What Can Make Crp and Bun/creatinine Ratio and Blood Platelets and Sodium High

Abstruse

The aim of this study was to determine whether decreased serum sodium concentration could be associated with the disease activity in SLE. We retrospectively analyzed the data of the ii independent cohorts of children and adults with SLE in 2 centers. Hyponatremia was associated with serum chloride (p = 0.004), albumin (p = 0.002) and SLE disease activity index (SLEDAI) (p = 0.026) in children with SLE. Serum sodium levels were correlated negatively with ESR (p =0.001) and positively with serum albumin levels (p < 0.0001) and C3 (p = 0.008) in children with SLE and those levels were correlated negatively with serum interleukin-half-dozen levels (p = 0.003) in adults with SLE. Independent take chances factors for the evolution of hyponatremia were the decreased serum C3 levels (OR 1.069, p = 0.031), the decreased serum chloride levels (OR ii.054, p = 0.006) and increased erythrocyte sedimentation charge per unit (ESR) (OR ane.066, p = 0.03) in children with SLE and increased C-reactive poly peptide (CRP) (OR ane.480, p = 0.023) in combined cohorts with SLE by multiple logistic regression analyses. Our study firstly showed that hyponatremia could reflect a disease action and severe inflammation of SLE.

Introduction

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune affliction with a highly variable clinical course^1,two. During the course of the affliction, decreased serum levels of C3, C4 and loftier anti-double stranded (anti-ds) Deoxyribonucleic acid antibody titers are reported to exist associated with the affliction activeness and poor survival³.

Hyponatremia is known to be one of the well-nigh common electrolyte abnormalities and can cause seizures, brain edema, encephalopathy, and even death^4,5. Hyponatremia has been reported to be poor clinical issue such as mortality in general population, dialyzed patients and those with eye failure, cirrhosis and sepsis^{half-dozen,seven,8}. However, the incidence and clinical significance of hyponatremia has non been studied in rheumatic diseases including SLE and only some case reports of hyponatremia have been reported in SLE^9,x. Also, at that place has been no study describing the relationship between the degree of hyponatremia and the disease activity in both childhood and adulthood SLE.

Therefore, the aim of this report was to evaluate the clinical and laboratory characteristics related to disease activity in children and adults with SLE and determine whether decreased serum sodium concentration could be associated with the affliction activity in SLE.

Results

A cohort of children and adolescents with SLE

Laboratory characteristics of the patients with (Group I, n = 11) and without hyponatremia (Group 2, northward = 63) are shown in Tabular array 1. In that location were no meaning differences in white blood prison cell (WBC) counts, hemoglobin, hematocrit, platelet counts, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), serum potassium, full carbon dioxide (tCO_ii), blood urea nitrogen (BUN), creatinine, full protein, cholesterol, uric acid, alanine aminotransferase (ALT) and total bilirubin between the two groups (p > 0.05). However, serum chloride (p = 0.004), albumin (p = 0.002), aspartate aminotransferase (AST) levels (p = 0.004) and SLE disease action alphabetize (SLEDAI) (p = 0.026) were significantly higher and serum calcium levels (p = 0.004) were significantly lower in SLE patients with hyponatremia than those without.

Table 1 Full general laboratory findings of children with lupus with or without hyponatremia.

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The positivity of antinuclear antibiotic (ANA), anti-ds DNA antibody and other autoantibodies, and the incidence of proteinuria did not differ betwixt the ii groups. However, serum C3 levels which reflect the disease activeness were significantly lower in SLE patients with hyponatremia than those without (p = 0.004) (Table two).

Tabular array two Immunologic laboratory findings and proteinuria of children with lupus with or without hyponatremia.

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Independent adventure factors for the development of hyponatremia were the decreased serum C3 levels (OR 1.069, p = 0.031), the decreased serum chloride levels (OR 2.054, p = 0.006) and increased erythrocyte sedimentation rate (ESR) (OR one.066, p = 0.03) in children with SLE by multiple logistic regression analysis (Tabular array 3).

Table iii Multiple logistic regression analysis of laboratory parameters associated with the evolution of lupus-associated hyponatremia in children with lupus.

