COVID-19 linked to rare kidney complication in woman with PNH

In a woman with paroxysmal nocturnal hemoglobinuria (PNH) who developed acute kidney damage and low numbers of red blood cells and platelets during a COVID-19 infection, doctors suspected another disease called complement-mediated thrombotic microangiopathy (TMA). Her condition rapidly improved after treatment with Soliris (eculizumab).

“Viral insults can serve as a potent ‘second hit’ that unmasks latent genetic or acquired complement vulnerabilities, requiring a high index of suspicion to ensure timely, targeted therapy,” researchers in Portugal wrote in “Complement-Mediated Hemolysis Beyond PNH: A Case of Complement-Mediated TMA in a Patient with Known PNH,” which was published online in Nefrología.

Recommended Reading

Aug. 17, 2026 News by Lila Levinson, PhD

New infusion therapy cuts need for blood transfusions in small PNH trial

PNH and complement-mediated TMA affect the blood in different ways

PNH and complement-mediated TMA both involve abnormal activity of the complement system, a part of the immune system. In PNH, complement attacks red blood cells. In complement-mediated TMA, uncontrolled complement activity damages the lining of small blood vessels. Both conditions can cause red blood cells to be destroyed prematurely, but their clotting problems differ: PNH increases the risk of blood clots, while complement-mediated TMA causes clots in small blood vessels.

While both can be treated with complement inhibitors such as Soliris, they develop differently. PNH is caused by acquired genetic mutations that render red blood cells vulnerable to complement-mediated attack, while complement-mediated TMA results from uncontrolled complement activity that damages small blood vessels. However, both can remain quiet until a trigger, called a “second hit,” causes the disease to become active.

In this case, an infection with SARS-CoV-2, the virus causing COVID-19, was thought to have triggered complement-mediated TMA in a 53-year-old woman who had already been diagnosed with PNH after developing aplastic anemia, which occurs when the bone marrow does not produce enough blood cells. About three years later, she developed a cough, fatigue, and dark urine and tested positive for SARS-CoV-2.

Blood tests showed anemia (low red blood cell counts), thrombocytopenia (a low number of platelets, which help the blood clot), and hemolysis (premature destruction of red blood cells). Because her kidney function was initially normal, doctors suspected a flare of her PNH and treated her with fluids and corticosteroids.

Within about two days, however, her symptoms worsened. Blood tests showed high levels of creatinine, indicating acute kidney damage that required dialysis to help filter the blood, as the kidneys could not do it properly. Her thrombocytopenia also worsened. However, her urine contained very little hemoglobin, the oxygen-carrying protein in red blood cells, making kidney damage caused by a PNH flare less likely.

Soliris started after doctors suspected complement-mediated TMA

Doctors suspected TMA and, after testing ruled out several other causes, made a presumptive diagnosis of complement-mediated TMA. The woman was started on Soliris, an antibody that blocks the complement protein C5. By blocking C5, Soliris helps prevent complement-mediated damage to red blood cells and blood vessels. Soliris is approved to treat PNH; in Europe, it can also be used to treat atypical hemolytic uremic syndrome, a type of complement-mediated TMA.

The response was rapid. Within about two days of receiving Soliris, she no longer needed additional dialysis. Genetic testing later showed two genetic deletions that led to a complete deficiency of CFHR1, a complement-regulating protein. Deletion of the CFHR1 gene is a “well-established predisposing factor” for complement-mediated TMA, the researchers wrote.

After four doses of Soliris, her kidney function had almost returned to normal, and her anemia and other signs of hemolysis had improved. She was discharged on Soliris every two weeks and remained on this therapy without another episode. The researchers said the case suggests COVID-19 may act as a trigger for complement-mediated TMA in someone with underlying PNH and other complement-related vulnerabilities, “requiring a high index of suspicion to ensure timely, targeted therapy.”