I’d suggest that the simplest, cheapest approach would be to a simple urinalysis that warns of “proteinuria” because sepsis activates the complement cascade, which generates thrombin that disintegrates fibrinogen into the alpha, beta, and gamma fragments of “soluble fibrin” that pass from blood into urine and are detected as “proteinuria.”

The second thing to watch for is hyaline casts in the urinalysis. These form when excessive soluble fibrin is present in the glomeruli

The third test would be thromboelastography (TEG) which detects hypercoagulability in blood. Sepsis exaggerates the generation of insoluble fibrin in blood, which causes hypercoagulability.

for sepsis per definition : a life-threatening organ dysfunction caused by a dysregulated host response to infection. So it's important to look for signs of end organ damage on laboratory studies you do. example rising levels of pro calcitonin ( PCT) is a Good sensitivity for bacterial sepsis. Rising lactate from an ABG also Reflects tissue hypoperfusion and anaerobic metabolism.CRP is sensitive but less specific; best used in combination with clinical scoring systems (SOFA, qSOFA). A septic screen with blood and urine cultures also help.