The cohort included 192 men, or 60.2 percent of participants, with a mean age of 51.8 years and a mean body mass index of 22.7 kg/m². Follow-up extended from the start of dialysis until death or administrative censoring on December 31, 2021. The SCI index itself is arithmetically simple: platelet count in thousands per liter multiplied by fibrinogen in grams per liter, divided by the white blood cell count in thousands per liter.

Each component carries distinct biological information. Platelets and fibrinogen sit at the heart of the coagulation cascade and the acute-phase inflammatory response, while white blood cells signal systemic inflammation. By combining them into a single ratio, the index attempts to capture the balance between thrombo-inflammatory activation and hematologic reserve in a single number that any dialysis unit could compute from an ordinary complete blood count and coagulation panel.

During follow-up, 115 of the 319 patients died, including 87 from cardiovascular causes and 28 from other causes. The researchers stratified patients into three SCI categories using outcome-specific cutoffs originally derived with X-tile software: below 47.8, 47.8 to below 118.7, and 118.7 or above for all-cause mortality, and slightly different thresholds for cardiovascular mortality. Kaplan-Meier curves showed clear separation in survival across the three groups, with a log-rank statistic of 41.612 and a P value below 0.001.

Cardiovascular cumulative incidence, analyzed with non-cardiovascular death treated as a competing event, also differed markedly, with Gray's test yielding a chi-squared value of 36.387. The magnitude of the associations was striking. In the primary model, which adjusted for age, sex, body mass index, hypertension, diabetes, and prior cardiovascular disease, patients in the lowest SCI category had a hazard ratio of 9.32 for all-cause mortality compared with the highest category (95 percent confidence interval, 4.55 to 19.08).

For cardiovascular mortality, the corresponding hazard ratio was 7.03 (95 percent confidence interval, 3.83 to 12.92). In the fully expanded model that additionally adjusted for hemoglobin, albumin, globulin, cholesterol, triglycerides, uric acid, parathyroid hormone, calcium, phosphorus, potassium, dialysis dose, and residual kidney function, the all-cause hazard ratio for low versus high SCI rose to 13.71, and the cardiovascular cause-specific hazard ratio reached 7.88, with closely matching subdistribution hazard ratios from Fine-Gray models. By 60 months of follow-up, the estimated cumulative incidence of cardiovascular death was 68.8 percent in the low SCI group, 33.3 percent in the middle group, and 20.1 percent in the high group.

The gradient ran in an unexpected direction: unlike in acute aortic dissection surgery, where low SCI has also been linked to poorer short-term survival, the authors note that in chronic kidney disease a low score may reflect inflammatory leukocyte elevation, impaired coagulation reserve, platelet abnormalities, or the malnutrition-inflammation syndrome rather than the platelet consumption and fibrinogen depletion seen in acute vascular catastrophe. The study did not directly test any of these mechanistic interpretations. Correlation analyses added context to the baseline picture.

The SCI index correlated positively with serum globulin (r = 0.288) and estimated glomerular filtration rate (r = 0.198), and negatively with creatinine (r = −0.226), all statistically significant. Patients in the low SCI group were younger, less likely to have hypertension or diabetes, had higher diastolic blood pressure and creatinine, and lower globulin and eGFR than those in higher categories. Subgroup analyses suggested the association between low SCI and mortality was most pronounced in patients older than 55 years and in those with hypertension, with statistically significant interaction tests, though the authors caution that these subgroup findings were sensitive to data-cleaning choices and rested on very small patient numbers.

How well did the index actually discriminate? Modestly, by its own authors' account. The area under the receiver operating characteristic curve was 0.681 for all-cause mortality and 0.688 for cardiovascular mortality.

For cardiovascular mortality, SCI beat white blood cell count and the systemic immune-inflammation index but did not demonstrate superiority over every comparator. The authors are explicit that these results do not establish SCI as a validated clinical prediction tool. Several limitations temper the findings.

The retrospective design, the absence of center identifiers in the analytic dataset, and the single baseline SCI measurement taken within three months of dialysis initiation all leave room for residual confounding and misclassification, since the index can fluctuate with infection, nutritional status, liver function, and medications. Extreme laboratory values were flagged and set to missing under a uniform statistical rule, which altered the analysis population and covariate distributions, and sensitivity analyses before and after this cleaning were compared. Ordinary ROC analyses did not adjust for censoring, the proportional hazards assumption showed departures in the fully adjusted model, and some subgroup strata contained no deaths in the reference category.

The authors conclude that lower SCI was independently associated with higher all-cause and cardiovascular mortality in this peritoneal dialysis cohort and may eventually serve as an adjunct to existing risk assessment, complementing evaluation of volume status and residual kidney function. But they draw a firm line between association and action: the data-derived cutoffs require independent external validation, the study did not test whether interventions that alter SCI improve survival, and the findings do not justify attempting to raise a patient's SCI or selecting antithrombotic treatment on this basis. Prospective studies of repeated measurements, incremental predictive value beyond established clinical variables, and trials of SCI-guided management remain the necessary next steps before this simple blood formula earns a place in dialysis care.

Subject of Research: Association between the systemic coagulation inflammation index and mortality in peritoneal dialysis patients

Article Title: Systemic coagulation inflammation index and risk of mortality in peritoneal dialysis patients: a multicenter cohort study

Article References: Zhang, T., Hua, X., Sun, D., Xie, X., Hu, H., & Xia, W. (2026). Systemic coagulation inflammation index and risk of mortality in peritoneal dialysis patients: a multicenter cohort study. Frontiers in Medicine, 13, Article 2005361. https://doi.org/10.3389/fmed.2026.2005361

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.2005361

Keywords: peritoneal dialysis, systemic coagulation inflammation index, end-stage renal disease, cardiovascular mortality, all-cause mortality, fibrinogen, platelet count, white blood cell count, biomarker, risk stratification, cohort study, nephrology