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Validation and comparison of three formulae to estimate sodium and potassium excretion from a single morning fasting urine compared to 24-h measures in 11 countries

Mente A, O'Donnell MJ, Dagenais G, Wielgosz A, Lear SA, McQueen MJ, et al.

J Hypertens, 2014 May;32(5):1005-14; discussion 1015.
PMID: 24569420 DOI: 10.1097/HJH.0000000000000122

Although 24-h urinary measure to estimate sodium and potassium excretion is the gold standard, it is not practical for large studies. We compared estimates of 24-h sodium and potassium excretion from a single morning fasting urine (MFU) using three different formulae in healthy individuals.

Matched MeSH terms: Potassium/urine*
Serum calcium and parathormone during normal pregnancy in Malay women

Singh HJ, Mohammad NH, Nila A

J Matern Fetal Med, 1999 May-Jun;8(3):95-100.
PMID: 10338062

To ascertain the calcium status in normal pregnant Malay women.

Matched MeSH terms: Potassium/urine
Effects of fasting during Ramadan on urinary excretion in Malaysian Muslims

Cheah SH, Ch'ng SL, Husain R, Duncan MT

Br J Nutr, 1990 Mar;63(2):329-37.
PMID: 2334668

Urine analysis was conducted on male Muslims before, during and after Ramadan. Various changes in urine volume, osmolality, total solute, sodium, potassium, titratable acidity and urea in response to altered feeding and activity regimens were found. There were no detectable levels of ketones, protein, glucose, urobilinogen and haemoglobin. It was concluded that the body adapted to fasting during Ramadan and that there were no adverse effects on renal function.

Matched MeSH terms: Potassium/urine
Study of low salt diet in hypertensive patients with chronic kidney disease

Koh KH, Wei-Soon LH, Jun L, Lui-Sian LN, Hui-Hong CT

Med J Malaysia, 2018 12;73(6):376-381.
PMID: 30647207

INTRODUCTION: The efficacy of blood pressure (BP) reduction with salt restriction in CKD subjects and its sustainability is not well established.
METHODS: We enrolled 75 hypertensive patients with CKD into one-month salt restricting diet. 24-hour urinary sodium and potassium was measured to verify their salt intake followed by 1½ year follow-up.
RESULTS: Their creatinine clearance was 43 ± standard deviation 33ml/min/1.73m2. Urinary Na excretion (24HUNa) was 173±129mmol/day, reducing to 148±81 by 31±6 day. Mean, systolic and diastolic BP (MBP, SBP, DBP) were reduced from 102±9 to 97±11 (p<0.001), 148±10 to 139±16 (p<0.001), 78±12 to 75±12 mmHg (p=0.012) respectively. Moderate correlations were shown between reductions in 24-hour urinary Na and MBP, SBP, DBP: r=0.366, 0.260, 0.365; p=0.001, 0.025, 0.001; whereas 24-hour urinary Na-K ratio showed mild correlation. Subjects have some tendency to drift back to previous Na intake profile in follow-up and thus repetitive education is necessary. In subanalysis, 34 subjects with baseline 24HUNa >150 mmol/day, benefited significantly with MBP, SBP, DBP reduction from 102±9 to 95±9 (p=0.001), 146±10 to 135±14 mmHg (p=0.001), 80±11 to 75±11 mmHg (p=0.002) in line with 24HUNa reduction from 253±154 to 163±87mmol/day (p=0.004) and urinary protein-creation ratio reduction from geometric mean of 95 to 65 g/mol. Thirty five subjects with 24HUNa reduction of >20mmol/day have significant reduction in MBP, SBP, DBP: -8 vs -2, -15 vs -4, -5 vs -2 mmHg (p=0.027, 0.006, 0.218) and urinary protein-creatinine ratio: -82 vs 2g/mol (p=0.030) compared to the other forty subjects.
CONCLUSION: Quantification of 24-hour urinary Na helps in predicting potential antihypertensive effect with dietary salt reduction of CKD subjects. Salt restriction reduces BP especially in patients with estimated daily sodium intake of >150mmol/day. Reduction in sodium intake beyond 20mmol/day reduced both BP and proteinuria.

