Current Management of Hyperkalemia in Non-Dialysis CKD: Longitudinal Study of Patients Receiving Stable Nephrology Care

Abstract

Background: No study has explored the limitations of current long-term management of hyperkalemia (HK) in outpatient CKD clinics. Methods: We evaluated the association between current therapeutic options and control of serum K (sK) during 12-month follow up in ND-CKD patients stratified in four groups by HK (sK ≥ 5.0 mEq/L) at baseline and month 12: Absent (no-no), Resolving (yes-no), New Onset (no-yes), Persistent (yes-yes). Results: We studied 562 patients (age 66.2 ± 14.5 y; 61% males; eGFR 39.8 ± 21.8 mL/min/1.73 m2, RAASI 76.2%). HK was “absent” in 50.7%, “resolving” in 15.6%, “new onset” in 16.6%, and “persistent” in 17.1%. Twenty-four hour urinary measurements testified adherence to nutritional recommendations in the four groups at either visit. We detected increased prescription from baseline to month 12 of bicarbonate supplements (from 5.0 to 14.1%, p < 0.0001), K-binders (from 2.0 to 7.7%, p < 0.0001), and non-K sparing diuretics (from 34.3 to 41.5%, p < 0.001); these changes were consistent across groups. Similar results were obtained when using higher sK level (≥5.5 mEq/L) to stratify patients. Mixed-effects regression analysis showed that higher sK over time was associated with eGFR < 60, diabetes, lower serum bicarbonate, lower use of non-K sparing diuretics, bicarbonate supplementation, and K-binder use. Treatment-by-time interaction showed that sK decreased in HK patients given bicarbonate (p = 0.003) and K-binders (p = 0.005). Conclusions: This observational study discloses that one-third of ND-CKD patients under nephrology care remain with or develop HK during a 12-month period despite low K intake and increased use of sK-lowering drugs.

Chronic Kidney Disease: Role of Diet for a Reduction in the Severity of the Disease

“…Additionally, Kalemic control is further compounded by extensive use of the renin–angiotensin–aldosterone system inhibitor (RAASI) therapy in CKD patients [ 77 ]. Development of hyperkalemia in CKD patients requires lowering the dose or discontinuation of the RAASI therapy to protect patients from developing cardiovascular events and end stage kidney disease.…”

Management of Chronic Hyperkalemia in Patients With Chronic Kidney Disease: An Old Problem With News Options

“…Studies in patients with CKD have shown a remarkable frequency in hyperkalemia in advanced CKD stages, hyporreninemic hypoaldosteronic diabetic patients, renal transplantation (RT), and patients with RAAS inhibition (4,6). Available information shows prevalence percentages ranging from 5 to 20% depending on the stage of CKD (13).…”

“…Compensatory mechanisms may help improving tolerance to hyperkalemia in patients with CKD and a J-shaped correlation was found between serum potassium and overall mortality risk in non-dialysis patients (16). Moreover, new onset or persistence of mild-to-moderate hyperkalemia (potassium 5.0-6.0 mmol/L) during 12 months of observation significantly increased by 30% the risk of End Stage Renal Disease (ESRD) (4,17,18). It has been suggested that CKD patients adapt to elevated potassium concentrations through modifications in gastrointestinal secretions which may favor intracellular potassium storage, or by increasing insulinmediated intracellular potassium uptake in splanchnic and peripheral muscle tissues (19).…”

“…Fresh fruits and vegetables, are considered healthy choices for most people and they are associated with a less renal complications except for hyperkalemia (3). Nevertheless, among patients with chronic kidney disease (CKD), a higher dietary potassium intake may be associated with a higher risk of kidney disease progression (4).…”

Chronic Hyperkaliemia in Chronic Kidney Disease: An Old Concern with New Answers

“…Moreover, a relationship between potassium intake and serum K + has never been demonstrated. Indeed, the studies evaluating potassium intake by urinary potassium excretion or food frequency questionnaire have shown a weak correlation between potassium intake and serum K + concentrations in patients with non-dialytic CKD (r = 0.05) [ 41 ] and ESKD [ 25 , 42 , 43 , 44 ]. This poor correlation between serum and potassium intake is likely due to an increase in gastrointestinal excretion and intracellular redistribution.…”