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it has long been known that proteinuria appears shortly after severe burns , and is detectable for several weeks until patients become critically ill .
proteinuria quantitatively varies from 0.5 to 3 to 4 g / day . from a nephrological point of view
, however , proteinuria accompanying severe burns is still an intriguing factor due to its entity and duration .
we still have no exhaustive understanding of its clinical significance and role , mainly because of a lack of data on its pathogenesis .
studies using sds polyacrylamide gel electrophoresis performed in the early 1980s demonstrated that the initial pattern of proteinuria is of mixed type , indicating a lesion of both glomerulus and tubule
. then , after a week , the protein excretion pattern gradually changes to typical tubular proteinuria , and persists like this for several weeks .
usually its duration and amount reflect the severity of burns : more severe burns lead to more proteinuria and worse patient outcome .
in the past 10 years many reports have focused on the relationship between severe burns , acute kidney injury ( aki ; staged using rifle or aki classification ) and proteinuria .
these studies demonstrated a high incidence of aki in burn patients , an association of aki with dysfunction of other organs , a pathogenetic role of sepsis in aki and , in particular , a direct correlation between aki and mortality .
the study of hu and coworkers   in the previous issue of critical care provides additional evidence on the clinical relevance of proteinuria on the outcome of burn patients .
it explores in a large cohort of 369 severe burn patients ( total burned surface area > 30% ) the determinants of proteinuria , and its influence on aki staged according to the rifle classification and on clinical outcome .
proteinuria , evaluated as positive urine dipstick readings , was absent in 31.5% of patients , mild ( 5 to 20 mg / dl ) in 45.5% and heavy ( > 100 mg / dl ) in 23% .
patients with proteinuria were older , with a higher incidence of inhalation injury , more severe burns and more incidence of sepsis ( 67% ) than in patients with mild ( 46% ) or absent ( 15% ) proteinuria .
in addition , proteinuric patients were more prone to develop aki ( incidence of 55% ) .
in contrast , none of the patients without proteinuria developed aki , suggesting that the persistent absence of proteinuria excludes the development of aki .
the mortality rate of patients with aki was 29% , significantly higher than that observed in patients without aki ( 12.50% ) .
finally , patients with proteinuria had significantly longer mechanical ventilation durations , longer icu stays , and higher mortality rates ( 30.8% ) than patients with mild ( 16.7% ) or absent ( 0.8% ) proteinuria .
proteinuria in thermally injured patients is considered the mirror of increased systemic capillary permeability . however , proteinuria ( or preferably proteinuria / creatininuria ratio to correct for variation of urinary flow rate ) is possibly a direct marker of renal injury .
in fact , it has been demonstrated that proteinuria negatively correlates with both decreased creatinine and urea clearance as an index of loss of glomerular function and positively correlates with both na+ and k+ fraction excretion reflecting loss of tubular function .
a plethora of inflammatory mediators ( cytokines , polypeptides , lipid mediators ) targeting endothelial cells have been implicated in glomerular and peritubular capillary dysfunction .
indeed , the plasma of burn patients contains pro - apoptotic factors at levels reflecting the presence of sepsis and aki .
these circulating pro - apoptotic factors reduce the viability and function of tubular cells and podocytes by a mechanism dependent on up - regulation of pro - inflammatory and pro - apoptotic genes and down - regulation of apoptosis inhibitors . moreover , they alter permeability by disrupting tight junctions and the polarity of tubular cells and by inducing nephrin loss in podocytes . therefore , proteinuria reflects a direct negative influence of plasma factors on renal parenchymal cells and requires further studies on new extracorporeal therapeutic approaches in burn patients [ 9 - 11 ] . in conclusion
, the study of hu and colleagues reminds us that proteinuria in burn patients should receive due consideration .
hu and coworkers in the previous issue of critical care provide evidence for the clinical relevance of proteinuria in the outcome of burn patients . 
 proteinuria is a common finding after severe burns , appears within a short period and is detectable for several weeks . 
 proteinuria ranging from 0.5 to 3 to 4 g / day is initially of mixed type , then , after a week , gradually changes to tubular proteinuria . 
 the clinical role of proteinuria is still unclear , mainly due to a lack of data on its pathogenesis . 
 recent studies have demonstrated an association between proteinuria and incidence of inhalation injury , sepsis , acute kidney injury and mortality rate . 
 proteinuria is considered the mirror of increased systemic capillary permeability , and possibly a direct marker of glomerular and tubular injury . 
 circulating plasma inflammatory mediators and pro - apoptotic factors reflecting burn injury , sepsis and acute kidney injury can affect the viability and function of tubular cells and podocytes . 
 these studies highlight that proteinuria in burn patients should receive due consideration .