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RAGE aktivuj tvorbu NF kappaB a aktivuje se intracelulrn oxidan stress a potlauj se nkter endogenn autoregulan funkce

doi: 10.3748/wjg.v25.i36.5543 106 WeirTLManterDKSheflinAMBarnettBAHeubergerALRyanEP

It has been reported that haemoglobinuria is an independent risk factor for the onset and progression of CKD in people suffering with SCA.11 Something similar occurs in paroxysmal nocturnal haemoglobinuria, a disease in which CKD secondary to the onset of renal vein thrombosis and haemoglobinuria is one of its most significant complications, which may affect 64% of patients and cause 18% of deaths.12 In the absence of treatment, the prognosis for atypical HUS (aHUS) is also poor, with a mortality rate during outbreak of 25%, and progression to CKD in over half of the patients the year after the diagnosis.13 Pathophysiological mechanisms involved in haemoproteins induced renal damage The main effect of haemoproteins on the kidneys is their direct tubule cell toxicity, regardless of what causes their release (haemo- or myoglobinuria) (Fig

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Quantification was performed using Salmon (v1.10.2) at the transcript level

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