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Macrophage migration inhibitory factor urinary excretion revisited – MIF a potent predictor of the immunosuppressive treatment outcomes in patients with proliferative primary glomerulonephritis.

Zwiech R - BMC Immunol. (2015)

Bottom Line: The highest pre-treatment urinary excretion of MIF was observed in NR-PGN (median 6.1), which was significantly higher than other subgroups (ANOVA P < 0.05).The treatment significantly reduced MIF urinary excretion only in R-PGN (P < 0.01).In Non-Responders, urinary MIF measurements may help to reconsider the choice of the immunosuppressive regimen at early stages of the treatment and act as an impulse to search for new therapeutic strategies.

View Article: PubMed Central - PubMed

Affiliation: Dialysis Department, Barlicki Memorial Teaching Hospital No1, Medical University of Łódź, Kopcińskiego 22, 90-153, Łódź, Poland. rzwiech@mp.pl.

ABSTRACT

Background: Macrophage migration inhibitory factor (MIF) is a cytokine that shares many activities with other pro-inflammatory cytokines in primary glomerulonephritis (GN). This study assesses the influence of immunosuppressive treatment on serum and urine MIF in patients with proliferative (PGN) and non-proliferative (NPGN) glomerulonephritis, and evaluates the potential of MIF in predicting outcomes.

Methods: Eighty-four patients (45 males and 39 females) with primary GN were included. Urinary excretion of MIF (ng/mg of urinary creatinine) was measured both pre- and post-treatment with combined steroids and cyclophosphamide. After a 12-month follow-up, the patients were retrospectively divided into four subgroups: responders of proliferative GN (R-PGN), non-responders of proliferative GN (NR-PGN), responders of non-proliferative GN (R-NPGN) and non-responders of non-proliferative GN (NR-NPGN).

Results: The median pre-treatment urinary MIF values were higher in PGN than in NPGN (3.6 versus 2.2; ANOVA P = 0.039). The highest pre-treatment urinary excretion of MIF was observed in NR-PGN (median 6.1), which was significantly higher than other subgroups (ANOVA P < 0.05). The treatment significantly reduced MIF urinary excretion only in R-PGN (P < 0.01). In NR-PGN, pre- (5.9 ± 2.9 pg/mgCr) and post-treatment mean MIF excretion (4.9 ± 2.3 pg/mgCr) exceeded the calculated cut off value (3.3 pg/mgCr).

Conclusion: MIF urinary excretion appears to be a prognostic marker of therapy outcomes only in proliferative glomerulonephritis, in which lower urinary MIF may be linked with good prognosis, whereas a higher MIF urinary excretion value was a marker of unfavorable therapy outcomes. In Non-Responders, urinary MIF measurements may help to reconsider the choice of the immunosuppressive regimen at early stages of the treatment and act as an impulse to search for new therapeutic strategies.

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Pre-treatment and post-treatment mean urinary excretion of MIF in proliferative and non-proliferative glomerulonephritis (GN) divided into Responder (R) and Non-Responder (NR) subgroups
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Fig1: Pre-treatment and post-treatment mean urinary excretion of MIF in proliferative and non-proliferative glomerulonephritis (GN) divided into Responder (R) and Non-Responder (NR) subgroups

Mentions: Urinary MIF was higher in PGN than in NPGN (P = 0.039). The treatment reduced urinary MIF in both primary glomerulonephritis types, irrespective of the response to treatment (R and NR subgroups), but MIF urinary excretion was only found to be significantly lower in Responders with PGN (P = 0.007) – Fig. 1. All results are presented in Table 3. The pre-treatment MIF urinary excretion value in PGN positively correlated with interstitium volume, glomerulosclerosis grade and serum creatinine concentration: ρ = 0.28, P = 0.03; ρ = 0.3, P = 0.037; ρ = 0.34, P = 0.026; respectively.Fig. 1


Macrophage migration inhibitory factor urinary excretion revisited – MIF a potent predictor of the immunosuppressive treatment outcomes in patients with proliferative primary glomerulonephritis.

