CD58 (PNH Marker), in Visit Clinic

PNH markers include flow cytometry demonstrating absent or reduced GPI‑anchored proteins (CD55 and CD59) on red cells and granulocytes. Laboratory evidence of hemolysis—elevated LDH, indirect bilirubin, reticulocytosis, low haptoglobin and hemoglobinuria—is typical. Historical sucrose lysis or Ham (acidified serum) tests may be positive. Patients may also show marrow abnormalities or thrombotic markers (e.g., elevated D‑dimer).

CD55 (decay‑accelerating factor) and CD59 (protectin) are GPI‑anchored complement regulators on red blood cells. In PNH, PIGA gene–mediated loss of GPI anchors removes CD55 and CD59, allowing unchecked complement activation. CD55 disrupts C3/C5 convertases; CD59 prevents membrane attack complex formation. Their absence causes intravascular hemolysis, hemoglobinuria, anemia and fatigue, with increased thrombosis risk.

The gold standard for diagnosing paroxysmal nocturnal hemoglobinuria (PNH) is flow cytometry demonstrating absence or reduced expression of GPI‑anchored proteins (especially CD55 and CD59) on red blood cells and granulocytes. FLAER‑enhanced flow cytometry (using fluorescent aerolysin) provides higher sensitivity and is preferred for detecting PNH clones in granulocytes and monocytes, confirming diagnosis and guiding management.

PNH is typically Coombs-negative. Hemolysis is complement-mediated due to loss of GPI-anchored proteins (CD55/CD59) on red cells, causing intravascular destruction without autoantibodies. Therefore the direct antiglobulin (Coombs) test is usually negative. Rarely, concomitant autoimmune hemolysis can yield a positive Coombs, but classic PNH is diagnosed by flow cytometry showing CD55/CD59 deficiency.

The gold-standard confirmatory test for paroxysmal nocturnal hemoglobinuria (PNH) is flow cytometry demonstrating deficiency of GPI-anchored proteins, especially CD55 and CD59, on red cells and myeloid cells. FLAER-based flow cytometry (fluorescent aerolysin) with anti-CD55/CD59 antibodies is the preferred, highly sensitive method; testing granulocytes/monocytes is more reliable than testing transfused red cells.

The hallmark of paroxysmal nocturnal hemoglobinuria (PNH) is complement‑mediated intravascular hemolysis due to loss of GPI‑anchored proteins (notably CD55 and CD59) on red cells. This causes episodic hemoglobinuria (often darker in the morning), hemolytic anemia, and risks of thrombosis and bone marrow failure; diagnosis is by flow cytometry showing absent CD55/CD59 on blood cells.