Altered IgG4 renal clearance in patients with inflammatory bowel diseases. Evidence for a subclinical impairment of protein charge renal selectivity

Monteleone, Giovanni; Cristina, G.; Parrello, Tiziana; Biancone, Livia; Pietravalle, P.; Sagratella, Elisabetta; Doldo, Patrizia; Luzza, Francesco; Mario, U. Di; Pallone, Francesco

doi:10.1093/ndt/15.4.498

Cited by 12 publications

(9 citation statements)

References 16 publications

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“…In this study, expression of NHE isoforms was examined in the renal cortex in colitic animals. The present findings demonstrate a selective induction of NHE-3 in the renal cortex of colitic animals, supporting earlier reports showing involvement of kidneys under IBD conditions [17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27]. However, lack of significant difference in the yield of renal crude microsomal proteins suggests that the induction of NHE-3 is not due to any overt change such as hyperplasia or hypertrophy.…”

Section: Discussionsupporting

confidence: 90%

“…Kidneys play an important role in maintaining the electrolyte and water homeostasis by having several ion-transporting systems [12, 13, 14, 15, 16], including NHE, however the role of renal cortical NHE remains to be established in colitis. In this context, changes in the renal structure and functions reported in inflammatory bowel disease (IBD) condition in humans are important [17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27]. For example, necrosis, tubular damage, changes in the renal permeability, IgA nephropathy or increased chances of renal stone formation are some well-documented extraintestinal manifestations reported in IBD patients [17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27].…”

Section: Introductionmentioning

confidence: 99%

“…In this context, changes in the renal structure and functions reported in inflammatory bowel disease (IBD) condition in humans are important [17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27]. For example, necrosis, tubular damage, changes in the renal permeability, IgA nephropathy or increased chances of renal stone formation are some well-documented extraintestinal manifestations reported in IBD patients [17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27]. Therefore, we raised a hypothesis that kidney being a major organ for the electrolyte and water balance should be associated with alterations in the expression of NHE isoforms.…”

Section: Introductionmentioning

confidence: 99%

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Antisense Inhibition of Cyclooxygenase-2 Causes a Selective Suppression of the Na+-H+ Exchanger Isoform 3 in Rat Kidney in Experimental Colitis

Khan¹

2002

Nephron

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Background: Experimental colitis induces the expression of Na⁺-H⁺ exchanger (NHE) isoforms 1 and 3 in the rat colon, however, their status in rat kidney is not established. Objectives: The renal cortical NHE-1 and -3 expression was examined in the colitic rats. Since cyclooxygenase-2 (cox-2) plays an important role in inflammation, its regulatory role on these isoforms was also investigated by using a cox-2-selective phosphorothioated antisense oligonucleotide (S-oligo). Methods: Male Sprague-Dawley rats having colitis induced by acetic acid or trinitrobenzenesulfonic acid (TNBS) were given injection of S-oligo (3 mg/kg, i.p.) and a mismatched control oligonucleotide (C-oligo) daily 2 h before inducing colitis. Colonic myeloperoxidase activity (MPO) was used to indicate colitis. The renal cortical levels of NHE-1, NHE-3 and α-actin, an internal control, were estimated by the Western blot analysis. Results: Colonic MPO activity was increased and urine output was decreased in both models of colitis. Serum, but not the renal cortical level of TNF-α, was increased in both cases. Only TNBS condition showed an increased PGE₂ level and a decreased body weight. Water intake and renal histology remained unchanged in either case. The NHE-3 protein, localized on the proximal tubules, was increased significantly without any change in NHE-1 and α-actin in both cases. These changes, except the body weight, were significantly reversed by the S-oligo. Conclusions: Selective induction of NHE-3 and TNF-α, and their reversal by cox-2 inhibition, suggest a cox-2-dependent regulation of NHE-3, which possibly involves TNF-α released from the site of inflammation and not from the kidney in colitis. The induction of NHE-3 is independent of the nature of colitides, and might be important to compensate for the loss of electrolyte and water in experimental colitis.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antisense Inhibition of Cyclooxygenase-2 Causes a Selective Suppression of the Na+-H+ Exchanger Isoform 3 in Rat Kidney in Experimental Colitis

Khan¹

2002

Nephron

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“…It has also been observed that glycation of protein increases its acidic nature [42]. At acidic pH, binding of protein to FcRn receptors is higher when compared to physiological pH [43].…”

Section: Discussionmentioning

confidence: 99%

Association Between Urinary IgG and Relative Risk for Factors Affecting Proteinuria in Type 2 Diabetic Patients

2012

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“…On the other hand, some authors have been unable to establish a correlation between several urinary markers of renal damage and 5-ASA treatment. 40,84 Furthermore, Riley et al 9 found that the incidence of elevated urinary markers (such as ␤-N-acetyl-D-glucosamidase) is low in patients with quiescent UC, which is independent of the dose and duration of 5-ASA treatment.…”

Section: Renal Markers Of Nephrotoxicitymentioning

confidence: 99%

5-Aminosalicylates and renal function in inflammatory bowel disease

Gisbert

González-Lama

Maté

2007

Inflammatory Bowel Diseases

201

144

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Nephrotoxicity has been described in some patients with inflammatory bowel disease (IBD) treated with 5-aminosalicylic acid (5-ASA). Studies with 5-ASA treatment in which serum creatinine or creatinine clearance was measured regularly show that nephrotoxicity is exceptional (mean rate of only 0.26% per patient-year). There have been several case reports, including 46 patients, of renal disease associated with 5-ASA treatment in patients with IBD. 5-ASA treatment-related nephrotoxicity is reported most often within the first 12 months, but also delayed presentation after several years has been shown. The absence of a clear relationship between 5-ASA dose and the risk of nephrotoxicity suggests that this complication is idiosyncratic rather than dose-related. Most of the patients with renal disease associated with 5-ASA treatment suffered interstitial nephritis, with symptoms and signs being nonspecific, which may delay detection for many months. The nephrotoxicity potential of mesalazine and sulfasalazine seems to be similar. The risk with different oral preparations of 5-ASA is probably too small to influence the choice of agent. Mesalazine should be withdrawn when renal impairment manifests in a patient with IBD; if this does not result in a fall in serum creatinine, then renal biopsy should be considered. A trial of high-dose steroid may be recommended in patients whose renal function does not respond to drug withdrawal. The optimal monitoring schedule of serum creatinine in patients receiving 5-ASA treatment remains to be established, as there is no evidence to date that either the test, or the frequency of testing, improves patient outcomes.

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Altered IgG4 renal clearance in patients with inflammatory bowel diseases. Evidence for a subclinical impairment of protein charge renal selectivity

Abstract: Renal protein charge permselectivity is impaired in 40% of patients with IBD with no overt proteinuria. Our data suggest that altered IgG(4) clearance may represent a subclinical marker of renal involvement in IBD.

Cited by 12 publications

References 16 publications

Antisense Inhibition of Cyclooxygenase-2 Causes a Selective Suppression of the Na<sup>+</sup>-H<sup>+</sup> Exchanger Isoform 3 in Rat Kidney in Experimental Colitis

Antisense Inhibition of Cyclooxygenase-2 Causes a Selective Suppression of the Na<sup>+</sup>-H<sup>+</sup> Exchanger Isoform 3 in Rat Kidney in Experimental Colitis

Association Between Urinary IgG and Relative Risk for Factors Affecting Proteinuria in Type 2 Diabetic Patients

5-Aminosalicylates and renal function in inflammatory bowel disease

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