1) Welcome to our #accredited#tweetorial on optimal mgt of #hyperkalemia in the patient with #CKD. Earn 0.5h #CME/CE credit by following this thread. I am Sourabh Sharma MD DNB FASN 🇮🇳 @iamnephrologist & u have found the ONLY source for CE credit delivered entirely on Twitter!
4) Re potassium #homeostasis: 98% of the body's K lies in intracellular space➡️ helping determine resting membrane potential & intracellular electronegativity.
10% of K secretion is via the colon (↑significantly in advancing CKD) 🔓kidney360.asnjournals.org/content/1/1/65#NephroNotes
6) Arrhythmia in Hyperkalemia
Moderate HyperK: Fast Na channel activation; ↑excitability/conduction velocity: Peaked T
Severe HyperK: Fast Na channel inactivation/Inwardly rectifying K channel activation: Wide QRS/Conduction block
🔓academic.oup.com/ndt/article/34…
11) A low-K diet is generally recommended in advanced #CKD, but @goKDIGO suggests interventional trials to determine optimal recommendations, as there is no direct evidence to link dietary K & serum K, and the benefits of K can’t be ignored
🔓kidney360.asnjournals.org/content/1/1/65 #NephroNotes
15) So when hyperK happens, how is it treated? Acutely:
👉IV calcium ↓cardiac membrane excitation (1-3 min)
👉Insulin/glucose & β agonist redistribute K to ICS (30-60 min) but not ↓total body K
👉β Agonists: short duration of effect (2-4hrs)
👉Sodium bicarbonate ↑K elimination
21) So now let's look at oral potassium binders, which are more useful in chronic mgt & can help facilitate #RAASi optimization. Which of the following binders has the most rapid onset of action after oral administration?
24) We were about to start talking about the oral K binders. (BTW earn MORE CE/#CME on this topic at cardiometabolic-ce.com/category/hyper…) Yes, prune juice is a K binder, but it's not quick, and it may make a bigger mess than Na polystyrene sulfonate. So the correct answer was D.
27) Start w/the old. Sodium/Calcium Polysterene Sulfonate clinical studies:
👉Limited evidence for effectiveness/safety
👉With sorbitol, can cause colonic necrosis
👉Nonselective for K, with affinity for Ca/Mg ions
👉Caution: Na & volume overload
🔓frontiersin.org/articles/10.33…
28) And then the new. First, #patiromer sorbitex calcium clinical studies:
👉Efficacy established in randomized, placebo-controlled, phase 2 and 3 trials (CKD/ HF/RAASi)
👉Onset of action~ 7 hours
👉No serious AEs
🔓frontiersin.org/articles/10.33… #NephPearls#FOAMed#MedEd
29) Sodium Zirconium Cyclosilicate (#SZC) clinical studies:
👉Efficacy & safety established in Ph 2 & 3 trials (#CKD/#HF/#DM/#RAASi)
👉assoc'd w/ ↑Bicarbonate
👉High selectivity for K & ammonium ions
👉fast onset, starts in small bowel
👉No serious AEs
🔓frontiersin.org/articles/10.33…
31) Treatment of #Hyperkalemia in #hemodialysis patients:
👉Hyperkalaemia contributes to mortality in HD (3-5% deaths)
👉K ⤴️is most common immediately post 3-day weekend break
👉Adjust dialysate K as per 🔓ukkidney.org/sites/renal.or…
32) In summary, the treatment of hyperkalemia is likely to evolve in the coming years with the availability of novel drugs & the development of new strategies to improve safety. Clinical decisions on when to treat & how aggressively to treat require a pt-centered approach ...
33) ... guided by the clinical setting and rate of change in serum K+ level. Patients with moderate levels of hyperkalemia pose the greatest dilemma, especially when acuity is low, but warrant intervention to avoid deterioration.
34) Severe hyperkalemia risks arrhythmias & cardiac arrest, therefore prompt recognition and intervention is required. How big a problem is it? In-hospital mortality is significantly higher in patients w/ hyperkalaemia (X%) hypokalaemia (Y%) vs normokalaemia (Z%). What are X,Y,Z?
35) Per NICE guidelines, the correct answer is B, more exactly hyperkalemia (18.1%) compared to those with hypokalemia (5.0%) or normokalemia (3.9%). Pts with severe hyperK (> 6.5 mmol/l) are most at risk & in one report (🔓pubmed.ncbi.nlm.nih.gov/23171442/), hospital mortality was 30.7%.
9) Many risk factors modulate the propensity of LDL-C to traverse the endothelium and enter the arterial intima. See 🔓academic.oup.com/eurheartj/arti….
10) It now appears that the passage of #LDL into the #intima is not a merely passive process whereby the concentration in blood & the permeability of the endothelium determine LDL accumulation.
11) It’s #Transcytosis (an active process), through a vesicular pathway involving #caveolae, scavenger receptors (#SRB1) and activin like receptor kinase 1 (#ALK1). Hence for a given blood level of LDL-C the amount of atherosclerosis is variable.
1) Welcome to an #accredited#tweetorial on the role of ⬆️ #LDL-C levels in the pathogenesis & pathophysiology of #ASCVD. I am Kausik Ray MD FRCP @profkausikray, Professor of Public Health & Cardiologist @imperialcollege London AND President of European Atherosclerosis Society
3) #Atherosclerosis starts in childhood, progresses in fits and spurts and presents in middle to late life in the form of major adverse cardiovascular events #MACE.
3) @PaulDThompsonMD took on education re mechanisms & use of ezetimibe & bempedoic acid. He proposes a case: 45 ♂️ w/history of inferior wall #MI treated with primary angioplasty.
3) It is an unfortunate fact of life that one cannot prescribe #anticoagulant or #antiplatelet (together, #antithrombotic) therapy without increasing a patient's #bleedingrisk. That is why it should be an individualized risk:benefit decision, ideally . . .
1) Welcome to a new #accredited#tweetorial on managing #VTE at the extremes of weight & renal function. Free CE/#CME credit for following along with expert author @AryaRoopen from King’s Thrombosis Centre at King's College Hospital in London! Only the best for our learners!