hyperkalemia following resection of a signficantly biochemically active and long-standing aldosteronoma, which was successfully managed with sodium bicarbonate. We attribute the post-operative hyperkalemia in this patient to a combination of hypoaldosteronism due to deep suppression of the mineralocorticoid production of the contralateral adrenal, as well as unmasking of more severe kidney dysfunction than was he previously thought to have once aldosterone excess was withdrawn.


2020 ◽  
Author(s):  
Priyank Patel ◽  
Andrew Frankel

Abstract Background Renin–angiotensin–aldosterone system (RAAS) inhibitors provide significant cardiorenal benefits with improved long-term outcomes for patients. This is most significant for patients receiving maximal RAAS inhibition, but some patients are unable to tolerate this therapy because of hyperkalaemia. Recently published National Institute for Health and Care Excellence (NICE) technology appraisal guidance recommended using sodium zirconium cyclosilicate (SZC) and patiromer for patients with chronic kidney disease (CKD) stage 3b to 5 or heart failure with reduced ejection fraction, who are not taking an optimised dosage of RAAS inhibitor because of hyperkalaemia. Objective Determine the impact of a locally produced guideline on effective implementation of NICE recommendation for use of SZC or patiromer to help maximise inhibition of the renin–angiotensin–aldosterone system within the general nephrology clinic. Methods A local guideline to practically support the implementation of recommendations made by NICE in the chronic use of new potassium binders was produced. One hundred sequential patients in a general nephrology clinic with non-immune chronic kidney disease (CKD 3 to 5) had their electronic records reviewed. Those with an indication for RAAS inhibition were identified. Results Of the 100 consecutive patients audited, 46 were female and 54 were male. The mean age of these patients was 64 and the mean estimated glomerular filtration rate (eGFR) was 33. Sixty-eight patients had an indication for being on RAAS inhibition with only 10 on maximal doses. Of the remaining 58 patients, 26 (45%) were limited by hyperkalaemia. Of these 26 patients, 12 of these patients (46%) had hyperkalaemia associated with an episode of acute kidney injury (AKI). Therefore, 14% of patients attending a general nephrology clinic were identified suitable for SZC and patiromer. Conclusions A significant proportion (14%) of unselected patients attending a general nephrology clinic were not on optimum RAAS inhibition due to hyperkalaemia. These patients would meet the criteria established within a working guideline for the implementation of the chronic use of SZC or patiromer and are likely to attain prognostic long-term benefit by using these new potassium binders to maximise RAAS inhibition. This analysis has implications for renal centres across the UK.


ESC CardioMed ◽  
2018 ◽  
pp. 218-221
Author(s):  
Keld P. Kjeldsen ◽  
Juan Tamargo ◽  
Thomas A. Schmidt

Potassium binders are used for the treatment of and prophylaxis against hyperkalaemia. Already in 1958, the United States Food and Drug Administration (FDA) approved sodium polystyrene sulfonate, a potassium binder exchanging sodium for potassium in the gastrointestinal tract. In 2015, the FDA approved a new potassium binder, patiromer sorbitex calcium (Veltassa®), exchanging calcium for potassium, and in 2017, it was approved by the European Medicines Agency (EMA). Furthermore, in 2018, the FDA and the EMA approved another new potassium binder, sodium zirconium cyclosilicate (Lokelma®), exchanging sodium for potassium. The clinical pharmacology aspects of potassium binders are reviewed in this chapter.


ESC CardioMed ◽  
2018 ◽  
pp. 218-221
Author(s):  
Keld P. Kjeldsen ◽  
Juan Tamargo ◽  
Thomas A. Schmidt

Potassium binders are used for the treatment of and prophylaxis against hyperkalaemia. Already in 1958, the United States Food and Drug Administration (FDA) approved sodium polystyrene sulfonate, a potassium binder exchanging sodium for potassium in the gastrointestinal tract. In 2015, the FDA approved a new potassium binder, patiromer sorbitex calcium (Veltassa®), exchanging calcium for potassium, and in 2017, it was approved by the European Medicines Agency (EMA). Furthermore, in January 2018 approval by the FDA of another new potassium binder, sodium zirconium cyclosilicate (ZS-9®), exchanging sodium for potassium, is pending. The clinical pharmacology aspects of potassium binders are reviewed in this chapter.


2020 ◽  
Vol 35 (8) ◽  
pp. 1446-1448
Author(s):  
Rakesh Dattani ◽  
Peter Hill ◽  
Nicholas Medjeral-Thomas ◽  
Megan E Griffith ◽  
Damien Ashby ◽  
...  
Keyword(s):  

Author(s):  
Agnieszka Tycinska ◽  
Ewa Jankowska
Keyword(s):  

No abstract


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
B L Neuen ◽  
M Oshima ◽  
V Perkovic ◽  
C Arnott ◽  
G Bakris ◽  
...  

Abstract Background Hyperkalaemia is a common complication of type 2 diabetes mellitus (T2DM) and limits the optimal use of agents that block the renin-angiotensin aldosterone system (RAAS), particularly in patients with chronic kidney disease (CKD). In patients with CKD, sodium glucose cotransporter 2 (SGLT2) inhibitors provide cardiorenal protection, but whether they affect the risk of hyperkalaemia remains uncertain. Purpose We sought to assess the effect of canagliflozin on hyperkalaemia and other potassium-related outcomes in people with T2DM and CKD by conducting a post-hoc analysis of the CREDENCE trial. Methods The CREDENCE trial randomized 4401 participants with T2DM and CKD to the SGLT2 inhibitor canagliflozin or matching placebo. In this post-hoc analysis using an intention-to-treat approach, we assessed the effect of canagliflozin on a composite outcome of time to either investigator-reported hyperkalaemia or the initiation of potassium binders. We also analysed effects on central laboratory-determined hyper- and hypokalaemia (serum potassium ≥6.0 and <3.5 mmol/L, respectively) and change in serum potassium. Results At baseline the mean serum potassium in canagliflozin and placebo arms was 4.5 mmol/L; 4395 (99.9%) participants were receiving renin angiotensin system blockade. Canagliflozin reduced the risk of investigator-reported hyperkalaemia or initiation of potassium binders (HR 0.78, 95% CI 0.64–0.95, p=0.014; Figure 1). The incidence of laboratory-determined hyperkalaemia was similarly reduced (HR 0.77, 95% CI 0.61–0.98, p=0.031; Figure 2); the risk of hypokalaemia (HR 0.92, 95% CI 0.71–1.20, p=0.53) was not increased. Mean serum potassium over time with canagliflozin was similar to that of placebo. Conclusion Among patients treated with RAAS inhibitors, SGLT2 inhibition with canagliflozin may reduce the risk of hyperkalaemia in people with T2DM and CKD without increasing the risk of hypokalaemia. FUNDunding Acknowledgement Type of funding sources: None. Figure 1 Figure 2


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