Kinin system in lupus nephritis

Dellalibera-Joviliano, Renata; Reis, Marina Lemos dos; Donadi, Eduardo Antônio

doi:10.1016/s1567-5769(01)00109-6

Cited by 17 publications

(17 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In line with the role of kallikreins as proinflammatory mediators, higher plasma levels of high-MW kininogen, low-MW kininogen, and kallikrein were found in 30 patients with active lupus nephritis compared with age- and sex-matched controls (14). In addition, plasma and urinary activities of tissue kallikrein and kininase II were also significantly increased in these patients.…”

Section: Kallikreins Sle and Lupus Nephritissupporting

confidence: 57%

Kallikreins and lupus nephritis

Ponticelli

Meroni

2009

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Kallikreins Sle and Lupus Nephritissupporting

confidence: 57%

Kallikreins and lupus nephritis

Ponticelli

Meroni

2009

J. Clin. Invest.

View full text Add to dashboard Cite

“…There were modest increases in the ratios of a number of proteins in the FH –/– mice that have been associated with tubular dysfunction; these included α 1 -microglobulin, high molecular weight (HMW) kininogenin-II, tissue kallikrenin 6 (mGK-6), and tissue amylase [23,24,25,26]. The presence of increased level of these proteins, albeit at low levels, is strongly suggestive of early tubular damage in the FH –/– mice.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling of Urinary Protein Excretion in the Factor H-Deficient Mouse

Braun

et al. 2006

Am J Nephrol

View full text Add to dashboard Cite

Background: Since the 1970s a variety of experimental techniques have been employed in an attempt to identify urinary biomarkers of renal injury. While these approaches have met with some success, modern proteomic tools now permit broad based high-throughput analysis of the urinary proteome. Methods: Using the ICAT isotopic labeling based LC/MS/MS approach, comparative urinary protein profiling was performed in a murine model of membranoproliferative glomerulonephritis. Paired samples were analyzed mice with a targeted deletion of the complement regulatory protein factor H (FH^–/–) and control mice. Results: 25 distinct urinary proteins were identified of which 7 were differentially expressed in the FH^–/– mice. Two proteins were markedly altered in the urine of FH^–/– mice compared to controls: uromodulin (5.5-fold lower) and the MHC class II molecule H2^e (8.6-fold higher). Differential expression was confirmed by Western blot and RT-PCR. Immunofluorescent staining demonstrated a marked increased expression of H2^e and a reduction of uromodulin expression in the tubular epithelium of FH^–/– mice. Conclusions: These findings provide insight into early complement-dependent alterations in tubular protein expression which may play critical roles in the development of tubulointerstitial disease, and provide experimental support for the use of urinary proteomic profiling in murine models of renal injury.

show abstract

“…Lupus nephritis, inflammation of the kidney, occurs when antibodies and complement components build up in the kidneys and cause inflammation. It often causes nephrotic syndrome (excessive protein excretion) and may progress to renal failure, whereby nitrogen waste products build up in the bloodstream[134]. Recent investigations have shown that patients with systemic lupus erthematosus, presented with increased plasma concentrations of kinin precursors and an increase in plasma kallikrein activity.…”

Section: Role Of the Plasma Kks In Cardiovascular Abnormalitiesmentioning

confidence: 99%

Human Plasma Kallikrein-Kinin System: Physiological and Biochemical Parameters

Bryant

Shariat‐Madar²

2009

CHAMC

118

View full text Add to dashboard Cite

The plasma kallikrein-kinin system (KKS) plays a critical role in human physiology. The KKS encompasses coagulation factor XII (FXII), the complex of prekallikrein (PK) and high molecular weight kininogen (HK). The conversion of plasma to kallikrein by the activated FXII and in response to numerous different stimuli leads to the generation of bradykinin (BK) and activated HK (HKa, an antiangiogenic peptide). BK is a proinflammatory peptide, a pain mediator and potent vasodilator, leading to robust accumulation of fluid in the interstitium. Systemic production of BK, HKa with the interplay between BK bound-BK receptors and the soluble form of HKa are key to angiogenesis and hemodynamics. KKS has been implicated in the pathogenesis of inflammation, hypertension, endotoxemia, and coagulopathy. In all these cases increased BK levels is the hallmark. In some cases, the persistent production of BK due to the deficiency of the blood protein C1-inhibitor, which controls FXII, is detrimental to the survival of the patients with hereditary angioedema (HAE). In others, the inability of angiotensin converting enzyme (ACE) to degrade BK leads to elevated BK levels and edema in patients on ACE inhibitors. Thus, the mechanisms that interfere with BK liberation or degradation would lead to blood pressure dysfunction. In contrast, anti-kallikrein treatment could have adverse effects in hemodynamic changes induced by vasoconstrictor agents. Genetic models of kallikrein deficiency are needed to evaluate the quantitative role of kallikrein and to validate whether strategies designed to activate or inhibit kallikrein may be important for regulating whole-body BK sensitivity.

show abstract

Kinin system in lupus nephritis

Cited by 17 publications

References 16 publications

Kallikreins and lupus nephritis

Kallikreins and lupus nephritis

Proteomic Profiling of Urinary Protein Excretion in the Factor H-Deficient Mouse

Human Plasma Kallikrein-Kinin System: Physiological and Biochemical Parameters

Contact Info

Product

Resources

About