Sp298renal Potassium Handling in Chronic Kidney Disease: Differences Between Patients With or Without Hyperkalemia

Caravaca-Fontán, Fernando; Díaz-Campillejo, Rosa; Valladares, Julián; Arnaldo, Cristina López; Barroso, Sérgio; Luna, Enrique; Caravaca, Francisco

doi:10.1093/ndt/gfz103.sp298

Cited by 2 publications

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“…As expected, all cases in our cohort had urine parameters indicative of a low/inadequate potassium excretion regardless of whether hyperkalemia was present or not in spite of a glomerular filtration rate > 30 ml/min/1.73 m 2 . Thus, the patients showed a descent of the FKE (which is expected to be > 30 in hyperkalemia ( 21 ) and > 7 in (normokalemia) ( 22 ), as well as a low Urinary K+/creatinine ratio (which is expected to be > 150 in hyperkalemia ( 23 )), a reduced TTKG (which is expected to be > 7, both in hyperkalemia and eukalemia, and even higher in hypovolemia ( 24 )), and an elevated value of Urinary Na+/K+ ratio (which is expected to be < 1 in hyperkalemia ( 25 – 27 )).In our cohort, hyperkalemia was the most consistent finding, documented in 106/112 (94.6%) cases at some time during the hypoaldosteronism episode. Thus, although the vast majority of patients developed hyperkalemia, 6 patients, over 5%, did not.…”

Section: Discussionmentioning

confidence: 99%

Clinical manifestations and associated factors in acquired hypoaldosteronism in endocrinological practice

et al. 2022

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IntroductionHypoaldosteronism can be congenital or acquired, isolated or part of primary adrenal insufficiency, and caused by an aldosterone deficit, resistance, or a combination of both. Reduced mineralocorticoid action can induce a decrease in urine K+ and H+ excretion and an increase in urine Na+ excretion, leading to hyperkalemia, and/or hyponatremia, often combined with metabolic acidosis. We aimed to characterize the clinical manifestations of hypoaldosteronism, and their associated factors.MethodsRetrospective analysis of 112 episodes of hypoaldosteronism diagnosed in 86 adult patients from 2012-2019 by the Endocrinology and Nutrition Department of a tertiary hospital. The frequency of hyperkalemia, hypovolemic hyponatremia (HH) and metabolic acidosis (MA), and their associated factors were evaluated.ResultsPatients had a median age of 77 [65 – 84], 55.4% were male. 94.6% cases showed hyperkalemia, 54.5% HH, and 60.3% MA. The mean serum K+ of all cases was 5.4 ± 0.5 mmol/L, Na+: 132.1 ± 6.3 mmol/L, HCO3: 22.6 ± 3.3 mmol/L. Hypoaldosteronism was isolated in the majority of cases: only 6/112 (5%) had primary adrenal insufficiency. Hypovolemia was associated with hyponatremia and a more florid clinical presentation. HH was associated with a combined presence of aldosterone-lowering and mineralocorticoid resistance factors. MA was associated with the presence of mineralocorticoid resistance factors.ConclusionsHypoaldosteronism in adult endocrinological clinical practice is primarily isolated, and acquired. It predisposes not only to the development of hyperkalemia and MA, but also to that of HH. Hypoaldosteronism must be considered in the differential diagnosis of HH with urinary sodium wasting.

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Section: Discussionmentioning

confidence: 99%

Clinical manifestations and associated factors in acquired hypoaldosteronism in endocrinological practice

et al. 2022

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“…When renal K + excretion is impaired, excessive K + intake can cause hyperkalemia [65]. Thus, in 212 predialysis patients with CKD stage 4-5, the main determinants of normal serum K + levels were the K + load (intake and absorption minus extrarenal excretion) relative to kidney function and fractional excretion of K + [80].…”

Section: Increased K + Loadmentioning

confidence: 99%

Hyperkalemia in Chronic Kidney Disease in the New Era of Kidney Protection Therapies

Valdivielso

Balafa

Ekart

et al. 2021

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Despite recent therapeutic advances, chronic kidney disease (CKD) is one of the fastest growing global causes of death. This illustrates limitations of current therapeutic approaches and, potentially, unidentified knowledge gaps. For decades, renin-angiotensin-aldosterone system blockers (RAAS) have been the mainstay of therapy for CKD. However, they favor the development of hyperkalemia that that is already common in CKD patients due to the CKDassociated decrease in urinary potassium (K + ) excretion and metabolic acidosis. Hyperkalemia may itself be life-threatening as it may trigger potentially lethal arrhythmia, and additionally may limit the prescription of RAAS blockers and lead to low K + diets associated to low dietary fiber intake. Indeed, hyperkalemia is associated with adverse kidney, cardiovascular and survival outcomes. Recently, novel kidney protective therapies, ranging from sodium/glucose cotransporter 2 (SGLT2) inhibitors to new mineralocorticoid receptor antagonists have shown efficacy in clinical trials. Herein, we review K + pathophysiology and the clinical impact and management of hyperkalemia considering these developments and the availability of the novel K + binders patiromer and sodium zirconium cyclosilicate, recent results from clinical trials targeting metabolic acidosis (sodium bicarbonate, veverimer) and an increasing understanding of the role of the gut microbiota in health and disease. Key points-Hyperkalemia is a potentially lethal consequence of CKD.-Some commonly used treatments in CKD patients, like inhibitors of the RAAS system, have a potential effect worsening hyperkalemia -New treatments available in the nephrologist's armamentarium can be used in order to maintain K levels in the safe range Declarations:

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Sp298renal Potassium Handling in Chronic Kidney Disease: Differences Between Patients With or Without Hyperkalemia

Cited by 2 publications

References 0 publications

Clinical manifestations and associated factors in acquired hypoaldosteronism in endocrinological practice

Clinical manifestations and associated factors in acquired hypoaldosteronism in endocrinological practice

Hyperkalemia in Chronic Kidney Disease in the New Era of Kidney Protection Therapies

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