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The values of expanse under the curves (AUC) for the prediction of hyponatremia in children with SLE were 0.749 (95% CI 0.589–0.908, p = 0.026) for high SLEDAI, 0.779 (95% CI 0.613–0.946, p = 0.012) for high ESR levels, 0.775 (95% CI 0.599–0.951, p = 0.013) for high AST levels, 0.758 (95% CI 0.563–0.953, p = 0.021) for decreased serum C3 levels and 0.778 (95% CI 0.650–0.906, p = 0.013) for decreased serum albumin levels.

In addition, serum sodium levels were correlated negatively with ESR (r = −0.399, p = 0.001) and serum AST levels (r = −0.334, p = 0.004), but positively with C3 (r = 0.304, p = 0.008), serum chloride (r = 0.372, p = 0.001), serum calcium (r = 0.549, p < 0.0001) and serum albumin levels (r = 0.479, p < 0.0001) (Tabular array four).

Table four Correlations among cardinal laboratory findings in children with lupus.

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Furthermore, changes in serum sodium levels (Na levels at the follow-up land– Na levels at the initial state, ΔNa) correlated positively with changes in serum C3 (ΔC3) (r = 0.476, p = 0.003), serum C4 (ΔC4) (r = 0.357, p = 0.03), hemoglobin (ΔHb) (r = 0.340, p = 0.039), hematocrit (ΔHct) (r = 0.425, p = 0.009), chloride (Δchloride) (r = 0.466, p = 0.004), calcium (Δcalcium) (r = 0.385, p = 0.019), phosphorus (Δphosphorus) (r = 0.391, p = 0.017) and albumin levels (Δalbumin) (r = 0.481, p = 0.003). However, ΔNa were non correlated with changes in SLEDAI (Δ SLEDAI) (r = −0.191, p = 0.313) (Table five).

Table 5 Correlations amidst changes in laboratory findings in children with lupus.

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A cohort of adolescents and adults with SLE

Laboratory characteristics of the patients with (due north = vii) and without hyponatremia (northward = 77) are shown in Supplementary Table S1. There were no meaning differences in WBC counts, SLEDAI, interleukin (IL)-6, IL-2, the dose of steroids and urine specific gravity between the 2 groups (p > 0.05). CRP levels were higher in SLE patients with hyponatremia than those without with a borderline significance (p = 0.077).

Serum sodium levels were correlated negatively with serum IL-6 levels (r = −0.317, p = 0.003), while those did not correlate to serum IL-two levels (p = 0.389). Serum IL-vi levels were also positively correlated with SLEDAI (r = 0.386, p = 0.032) (Table 6). The significant correlations between serum sodium and IL-6 levels were more than prominent in SLE patients who were not treated with steroids (r = −0.424, p = 0.017) than those who were treated with steroids (r = −0.247, p = 0.075). In SLE patients who were not treated with steroids, serum sodium levels were correlated negatively with urine specific gravity which reflect the result of ADH with a borderline significance (r = −0.326, p = 0.073) (Supplementary Tables S2–S3).

Table 6 Correlations among primal laboratory findings in adults with lupus.

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Two combined cohorts of children and adults with SLE

In univariate analyses, there were no significant differences in WBC counts and SLEDAI between the two groups (p > 0.05) and ESR (p = 0.053) and CRP levels (p = 0.053) were college in SLE patients with hyponatremia (northward = 18) than those without (north = 140) with borderline significances (Supplementary Table S4).

Multiple logistic regression analysis showed that increased CRP level (OR i.480, p = 0.023) was an contained risk factor for the evolution of hyponatremia in combined cohorts of children and adults with SLE (Supplementary Tabular array S5). In addition, serum sodium levels were correlated negatively with CRP (r = −0.368, p < 0.0001) and ESR levels (r = −0.189, p = 0.023) (Supplementary Tabular array S6).

Receiver operating characteristic (ROC) curves

To establish the predictive value of the parameters for predicting hyponatremia in patients with lupus, ROC curves were plotted for SLEDAI, ESR, AST, serum C3 and albumin levels.

AUC values from ROC curve analyses for SLEDAI, ESR, AST, serum C3 and albumin levels were 0.743 (P = 0.029), 0.768 (P = 0.016), 0.770 (P = 0.015), 0.746 (P = 0.027) and 0.777 (P = 0.013), respectively (Supplementary Table S7 and Figure S1).

