Hypochloremia ja sydän

https://www.ncbi.nlm.nih.gov/pubmed/27507113

Circ Heart Fail. 2016 Aug;9(8). pii: e003180. doi: 10.1161/CIRCHEARTFAILURE.116.003180.

Hypochloremia and Diuretic Resistance in Heart Failure: Mechanistic Insights.

Hanberg JS¹, Rao V¹, Ter Maaten JM¹, Laur O¹, Brisco MA¹, Perry Wilson F¹, Grodin JL¹, Assefa M¹, Samuel Broughton J¹, Planavsky NJ¹, Ahmad T¹, Bellumkonda L¹, Tang WH¹, Parikh CR¹, Testani JM².

Author information

Abstract

BACKGROUND:

Recent epidemiological studies have implicated chloride, rather than sodium, as the driver of poor survival previously attributed to hyponatremia in heart failure. Accumulating basic science evidence has identified chloride as a critical factor in renal salt sensing. Our goal was to probe the physiology bridging this basic and epidemiological literature.

METHODS AND RESULTS:

Two heart failure cohorts were included: (1) observational: patients receiving loop diuretics at the Yale Transitional Care Center (N=162) and (2) interventional pilot: stable outpatients receiving ≥80 mg furosemide equivalents were studied before and after 3 days of 115 mmol/d supplemental lysine chloride (N=10). At the Yale Transitional Care Center, 31.5% of patients had hypochloremia (chloride ≤96 mmol/L). Plasma renin concentration correlated with serum chloride (r=-0.46; P<0 .001="" b=""> with no incremental contribution from serum sodium

(P=0.49).  Hypochloremic versus nonhypochloremic patients exhibited renal wasting of chloride (P=0.04) and of chloride relative to sodium (P=0.01), despite better renal free water excretion (urine osmolality 343±101 mOsm/kg versus 475±136; P<0 .001="" b="">Hypochloremia was associated with poor diuretic
response (odds ratio, 7.3; 95% confidence interval, 3.3-16.1; P<0 .001="" b="" in="" interventional="" pilot="" the="">lysine chloride supplementation was associated with an increase in serum chloride levels of 2.2±2.3 mmol/L, and the majority of participants experienced findings such as hemoconcentration, weight loss, reduction in amino terminal, pro B-type natriuretic peptide, increased plasma renin activity, and increased blood urea nitrogen to creatinine ratio.

CONCLUSIONS:

Hypochloremia is associated with neurohormonal activation and diuretic resistance with chloride depletion as a candidate mechanism. Sodium-free chloride supplementation was associated with increases in serum chloride and changes in several cardiorenal parameters.

CLINICAL TRIAL REGISTRATION:

URL: http://www.clinicaltrials.gov. Unique identifier: NCT02031354.

© 2016 American Heart Association, Inc.

KEYWORDS:

cardiorenal syndrome; chloride; diuretics

PMID:

27507113

PMCID:

PMC4988527

[Available on 2017-08-01]

DOI:

10.1161/CIRCHEARTFAILURE.116.003180