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The JAK/STAT signaling pathway is an intracellular signal transduction pathway, that is universally expressed and involved in diverse biological processes, including cell proliferation, differentiation, apoptosis and regulation of the immune system. Recent studies have explored abnormal receptor tyrosine kinase activation in the pathogenesis of IgA Nephropathy(IgAN).
A retrospective study was performed between 2002 and 2016 in 63 patients with biopsy-proved IgAN. Clinical and laboratory data were collected at baseline and at the end of follow up. Kidney tissue sections were stained with antibodies specific for components of JAK-STAT pathway.
As controls 6 renal tumor border tissues were used.
Clinical features are summarized in Table 1. Mean follow-up time in the study population was 102 months. More than half of patients achieved remission and 31.1% achieved the primary outcome primary outcome that was defined as end-stage renal disease (ESRD) or doubling of baseline creatinine. Staining for JAK3 was observed observed in the renal tubule and glomeruli. Staining for JAK3 was enhanced in patients with IgAN compared to controls.
Table 1 - Clinical and laboratory data at the time of biopsy and at the end of follow-up
n
63
Age (years)
33.00 [24.50-46.00]
Woman (n/%)
35 (55.6)
Not White (n/%)
17 (27.0)
Creatinine mg/dL
1.39 [0.94-2.21]
eGFR CKD-EPI (ml/min/1,73 m2)
58.00 [31.00-95.00]
Hematuria (n/%)
54(85.7)
Follow up (months)
102.00[34.00-144.50]
Remission n(%)
31(54.4)
Creatinine duplication or ESRD(%)
19(31.1)
Figure 1 - Comparison of JAK3 cell density in patients with IgAN and controls
The presence of activation of the JAK/STAT signaling pathway has been demonstrated in patients with IgAN. This pathway may represent a therapeutic target in this pathology.