Hypokalemia, Its Contributing Factors and Renal Outcomes in Patients with Chronic Kidney Disease

Wang, Hsiao Han; Hung, Chi Chih; Hwang, Daw Yang; Kuo, Mei Chuan; Chiu, Ya Wen; Chang, Jer Ming; Tsai, Jason; Hwang, Shang Jyh; Seifter, Julian L.; Chen, Hung Chun

doi:10.1371/journal.pone.0067140

Cited by 46 publications

(43 citation statements)

References 43 publications

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“…For hypokalemia, management is reasonably straightforward because most patients can be corrected with oral supplements (13). Clinicians should be particularly vigilant in monitoring for hypokalemia, a potent precipitant in the setting of diuretic use, as this and other studies have shown (14).…”

Section: Discussionmentioning

confidence: 99%

Association between Serum Potassium and Outcomes in Patients with Reduced Kidney Function

Luo

Brunelli

Jensen

et al. 2016

Clinical Journal of the American Society of Nephrology

231

208

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Background and objectives Patients with CKD are more likely than others to have abnormalities in serum potassium (K + ). Aside from severe hyperkalemia, the clinical significance of K + abnormalities is not known. We sought to examine the association of serum K + with mortality and hospitalization rates within narrow eGFR strata to understand how the burden of hyperkalemia varies by CKD severity. Associations were examined between serum K + and discontinuation of medications that block the renin-angiotensin-aldosterone system (RAAS), which are known to increase serum K + .Design, setting, participants, & measurements A cohort of patients with CKD (eGFR,60 ml/min per 1.73 m 2 ) with serum K + data were studied (n=55,266) between January 1, 2009, and June 30, 2013 (study end). Serum K + , eGFR, and covariates were considered on a time-updated basis. Mortality, major adverse cardiovascular events (MACE), hospitalization, and discontinuation of RAAS blockers were considered per time at risk.Results During the study, serum K + levels of 5.5-5.9 and $6.0 mEq/L were most prevalent at lower eGFR: they were present, respectively, in 1.7% and 0.2% of patient-time for eGFR of 50-59 ml/min per 1.73 m 2 versus 7.6% and 1.8% of patient-time for eGFR,30 ml/min per 1.73 m 2 . Serum K + level ,3.5 mEq/L was present in 1.2%-1.4% of patient-time across eGFR strata. The median follow-up time was 2.76 years. There was a U-shaped association between serum K + and mortality; pooled adjusted incidence rate ratios were 3.05 (95% confidence interval, 2.53 to 3.68) and 3.31 (95% confidence interval, 2.52 to 4.34) for K + levels ,3.5 mEq/L and $6.0 mEq/L, respectively. Within eGFR strata, there were U-shaped associations of serum K + with rates of MACE, hospitalization, and discontinuation of RAAS blockers.Conclusions Both hyperkalemia and hypokalemia were independently associated with higher rates of death, MACE, hospitalization, and discontinuation of RAAS blockers in patients with CKD who were not undergoing dialysis. Future studies are needed to determine whether interventions targeted at maintaining normal serum K + improve outcomes in this population.

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Section: Discussionmentioning

confidence: 99%

Association between Serum Potassium and Outcomes in Patients with Reduced Kidney Function

Luo

Brunelli

Jensen

et al. 2016

Clinical Journal of the American Society of Nephrology

231

208

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“…Multivariate logistic regression analysis was used to evaluate the association between glycosuria and rapid renal function decline. The covariates were selected according to our previous studies29. The continuous variables with skewed distributions were log-transformed to reduce the skewness.…”

Section: Methodsmentioning

confidence: 99%

Glycosuria and Renal Outcomes in Patients with Nondiabetic Advanced Chronic Kidney Disease

Hung

Lin

Lee

et al. 2016

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Sodium glucose cotransporter 2 inhibitors have shown a potential for renoprotection beyond blood glucose lowering. Glycosuria in nondiabetic patients with chronic kidney disease (CKD) is sometimes noted. Whether glycosuria in CKD implies a channelopathy or proximal tubulopathy is not known. The consequence of glycosuria in CKD is also not studied. We performed a cross-sectional study for the association between glycosuria and urine electrolyte excretion in 208 nondiabetic patients. Fractional excretion (FE) of glucose >4% was 3.4%, 6.3% and 62.5% in CKD stage 3, 4 and 5, respectively. These patients with glycosuria had higher FE sodium, FE potassium, FE uric acid, UPCR, and urine NGAL-creatinine ratio. We conducted a longitudinal study for the consequence of glycosuria, defined by dipstick, in 769 nondiabetic patients with stage 4–5 CKD. Glycosuria was associated with a decreased risk for end-stage renal disease (adjusted hazard ratio: 0.77; CI = 0.62–0.97; p = 0.024) and for rapid renal function decline (adjusted odds ratio: 0.63; CI = 0.43–0.95; p = 0.032); but glycosuria was not associated with all-cause mortality or cardiovascular events. The results were consistent in the propensity-score matched cohort. Glycosuria is associated with increased fractional excretion of electrolytes and is related to favorable renal outcomes in nondiabetic patients with stage 5 CKD.

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“…In an observational study of pre-dialysis CKD patients ( n = 2,500), followed up for 2.7 years [39] , Wang et al [39] reported that more than 50% of the patients with CKD stages 1 and 2 and more than 25% of the CKD stages 3 and 4 had serum K + of <4 mEq/L. About 5.6% of the CKD stage 4 patients had serum K + below 3.5 mEq/L.…”

Section: Hypokalemiamentioning

confidence: 99%

Inflammation: A Key Contributor to the Genesis and Progression of Chronic Kidney Disease

Qian

2017

Expanded Hemodialysis: Innovative Clinical Approach in Dialysis

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It has become apparent that inflammation and inflammatory reactions can evoke renal injury and promote chronic kidney disease (CKD) progression. Under physiological condition, intrarenal vascular distribution is heterogeneous, and medulla is hypoxic. To avoid energy deprivation in the low pO 2 regions of the kidney, an array of hormones, autocoids, and vasoactive substances, including medullipin, prostaglandins, endothelins, nitric oxide, angiotensin II, kinins, and adenosine, tonically regulates the microvasculature to ensure a perfect match of the microcirculation (O 2 supply) and renal tubules (O 2 demand). Inflammation, systemic or intrarenal, not only can abolish the microvascular response to its regulators, but also induces an array of tubular toxins, including reactive oxygen species, leading to tubular injury, nephron dropout, and onset of CKD. Positive acid balance, electrolyte alterations, and intestinal dysbiosis can perpetuate CKD progression. Understanding the role of inflammation in the genesis and progression of CKD will foster the development of strategies to prevent and treat the underlying inflammation and improve CKD outcomes.

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Hypokalemia, Its Contributing Factors and Renal Outcomes in Patients with Chronic Kidney Disease

Cited by 46 publications

References 43 publications

Association between Serum Potassium and Outcomes in Patients with Reduced Kidney Function

Association between Serum Potassium and Outcomes in Patients with Reduced Kidney Function

Glycosuria and Renal Outcomes in Patients with Nondiabetic Advanced Chronic Kidney Disease

Inflammation: A Key Contributor to the Genesis and Progression of Chronic Kidney Disease

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