Matched MeSH terms: Potassium/urine
Spot urine potassium as a potential screening test for aldosterone breakthrough

Sakthiswary R, Wong M, Isa ZM, Nor Azmi K

Clin Ter, 2012;163(3):195-8.
PMID: 22964690

Treatment with angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) may suppress aldosterone production only in the initial phase of treatment and subsequently lead to a rising level of aldosterone to baseline or higher. This phenomenon is described as aldosterone breakthrough. Apart from serial plasma aldosterone levels, there are no other test to identify this condition. The purpose of this study was to evaluate the role of spot urine potassium as a potential screening test for aldosterone breakthrough.

Matched MeSH terms: Potassium/urine*
Twenty-four hour and spot urine metabolic evaluations: correlations versus agreements

Hong YH, Dublin N, Razack AH, Mohd MA, Husain R

Urology, 2010 Jun;75(6):1294-8.
PMID: 19914693 DOI: 10.1016/j.urology.2009.08.061

OBJECTIVES: To investigate the correlations and agreements between the solute/creatinine ratios from the 24-hour and early morning spot urine samples for metabolic evaluation in stone-formers given the various pitfalls with the 24-hour urinary metabolic evaluation in stone-formers.
METHODS: 30 urinary stone-formers out of an initial 62 recruited provided a complete 24-hour urine and early morning spot urine samples for metabolic evaluation. Pearson correlation and Bland and Altman Test were used to assess the correlations and agreements.
RESULTS: Significant correlations were established between the 24-hour urinary solute excretions and the corresponding early morning spot urine solute/creatinine ratios for calcium, magnesium, urate, potassium, oxalate, citrate, and the Differential Gibb's free energy value of calcium oxalate DG(CaOx) values. However, all these solute/creatinine measurements between the 24-hour and early morning spot urine samples were judged to be not within the acceptable limits based on the estimated "limit of agreement" by the Bland and Altman Test of Agreement. Diurnal circadian rhythm and postprandial excretion surge are thought to be responsible for the disagreements.
CONCLUSIONS: Thus, the early morning spot urine is not suitable to be used interchangeably to replace the 24-hour urine collection in the evaluation of urinary metabolic abnormalities in stone-formers. A good correlation does not translate to an agreement between the 2 measurements.

Matched MeSH terms: Potassium/urine
Plasma renin and aldosterone in thyroid diseases

Asmah BJ, Wan Nazaimoon WM, Norazmi K, Tan TT, Khalid BA

Horm. Metab. Res., 1997 Nov;29(11):580-3.
PMID: 9479560 DOI: 10.1055/s-2007-979105

The effect of thyroid hormones on the renin-angiotensin-aldosterone system has not been fully resolved. Highly specific immunoassays for measurement of renin, aldosterone, free T4 (fT4), free T3 (fT3) and ultrasensitive TSH enables a direct and more accurate measurement of these hormones. We investigated the relationship between plasma renin, aldosterone and thyroid hormones in the basal state and after intravenous frusemide. This is a cross-sectional study involving 37 patients with thyrotoxicosis, 42 rendered euthyroid with normal fT4, fT3 and TSH levels, 17 with euthyroid levels of fT4 and fT3 but suppressed TSH, and 11 with hypothyroidism. Basal plasma renin was significantly higher in thyrotoxicosis (63.4 +/- 9.8 microU/ml, mean +/- SEM) compared to euthyroid (32.7 +/- 4.4 microU/ml) and hypothyroid (26.7 +/- 9.8 microU/ml). Basal plasma renin for euthyroid with suppressed TSH (41.0 +/- 7.4 microU/ml) was significantly higher than hypothyroid (p = 0.02). Basal plasma aldosterones were not significantly different except for suppressed TSH (157.7 +/- 13 pg/ml), which was higher than normal (109.9 +/- 10.4 pg/ml; p = 0.04). Following frusemide, plasma renin and aldosterone were significantly increased in all groups. Plasma renin was highly correlated to fT3 (r = 0.405, p < 0.001), total T3 (r = 0.359, p < 0.001), fT4 (r = 0.331, p < 0.001) and TSH (r = 0.300, p < 0.001) in the basal state, but less to total T4 (r = 0.248, p < 0.01). Plasma renin correlated poorly to serum aldosterone (r = 0.212, p < 0.03). This study clearly showed that regulation of renin was mainly influenced by fT3, and that aldosterone response to frusemide was blunted in thyrotoxicosis despite normal electrolytes.

