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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Nephrol
2015 ; 28
(3
): 315-20
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Increased urine semaphorin-3A is associated with renal damage in hypertensive
patients with chronic kidney disease: a nested case-control study
#MMPMID24756974
Viazzi F
; Ramesh G
; Jayakumar C
; Leoncini G
; Garneri D
; Pontremoli R
J Nephrol
2015[Jun]; 28
(3
): 315-20
PMID24756974
show ga
BACKGROUND: Semaphorins are guidance proteins implicated in several processes
such as angiogenesis, organogenesis, cell migration, and cytokine release.
Experimental studies showed that semaphorin-3a (SEMA3A) administration induces
transient massive proteinuria, podocyte foot process effacement and endothelial
cell damage in healthy animals. While SEMA3A signaling has been demonstrated to
be mechanistically involved in experimental diabetic glomerulopathy and in acute
kidney injury, to date its role in human chronic kidney disease (CKD) has not
been investigated. METHODS: To test the hypothesis that SEMA3A may play a role in
human CKD, we performed a cross-sectional, nested, case-control study on 151
matched hypertensive patients with and without CKD. SEMA3A was quantified in the
urine (USEMA) by ELISA. Glomerular filtration rate was estimated (eGFR) by the
CKD-EPI formula and albuminuria was measured as albumin-to-creatinine ratio
(ACR). RESULTS: USEMA levels were positively correlated with urine ACR (p =
0.001) and serum creatinine (p < 0.001). USEMA was higher in patients with both
components of renal damage as compared to those with only one and those with
normal renal function (p < 0.007 and <0.001, respectively). The presence of
increased USEMA levels (i.e. top quartile) entailed a fourfold higher risk of
combined renal damage (p < 0.001) and an almost twofold higher risk of
macroalbuminuria (p = 0.005) or of reduced eGFR, even adjusting for confounding
factors (p = 0.002). CONCLUSIONS: USEMA is independently associated with CKD in
both diabetic and non diabetic hypertensive patients. Further studies may help
clarify the mechanisms underlying this association and possibly the pathogenic
changes leading to the development of CKD.