Keyword: Disseminated Intravascular Coagulation
2 results found.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A26, https://doi.org/10.63946/cajn/19515
ABSTRACT:
Background: Treatment of rheumatoid arthritis (RA) in patients with end-stage chronic kidney disease (CKD stage 5D) on maintenance hemodialysis is challenging because of limited therapeutic options and increased drug toxicity. Stevens–Johnson syndrome (SJS) is a rare, life-threatening drug reaction that may cause severe systemic complications. This case is noteworthy for severe SJS complicated by sepsis and progressive coagulation abnormalities in a patient with seropositive RA, secondary renal amyloidosis, and CKD stage 5D.
Case Presentation: A 61-year-old woman with seropositive RA (anti-CCP+, RF+), late-stage disease, high activity (DAS28 5.3), secondary renal amyloidosis, and CKD stage 5D had received maintenance hemodialysis since December 2025. From January 21 to February 2, 2026, she was hospitalized due to RA exacerbation. Before therapy, hemoglobin was 106 g/L, erythrocytes 3.64 × 10¹²/L, leukocytes 21.57 × 10⁹/L, hematocrit 32.4%, neutrophils 17.99 × 10⁹/L, ESR 30 mm/h. Creatinine was 405 μmol/L, urea 14.1 mmol/L, total protein 63 g/L, potassium 4.05 mmol/L, glucose 6.77 mmol/L, ALT 18 U/L, AST 16 U/L. Hemostasis lab tests: PTI 79%, INR 1.24, fibrinogen 684 mg/dL, aPTT 26.0 s. Therapy included methotrexate 15 mg, colchicine 1.0 mg, infliximab 200 mg, denosumab 60 mg, and prednisolone 10 mg. Subsequently, severe stomatitis and generalized skin eruptions developed. On March 24, she was hospitalized; on March 25, was diagnosed drug-induced SJS. On March 27, she was transferred to the intensive care unit. At admission, hemoglobin was 67 g/L, leukocytes 1.68 × 10⁹/L, platelets 88 × 10⁹/L, creatinine 605.3 μmol/L, urea 21.99 mmol/L, and total protein 53.6 g/L. By March 29, platelets decreased to 12 × 10⁹/L, total protein to 36.3 g/L, and albumin to 17.6 g/L. Hemostasis lab tests deteriorated: PTI 79%-74%-59%, INR 1.24-1.31-1.60, and aPTT 26.0-26.9-77.3 s (January 21, March 24, and March 29, respectively). Sepsis developed, requiring antibacterial and antifungal therapy, platelet concentrates, fresh frozen plasma, and maintenance hemodialysis. Despite intensive treatment, her condition progressively deteriorated. Treatment was stopped at her family's request.
Conclusion: This case highlights the high risk of severe drug-related complications in patients with RA and CKD stage 5D on hemodialysis. Individualized antirheumatic therapy, careful assessment of drug toxicity and renal status, early recognition of severe mucocutaneous reactions, and prompt multidisciplinary management of SJS, sepsis, and coagulation abnormalities are essential to improve outcomes. Early withdrawal of suspected offending agents and close monitoring of hematological and hemostatic parameters are critical to prevent progression.