Matched MeSH terms: Potassium/urine
Composition of normal urine in students of the University of Malaya

Chandra N, Bhattathiry EP

Trop Geogr Med, 1967 Dec;19(4):300-3.
PMID: 5585976
Matched MeSH terms: Potassium/urine
Diuretic properties of Orthosiphon stamineus Benth

Adam Y, Somchit MN, Sulaiman MR, Nasaruddin AA, Zuraini A, Bustamam AA, et al.

J Ethnopharmacol, 2009 Jul 6;124(1):154-8.
PMID: 19375494 DOI: 10.1016/j.jep.2009.04.014

Orthosiphon stamineus has been used in traditional medicine for centuries especially to treat diseases of the urinary system.

Matched MeSH terms: Potassium/urine*
Fulltext Lysine-Specific Demethylase-1 Deficiency Increases Agonist Signaling Via the Mineralocorticoid Receptor

Treesaranuwattana T, Wong KYH, Brooks DL, Tay CS, Williams GH, Williams JS, et al.

Hypertension, 2020 04;75(4):1045-1053.
PMID: 32160100 DOI: 10.1161/HYPERTENSIONAHA.119.13821

LSD1 (lysine-specific demethylase-1) is an epigenetic regulator of gene transcription. LSD1 risk allele in humans and LSD1 deficiency (LSD1+/-) in mice confer increasing salt-sensitivity of blood pressure with age, which evolves into salt-sensitive hypertension in older individuals. However, the mechanism underlying the relationship between LSD1 and salt-sensitivity of blood pressure remains elusive. Here, we show that LSD1 genotype (in humans) and LSD1 deficiency (in mice) lead to similar associations with increased blood pressure and urine potassium levels but with decreased aldosterone levels during a liberal salt diet. Thus, we hypothesized that LSD1 deficiency leads to an MR (mineralocorticoid receptor)-dependent hypertensive state. Yet, further studies in LSD1+/- mice treated with the MR antagonist eplerenone demonstrate that hypertension, kaliuria, and albuminuria are substantially improved, suggesting that the ligand-independent activation of the MR is the underlying cause of this LSD1 deficiency-mediated phenotype. Indeed, while MR and epithelial sodium channel expression levels were increased in LSD1+/- mouse kidney tissues, aldosterone secretion from LSD1+/- glomerulosa cells was significantly lower. Collectively, these data establish that LSD1 deficiency leads to an inappropriate activation and increased levels of the MR during a liberal salt regimen and suggest that inhibiting the MR pathway is a useful strategy for treatment of hypertension in human LSD1 risk allele carriers.

Matched MeSH terms: Potassium/urine
Fulltext Dysregulated aldosterone secretion in persons of African descent with endothelin-1 gene variants

Tan JW, Gupta T, Manosroi W, Yao TM, Hopkins PN, Williams JS, et al.

JCI Insight, 2017 12 07;2(23).
PMID: 29212952 DOI: 10.1172/jci.insight.95992

Compared with persons of European descent (ED), persons of African descent (AD) have lower aldosterone (ALDO) levels, with the assumption being that the increased cardiovascular disease (CVD) risk associated with AD is not related to ALDO. However, the appropriateness of the ALDO levels for the volume status in AD is unclear. We hypothesized that, even though ALDO levels are lower in AD, they are inappropriately increased, and therefore, ALDO could mediate the increased CVD in AD. To test this hypothesis, we analyzed data from HyperPATH - 1,788 individuals from the total cohort and 765 restricted to ED-to-AD in a 2:1 match and genotyped for the endothelin-1 gene (EDN1). Linear regression analyses with adjustments were performed. In the total and restricted cohorts, PRA, ALDO, and urinary potassium levels were significantly lower in AD. However, in the AD group, greater ALDO dysregulation was present as evidenced by higher ALDO/plasma renin activity (PRA) ratios (ARR) and sodium-modulated ALDO suppression-to-stimulation indices. Furthermore, EDN1 minor allele carriers had significantly greater ARRs than noncarriers but only in the AD group. ARR levels were modulated by a significant interaction between EDN1 and AD. Thus, EDN1 variants may identify particularly susceptible ADs who will be responsive to treatment targeting ALDO-dependent pathways (e.g., mineralocorticoid-receptor antagonists).

Matched MeSH terms: Potassium/urine