Discussion

The principal goal of this report was to investigate the significance of hyponatremia in children and adults with SLE and determine whether hyponatremia is associated with disease activity. Our study firstly demonstrated the clan of hyponatremia with the decreased C3 and increased ESR levels and SLEDAI which reflect illness activity of SLE in a cohort of children with SLE and serum sodium levels were correlated negatively with serum IL-six levels in an independent cohort of adults with SLE, which have non been investigated in both adults and children over the past decade.

Hyponatremia can occur in patients with SLE by various causes such every bit renal disease, acute kidney injury, and medication apply, only only very few case reports were found in literatures on hyponatremia in SLE^nine,10. Although the exact mechanism of hyponatremia in SLE flare patients is not established still, we speculate that inflammation can exist i of the mechanisms in the pathogenesis of hyponatremia in SLE patients. In a cohort of children with SLE, we constitute that decreased serum chloride levels were independent risk factors for the development of hyponatremia in children with SLE. Urinary loss of sodium chloride could cause hyponatremia and hypochloremia and it can be caused by renal tubular damage or increased renal sodium loss past a reduction in renal tubular sodium absorption in inflammatory conditions^{11,12,13,14,15,xvi,17,18,19,20}. Withal, we excluded the SLE patients with evident renal failure, because tubular injury tin cause natriuresis and hyponatremia which obscure the relationship betwixt lupus activity and serum sodium levels. Therefore, serum creatinine levels and the caste of proteinuria did not differ in SLE patients with hyponatremia than those without.

Eisenhut pointed out that inflammatory mediators such every bit IL-i and tumor necrosis factor (TNF)-α have been reported to reduce sodium send in epithelial cells past a reduction in the expression and function of the upmost epithelial sodium channel (ENaC) and/or the sodium potassium ATPase (Na/K ATPase) at the basolateral membrane^11,12. Information technology was also demonstrated that IL-1 could induce natriuresis in the rat model¹³. Using cultures of inner medullary, cortical collecting duct and proximal tubular renal cells in vitro, the potential mechanisms were establish to involve a reduction in the Na/Yard ATPase part mediated by prostaglandin E2^{fourteen,15,16,17,18} and past increasing tissue levels of nitric oxide, which is a potent suppressor of the epithelial Na/Thousand ATPase past the intracellular messenger cGMP and through protein kinase G modification^xix,20. An activation of the autoimmune organisation in SLE tin cause CD8 + T-cells and macrophages to produce pro-inflammatory cytokines and chemokines, such equally interleukin (IL)-1, IL-6, IL-8 and TNF-α^21,22,23,24.

Because the degree of proteinuria did non differ in SLE children with hyponatremia than those without and our children with SLE did not accept nephrotic syndrome or severe renal illness, hypoalbuminemia might occur by severe inflammation through a disease activity of SLE. Hypoalbuminemia has been regarded every bit an important cause of observable hypovolemic hyponatremia²⁵. Also, it was thought that decreased serum calcium levels could be caused by hypoalbuminemia in our children's cohort.

Nosotros found that hyponatremia was associated with increased ESR, CRP, and SLEDAI and decreased serum albumin and C3 levels past various statistical methods (univariate, multivariate and correlation analyses) in our cohorts of SLE, suggesting that hyponatremia in SLE is closely related to more severe inflammation. Although not studied nonetheless in SLE, at that place accept been some evidences and our hypothetical background showing that IL-1β or IL-6 might increase antidiuretic hormone (ADH) secretion, leading to hyponatremia^{26,27,28,29,30,31}. Mastorakos et al. reported that plasma ADH levels were increased afterward injection of IL-6 in cancer patients, suggesting that IL-6 activated the magnocellular ADH-secreting neurons, which could be involved in the development of SIADH²⁶. Ohta et al. performed fauna experiments and intravenous administrations of IL-1β increased ADH²⁷. Because IL-six and IL-1β are all important cytokines in the pathogenesis of SLE both in animal models and human being SLE^21,22,23,24, there is a possibility that increased these cytokines could be implicated in the pathogenesis of hyponatremia in the patients with SLE. To validate this hypothesis, we analyzed the relationship between serum sodium and IL-vi levels in an contained cohort of adults with SLE and institute that serum sodium levels were correlated negatively with serum IL-half dozen levels (r = −0.317, p = 0.003), which was more prominent in SLE patients who were non treated with steroids (r = −0.424, p = 0.017). In SLE patients who were not treated with steroids, serum sodium levels were correlated negatively with urine specific gravity which reflect the effect of ADH with a deadline significance (r = −0.326, p = 0.073).

