Explore chapters and articles related to this topic
The Patient with Renal Dysfunction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Alexandros Briasoulis, Ily Kristine T. Yumul-Non, Paulino Alvarez
Patiromer and sodium zirconium cyclosilicate are novel potassium binders that may help mitigate hyperkalemia with angiotensin blockade and AA specifically in CKD patients. Patiromer (RLY5016) is a non-absorbed, sodium-free polymer that exchanges calcium for potassium in the gastrointestinal (GI) tract, promoting fecal potassium excretion.78 In PEARL-HF (Parallel Evaluation of RLY5016 in Heart Failure), patiromer prevented hyperkalemia in HF patients with CKD who had been on an angiotensin blockade regimen and spironolactone (25–50 mg/day).78 Sodium zirconium cyclosilicate (ZS-9) is a highly selective cation exchanger that entraps potassium in the GI tract, exchanging it for hydrogen and sodium. It can correct hyperkalemia within 48 hours and its effects are noted to be most significant in higher potassium levels at baseline.79 Prior to administration of either of these agents, careful consideration of potential adverse effects is required, such as constipation, hypomagnesemia and drug interactions (metformin, levothyroxine) with patiromer, or edema with ZS-9. Also, a low-potassium diet and loop diuretics should be attempted first before initiation of these agents.
Managing Crush Injuries on Arrival
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Sarvdeep Singh Dhatt, Deepak Neradi
Mannitol (osmotic diuretic and free radical scavenger) may be used to treat and prevent ARF. It also helps to reduce compartment pressure by osmotic diuresis and decreasing vascular permeability. However, due to possible complications [nephrotoxicity/congestive heart failure (CHF)], its use is controversial and should be started/titrated according to urine output. Furosemide (loop diuretic) should be avoided, as it acidifies urine and promotes myoglobulin precipitation. Hyperkalaemia is an early sign of cardiac arrhythmia and needs early corrective measures. Early administration of 15 g/day of sodium polystyrene sulfonate (potassium binder) can be used to prevent fatal hyperkalaemia due to reperfusion injury. Correction of hypocalcaemia should be avoided, as administered calcium gets trapped in injured muscles and causes metastatic calcification and rebound hypercalcaemia. Calcium should be used only to prevent hyperkalaemic cardiac arrhythmia. Allopurinol (xanthine oxidase inhibitor) given early may be used to protect from reperfusion injury to ischaemic cells by reducing free radical formation. Dialysis is required in hyperkalaemia/metabolic acidosis resistant to medical therapy, volume overload and uraemia. Dialysis is usually required two to three times daily for 2 weeks to restore renal function. Crush victims are at increased risk of sepsis, systemic inflammatory response syndrome (SIRS) or multi-organ failure; therefore, they require intensive care monitoring, aggressive treatment of open injuries and nutritional supplementation.
The Nephroprotective Effect of Antihypertensive Treatment
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Luis M. Ruilope, Jose R. Banegas
In recent years, aldosterone is regarded as a mediator of progressive renal damage (53). It is therefore relevant that aldosterone antagonists reduce proteinuria in patients with chronic kidney disease, even if they are already on a RAAS blocker (54,55). In a meta-analysis, the addition of an aldosterone antagonist to an ACEi or an ARB, decreased proteinuria by an estimate of 30–40% (55). A limiting factor for the wide use of aldosterone antagonists is linked with the risk of inducing hyperkalaemia, which becomes a prominent concern as renal function deteriorates (54,55). The recent appearance of new potassium binders could facilitate the maintenance of RAAS blockade including an ACEi or an ARB plus an aldosterone blocker in patients with stage 3–4 or more advanced CKD (56) because of their capacity to control increases in serum potassium that impede adequate RAAS blockade.