Case Presentation: A 61-year-old woman with seropositive RA (anti-CCP+, RF+), late-stage disease, high activity (DAS28 5.3), secondary renal amyloidosis, and CKD stage 5D had received maintenance hemodialysis since December 2025. From January 21 to February 2, 2026, she was hospitalized due to RA exacerbation. Before therapy, hemoglobin was 106 g/L, erythrocytes 3.64 × 10¹²/L, leukocytes 21.57 × 10⁹/L, hematocrit 32.4%, neutrophils 17.99 × 10⁹/L, ESR 30 mm/h. Creatinine was 405 μmol/L, urea 14.1 mmol/L, total protein 63 g/L, potassium 4.05 mmol/L, glucose 6.77 mmol/L, ALT 18 U/L, AST 16 U/L. Hemostasis lab tests: PTI 79%, INR 1.24, fibrinogen 684 mg/dL, aPTT 26.0 s. Therapy included methotrexate 15 mg, colchicine 1.0 mg, infliximab 200 mg, denosumab 60 mg, and prednisolone 10 mg. Subsequently, severe stomatitis and generalized skin eruptions developed. On March 24, she was hospitalized; on March 25, was diagnosed drug-induced SJS. On March 27, she was transferred to the intensive care unit. At admission, hemoglobin was 67 g/L, leukocytes 1.68 × 10⁹/L, platelets 88 × 10⁹/L, creatinine 605.3 μmol/L, urea 21.99 mmol/L, and total protein 53.6 g/L. By March 29, platelets decreased to 12 × 10⁹/L, total protein to 36.3 g/L, and albumin to 17.6 g/L. Hemostasis lab tests deteriorated: PTI 79%-74%-59%, INR 1.24-1.31-1.60, and aPTT 26.0-26.9-77.3 s (January 21, March 24, and March 29, respectively). Sepsis developed, requiring antibacterial and antifungal therapy, platelet concentrates, fresh frozen plasma, and maintenance hemodialysis. Despite intensive treatment, her condition progressively deteriorated. Treatment was stopped at her family's request.
Conclusion: This case highlights the high risk of severe drug-related complications in patients with RA and CKD stage 5D on hemodialysis. Individualized antirheumatic therapy, careful assessment of drug toxicity and renal status, early recognition of severe mucocutaneous reactions, and prompt multidisciplinary management of SJS, sepsis, and coagulation abnormalities are essential to improve outcomes. Early withdrawal of suspected offending agents and close monitoring of hematological and hemostatic parameters are critical to prevent progression.
Congress Abstract
Central Asian Journal of Nephrology, 2(2, Suppl. 1), 2026, cajn_A24, https://doi.org/10.63946/cajn/19514
ABSTRACT:
Background: Patients with type 2 diabetes mellitus (T2DM) on maintenance hemodialysis represent one of the highest-risk populations in nephrology practice. End-stage kidney disease (ESKD) and T2DM create a state of profound immunosuppression that predisposes patients to life-threatening infections.
Central venous catheters (CVCs), frequently required for hemodialysis access, are a well-recognized gateway for bacteremia. When bacteremia is complicated by coagulopathy, the clinical course can rapidly evolve toward disseminated intravascular coagulation (DIC).
Case Presentation: A 58-year-old woman was admitted with a 3-day history of nausea, vomiting, and body pain. Examination revealed anasarca, lower-extremity purpura, and petechial rash, with concern for coagulopathy. T2DM diagnosed in 2007 and ESKD on maintenance hemodialysis since October 2025 (three 4-hour sessions weekly). Vascular access was a right internal jugular CVC.
On admission, hemoglobin 62 g/L, RBC 2.02 ×10¹²/L, platelets 93 ×10⁹/L, WBC 11.18 ×10⁹/L, glucose 24.28 mmol/L, total protein 63 g/L, D-dimer 2,680 ng/mL, procalcitonin (PCT) 14.8 ng/mL, creatinine 405 μmol/L, urea 13.9 mmol/L, INR 1.46, Prothrombin Index 66%, fibrinogen 4.0 g/L, APTT 28.2 sec. Antibiotics had been started at home without improvement. In hospital, broad-spectrum therapy was escalated to a carbapenem plus a fluoroquinolone, with packed red blood cell and fresh frozen plasma transfusions. Hemoglobin increased to 87 g/L, PCT decreased to 1.78 ng/mL, and D-dimer to 1,178 ng/mL; thrombocytopenia persisted. After treatment, creatinine 592 μmol/L, urea 20.7 mmol/L, glucose 16.55 mmol/L, albumin 26 g/L, total protein 53 g/L, INR 1.39, Prothrombin Index 69%, fibrinogen 7.55 g/L, APTT 25.4 sec.