Our written report has some limitations, such equally small-scale sample size due to the rarity of lupus in Korea, retrospective written report pattern. Nevertheless, the current information are noteworthy because we firstly showed that hyponatremia reflected affliction activity of SLE in two independent cohorts of children and adults with SLE. Therefore, clinicians should recognize this electrolyte disturbance in SLE and pediatricians should pay more attention to the risk for exacerbating hyponatremia by administering a hypotonic fluid in children. Further studies are necessary to evaluate the verbal molecular machinery of hyponatremia in SLE and to elucidate whether our findings are also relevant in a large cohort of SLE in the future.

Patients and Methods

A cohort of children and adolescents with SLE

We retrospectively analyzed the information of 37 children (male:female = 4:33) who had been diagnosed with SLE in Severance Children'southward Hospital for 20 years from the years 1991 to 2010. Laboratory examinations were collected two times at the stage of affliction activity and at follow-up after 22.ii ± 28.3 months (range 1–123 months) in all patients. Nosotros divided the patients into two groups: group I (north = 11 samples, hyponatremia) and group II (n = 63 samples, no hyponatremia).

Medical charts were reviewed for clinical characteristics, such as age at onset, gender, and laboratory data, including WBC counts, hemoglobin, hematocrit, platelet counts, ESR, CRP, serum sodium, potassium, chloride, tCO₂, calcium, phosphorus, BUN, creatinine, total poly peptide, albumin, cholesterol, uric acid, AST, ALT, total bilirubin, and urinalysis.

Serum sodium assay was evaluated by using ion selective electrodes measurement by an automated chemical science analyzer (Olympus AU-2700, Beckman coulter, Mishima, Nippon). Complete claret counts including platelet counts were analyzed by the Advia 2120i automated analyzer (Siemens Healthcare Diagnostics, Deerfield, IL, United states of america). CRP levels were measured by the latex-enhanced turbidimetric assay method using a Hitachi 7600 P module (Hitachi, Tokyo, Japan). ESR levels were measured past the Examination i (Alifax, Padova, Veneto, Italian republic). Serum C3 and C4 levels were measured past the automated Roche Diagnostics analyzer (Hitachi Cobas C501, Roche Diagnostics GmbH, Mannheim, Germany). Antinuclear antibodies and anti-ds DNA antibodies were detected by immunofluorescence using Crithidia luciliae (Section of Laboratory Medicine, Severance Hospital, Seoul). Strict quality control procedures were adopted.

A cohort of adolescents and adults with SLE

Among 166 SLE patients who were followed up at Ajou University Hospital and in whom IL-6 levels were measured²³, 84 were included in the written report (age: mean 34.4 ± 12.i years [range 16–69 years], male person : female = 8:76) in whom serum sodium levels were available. Laboratory parameters of disease activity were recorded such every bit WBC counts, ESR, CRP, and urine specific gravity and SLEDAI was likewise calculated. Measurements of IL-2 and IL-half-dozen in serum samples were performed by sandwich enzyme-linked immunosorbent assay (ELISA) using BD OptEIA sets (Pharmingen, San Diego, CA). All serum samples were measured in triplicate and diluted 1:one in assay diluent for OptEIA ELISA sets. Briefly, afterward coating with main anti-human IL-2 and IL-half-dozen antibodies (Pharmingen) and blocking, 100 μg of diluted serum was loaded, and biotinylated secondary anti-human being IL-2 and IL-6 monoclonal antibodies (Pharmingen) were added, respectively. The wells were incubated with streptavidine horseradish peroxidase cohabit, and colorimetric reaction was developed with 3,3′,5,5′-tetramethylbenzidine (TMB) substrate solution and terminated with 2 N H_iiSO_iv. And so, absorbance at 450 nm (reference, 570 nm) was read by an automated microplate reader (Criterion, Bio-RAD, Hercules, CA). The serum cytokine levels were determined by comparing with a standard curve obtained using recombinant human IL-two and IL-vi, respectively²³.