Zwiech R - BMC Immunol. (2015)

Pre-treatment and post-treatment mean urinary excretion of MIF in proliferative and non-proliferative glomerulonephritis (GN) divided into Responder (R) and Non-Responder (NR) subgroups
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4536780&req=5

Fig1: Pre-treatment and post-treatment mean urinary excretion of MIF in proliferative and non-proliferative glomerulonephritis (GN) divided into Responder (R) and Non-Responder (NR) subgroups
Mentions: Urinary MIF was higher in PGN than in NPGN (P = 0.039). The treatment reduced urinary MIF in both primary glomerulonephritis types, irrespective of the response to treatment (R and NR subgroups), but MIF urinary excretion was only found to be significantly lower in Responders with PGN (P = 0.007) – Fig. 1. All results are presented in Table 3. The pre-treatment MIF urinary excretion value in PGN positively correlated with interstitium volume, glomerulosclerosis grade and serum creatinine concentration: ρ = 0.28, P = 0.03; ρ = 0.3, P = 0.037; ρ = 0.34, P = 0.026; respectively.Fig. 1

Bottom Line: The highest pre-treatment urinary excretion of MIF was observed in NR-PGN (median 6.1), which was significantly higher than other subgroups (ANOVA P < 0.05).The treatment significantly reduced MIF urinary excretion only in R-PGN (P < 0.01).In Non-Responders, urinary MIF measurements may help to reconsider the choice of the immunosuppressive regimen at early stages of the treatment and act as an impulse to search for new therapeutic strategies.

View Article: PubMed Central - PubMed

Affiliation: Dialysis Department, Barlicki Memorial Teaching Hospital No1, Medical University of Łódź, Kopcińskiego 22, 90-153, Łódź, Poland. rzwiech@mp.pl.

ABSTRACT

Background: Macrophage migration inhibitory factor (MIF) is a cytokine that shares many activities with other pro-inflammatory cytokines in primary glomerulonephritis (GN). This study assesses the influence of immunosuppressive treatment on serum and urine MIF in patients with proliferative (PGN) and non-proliferative (NPGN) glomerulonephritis, and evaluates the potential of MIF in predicting outcomes.

Methods: Eighty-four patients (45 males and 39 females) with primary GN were included. Urinary excretion of MIF (ng/mg of urinary creatinine) was measured both pre- and post-treatment with combined steroids and cyclophosphamide. After a 12-month follow-up, the patients were retrospectively divided into four subgroups: responders of proliferative GN (R-PGN), non-responders of proliferative GN (NR-PGN), responders of non-proliferative GN (R-NPGN) and non-responders of non-proliferative GN (NR-NPGN).

Results: The median pre-treatment urinary MIF values were higher in PGN than in NPGN (3.6 versus 2.2; ANOVA P = 0.039). The highest pre-treatment urinary excretion of MIF was observed in NR-PGN (median 6.1), which was significantly higher than other subgroups (ANOVA P < 0.05). The treatment significantly reduced MIF urinary excretion only in R-PGN (P < 0.01). In NR-PGN, pre- (5.9 ± 2.9 pg/mgCr) and post-treatment mean MIF excretion (4.9 ± 2.3 pg/mgCr) exceeded the calculated cut off value (3.3 pg/mgCr).

Conclusion: MIF urinary excretion appears to be a prognostic marker of therapy outcomes only in proliferative glomerulonephritis, in which lower urinary MIF may be linked with good prognosis, whereas a higher MIF urinary excretion value was a marker of unfavorable therapy outcomes. In Non-Responders, urinary MIF measurements may help to reconsider the choice of the immunosuppressive regimen at early stages of the treatment and act as an impulse to search for new therapeutic strategies.

Show MeSH
Related in: MedlinePlus