On days 5–6, livedo reticularis, worsening dyspnea, and persistent coagulopathy prompted chest MSCT. It revealed bilateral peribronchial foci with formed cavities, consistent with abscessing (necrotizing) pneumonia. The bilateral cavitary pattern suggested hematogenous dissemination, likely from the indwelling CVC. Patient transferred to the ICU with sepsis-associated DIC.
Linezolid 600 mg IV twice a day was added to provide coverage for possible methicillin-resistant Staphylococcus aureus and other gram-positive organisms. Following treatment escalation, hemoglobin reached 118 g/L, PCT decreased to 0.9 ng/mL, INR normalized to 0.92, and Prothrombin Index increased to 117%.
Conclusion: CVC-related bacteremia should be considered early in hemodialysis patients with unexplained coagulopathy or bilateral pulmonary infiltrates. Purpura followed by livedo reticularis may indicate DIC progression and should prompt urgent reassessment. Cavitation despite antibiotics signals treatment failure and need to reassess pathogen coverage, including biofilm-forming gram-positive organisms. T2DM and ESKD create a multiplicative immunocompromised state, requiring multimodal management and glycemic control.
Central venous catheters (CVCs), frequently required for hemodialysis access, are a well-recognized gateway for bacteremia. When bacteremia is complicated by coagulopathy, the clinical course can rapidly evolve toward disseminated intravascular coagulation (DIC).
Case Presentation: A 58-year-old woman was admitted with a 3-day history of nausea, vomiting, and body pain. Examination revealed anasarca, lower-extremity purpura, and petechial rash, with concern for coagulopathy. T2DM diagnosed in 2007 and ESKD on maintenance hemodialysis since October 2025 (three 4-hour sessions weekly). Vascular access was a right internal jugular CVC.
On admission, hemoglobin 62 g/L, RBC 2.02 ×10¹²/L, platelets 93 ×10⁹/L, WBC 11.18 ×10⁹/L, glucose 24.28 mmol/L, total protein 63 g/L, D-dimer 2,680 ng/mL, procalcitonin (PCT) 14.8 ng/mL, creatinine 405 μmol/L, urea 13.9 mmol/L, INR 1.46, Prothrombin Index 66%, fibrinogen 4.0 g/L, APTT 28.2 sec. Antibiotics had been started at home without improvement. In hospital, broad-spectrum therapy was escalated to a carbapenem plus a fluoroquinolone, with packed red blood cell and fresh frozen plasma transfusions. Hemoglobin increased to 87 g/L, PCT decreased to 1.78 ng/mL, and D-dimer to 1,178 ng/mL; thrombocytopenia persisted. After treatment, creatinine 592 μmol/L, urea 20.7 mmol/L, glucose 16.55 mmol/L, albumin 26 g/L, total protein 53 g/L, INR 1.39, Prothrombin Index 69%, fibrinogen 7.55 g/L, APTT 25.4 sec.
On days 5–6, livedo reticularis, worsening dyspnea, and persistent coagulopathy prompted chest MSCT. It revealed bilateral peribronchial foci with formed cavities, consistent with abscessing (necrotizing) pneumonia. The bilateral cavitary pattern suggested hematogenous dissemination, likely from the indwelling CVC. Patient transferred to the ICU with sepsis-associated DIC.
Linezolid 600 mg IV twice a day was added to provide coverage for possible methicillin-resistant Staphylococcus aureus and other gram-positive organisms. Following treatment escalation, hemoglobin reached 118 g/L, PCT decreased to 0.9 ng/mL, INR normalized to 0.92, and Prothrombin Index increased to 117%.
Conclusion: CVC-related bacteremia should be considered early in hemodialysis patients with unexplained coagulopathy or bilateral pulmonary infiltrates. Purpura followed by livedo reticularis may indicate DIC progression and should prompt urgent reassessment. Cavitation despite antibiotics signals treatment failure and need to reassess pathogen coverage, including biofilm-forming gram-positive organisms. T2DM and ESKD create a multiplicative immunocompromised state, requiring multimodal management and glycemic control.