Finerenone: a mineralocorticoid receptor antagonist for the treatment of chronic kidney disease associated with type 2 diabetes
Published in Expert Review of Clinical Pharmacology, 2022
Edgar V. Lerma, Daniel J. Wilson
Finerenone has a unique pharmacokinetic and pharmacodynamic profile characterized by a high potency and selectivity, unique MR binding with cofactor recruitment inhibition, short plasma half-life, lack of active metabolites, and a balanced distribution in heart and kidneys. Hyperkalemia may occur with finerenone but not to the extent observed with steroidal MRAs (spironolactone and eplerenone) and can be managed with an effective monitoring and mitigation strategy. Some patients who develop hyperkalemia may require sporadic or intermittent treatment with a potassium binder such as patiromer, sodium zirconium cyclosilicate, or sodium polystyrene. Hypotension and hyponatremia occur infrequently, and breast tenderness, gynecomastia, and sexual AEs have been reported by <1% of patients taking finerenone. Importantly, cardiorenal event reduction in the phase III clinical trial program occurred in high-risk patients, many of whom had established CV disease and were receiving a variety of different medications for glycemic control. Finerenone has a novel mechanism of action and, through its MR antagonism, appears to reduce inflammation and fibrosis, providing an important addition to glycemic and BP control, and risk factor modification in the treatment of CKD associated with T2D.
Inpatient management and post-discharge outcomes of hyperkalemia
Published in Hospital Practice, 2021
Jill Davis, Rubeen Israni, Fan Mu, Erin E. Cook, Harold Szerlip, Gabriel Uwaifo, Vivian Fonseca, Keith A. Betts
However, despite frequent treatment, monitoring, and normalization of serum potassium levels during the inpatient stay, death, readmission, and hyperkalemia recurrence were fairly common across all cohorts. Furthermore, less than 1% of patients received any potassium binder treatment at discharge in this study despite the fact that approximately 18% of patients did not have normalized serum potassium levels. The lack of potassium binder treatment use at discharge as well as the subsequent high hyperkalemia recurrence and hyperkalemia-related readmissions may demonstrate the continued unmet treatment need in this patient population. However, this study was descriptive in nature and the cause of the readmissions was not examined. Currently, newer treatments, such as patiromer (approved by the FDA in 2015) and sodium-zirconium cyclosilicate (approved by the FDA in 2018), are available to patients. While not commonly used or available during this study period, these treatments have improved tolerability profiles compared to other treatments for hyperkalemia [36–38]. Further studies examining how these treatments impact potassium normalization, recurrence and readmission in real-world settings would be beneficial.
Patiromer for the treatment of hyperkalemia
Published in Expert Review of Clinical Pharmacology, 2020
Gates B. Colbert, Dhwanil Patel, Edgar V. Lerma
Historically sodium polystyrene sulfonate (SPS) or Kayexalate has been used as an oral potassium binder. SPS is a sodium-exchange resin that is orally administered with water that promotes excretion of potassium in the colon lumen with voluminous stool outputs [14]. This medication was released into the market prior to the Food and Drug Administration creation, thus rigorous clinical trials and efficacy are lacking. Only oncea small trial of only 33 patients has shown any data to prove efficacy and safety [15]. In 1961, sorbitol was recognized as an effective addition to SPS to promote diarrhea and allow for further increases in potassium excretion [16]. Unfortunately, there are limitations to SPS palatability due to a gritty sensation when administered orally. As well, the propensity for voluminous diarrhea is not well tolerated by many patients. Fifteen grams of SPS contains approximately 60 mg of sodium [17], which can add up to a high sodium load if given in increasing and multiple doses, as is common in daily practice. This potentially can lead to worsening volume overload and resistant hypertension control. There is also increased morbidity associated with SPS and colonic necrosis reported [18]. As a result, after over 50 years of its addition to SPS, sorbitol was recommended not to be given concomitantly by the FDA to lower this life-threatening complication [19]. Recently in 2019, results of an Swedish observational analysis in adults with at least CKD Stage 4 described the use of SPS to be associated with a higher risk of gastrointestinal events, including a composite of hospitalization or death due to intestinal ischemia or thrombosis, GI ulcers, and perforation (adjusted HR 1.25) [18,20]. Newer guidelines by the FDA recommend a 3-h separation window between SPSother oral medications.