Definitions

The diagnosis of SLE was based on the revised classification criteria of the American College of Rheumatology in 1997 in two cohorts of SLE². The nomenclature is based on eleven criteria and the diagnosis of SLE was made if any 4 or more than of the xi criteria are present, serially or simultaneously, during any interval of observation. The 11 criteria are as follows: malar rash, discoid rash, photosensitivity, oral ulcers, nonerosive arthritis involving two or more than peripheral joints, pleuritis or pericarditis, renal disorder (persistent proteinuria >0.5 grams per day or >than 3+ if quantitation non performed or cellular casts–may be cherry-red cell, hemoglobin, granular, tubular, or mixed), neurologic disorder (seizures or psychosis), hematologic disorder (hemolytic anemia with reticulocytosis or leukopenia <iv,000/mm^three on ≥2 occasions or lymphopenia <1,500/mm³ on ≥2 occasions or thrombocytopenia <100,000/mm³ in the absenteeism of offending drugs), immunologic disorder (anti-ds DNA in abnormal titer or anti-Sm or positive finding of antiphospholipid antibodies) and positive antinuclear antibiotic^two.

Hyponatremia was defined as serum sodium level ≤135 mEq/Fifty. SLE activity was considered serologically as the increased titers of anti-ds Dna antibodies and decreased complement levels, such as C3 < 90 mg/dL and C4 < 10 mg/dL and SLEDAI was also measuredⁱ.

Statistical methods

Statistical analyses were performed, using the SPSS for Windows (SPSS Inc., Chicago, Illinois, U.s.) and MedCalc version 15.8 (MedCalc Software, Ostend, Belgium). The independent t-test and Isle of man-Whitney U test was used for continuous variables and expressed equally mean ± standard deviation. Fisher'due south exact test was used to analyze chiselled variables. Correlation analysis was likewise carried out to determine the relationship between 2 variables by Spearman or Pearson correlation. Nosotros also analyzed whether the changes (Δ: follow-upwards levels- initial levels) of serum sodium correlated with the changes (Δ) of other parameters in a cohort of children with SLE. Multiple logistic regression analysis was used to detect contained predictive factors for hyponatremia in lupus. To establish the predictive value of the parameters for predicting hyponatremia, ROC curves were plotted for laboratory tests. All differences were considered significant at a value of p < 0.05

This study blueprint and the utilise of patients' data stored in the hospital database were approved by the Institutional Review Board and the research ethics committee of Yonsei Severance Hospital and Ajou University Infirmary. We were given exemption from getting informed consents past the ii IRBs because the present report is a retrospective study and personal identifiers were completely removed and the data were analyzed anonymously. Our study was conducted according to the ethical standards laid down in the 1964 Declaration of Helsinki and its afterward amendments.

Additional Data

How to cite this commodity: Shin, J. I. et al. Hyponatremia in patients with systemic lupus erythematosus. Sci. Rep. six, 25566; doi: 10.1038/srep25566 (2016).

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Author notes

1. Jae Il Shin, Se Jin Park and Chang-Hee Suh: These authors contributed equally to this work.

Affiliations

1. Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea

   Jae Il Shin, Geum Hwa Lee, Min Woo Hur, Song Yi Han, Dong Soo Kim & Ji Hong Kim

2. Section of Pediatric Nephrology, Severance Children'due south Hospital, Seoul, Korea

   Jae Il Shin

3. Department of Pediatrics, Ajou University School of Medicine, Daewoo General Infirmary, Geoje, Korea

   Se Jin Park

4. Section of Rheumatology, Ajou Academy School of Medicine, Suwon, Korea

   Chang-Hee Suh

5. Department of Pediatrics, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea

   Ji Hong Kim

Contributions

J.I.Southward., Due south.J.P., C.H.South., Southward.Y.H., G.H.L., M.W.H., D.S.Thousand. and J.H.K. designed report, coordinated data conquering, performed the statistical analysis, interpreted the information, drafted and revised the manuscript. All authors read and approved the final manuscript.

Respective writer

Correspondence to Ji Hong Kim.

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The authors declare no competing financial interests.

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Il Shin, J., Park, Due south., Suh, CH. et al. Hyponatremia in patients with systemic lupus erythematosus. Sci Rep 6, 25566 (2016). https://doi.org/ten.1038/srep25566

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• Received: 12 October 2015

• Accepted: xix April 2022

• Published: 19 May 2022

• DOI : https://doi.org/ten.1038/srep25566

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