A Study Evaluating the Efficacy, Safety, Pharmacokinetics and Pharmacodynamics of Crovalimab in Pediatric Participants With Atypical Hemolytic Uremic Syndrome (aHUS)

Inclusion Criteria:

• Body weight >= 5 kg at screening.

• Vaccination against Neisseria meningitis serotypes A, C, W, and Y; vaccinationagainst serotype B, according to national vaccination recommendations.

• Vaccination against Haemophilus influenzae type B and Streptococcus pneumoniae,according to national vaccination recommendations.

• For patients continuing to receive other therapies concomitantly with crovalimab (e.g., immunosuppressants, corticosteroids, mammalian target of rapamycin inhibitor (mTORi), or calcineurin inhibitors): stable dose for >=28 days prior to screeningand up to the first crovalimab administration.

• For female participants of childbearing potential: an agreement to remain abstinentor use contraception.

• Participants with a prior kidney transplant are eligible if they have a knownhistory of complement-mediated aHUS prior to the kidney transplant.

• Onset of initial TMA presentation within 28 days prior to the first dose ofcrovalimab (for Naive Cohort only).

• Documented treatment with either eculizumab or ravulizumab (for Switch Cohort only).

• Clinical evidence of response to a C5 inhibitor (for Switch Cohort only).

• Poorly controlled TMA following treatment with another C5 inhibitor (for C5 SNPparticipants in the Pretreated Cohort only).

• Known C5 polymorphism (for C5 SNP participants in the Pretreated Cohort only).

Exclusion Criteria:

• TMA associated with non-aHUS related renal disease.

• Positive direct Coombs test.

• Chronic dialysis within 90 days prior to first crovalimab administration , and /orend stage renal disease

• Identified drug exposure-related TMA.

• Presence or history of a condition that could trigger TMA, such as malignancy, bonemarrow or organ transplant (other than kidney transplant) or autoimmune disease.

• History of a kidney disease, other than aHUS.

• History of Neisseria meningitidis infection within 6 months of study enrollment.

• Known or suspected immune deficiency (e.g., history of frequent recurrentinfections).

• Positive HIV test.

• Active systemic bacterial, viral, or fungal infection within 14 days before firstcrovalimab administration.

• Presence of fever (>= 38°C) before the first crovalimab administration (If feversare solely due to the underlying aHUS pathology, and there is no evidence orsuspicion of a systemic infection, participants may enroll).

• Multi-system organ dysfunction or failure.

• Recent intravenous immunoglobulin (IVIg) treatment.

• Pregnant or breastfeeding or intending to become pregnant.

• Participation in another interventional treatment study with an investigationalagent or use of any experimental therapy within 28 days of screening or within fivehalf lives of that investigational product, whichever is greater.

• Recent use of tranexamic acid.

• Current or previous treatment with a complement inhibitor (for Naive Cohort only).

• First initiation of plasma exchange/plasma infusions (PE/PI) should not be more than 28 days prior to first crovalimab administration (for Naive Cohort only).

• Last PE/PI completed less than 2 hours prior to first crovalimab administration (forNaive Cohort only).

• Receiving PE/PI within 8 weeks of the first crovalimab administration (Switch Cohortonly).

• Normalization of serum creatinine values at baseline (<97.5th percentile for age), (for Naive Cohort only).

• Positive for active Hepatitis B and/or C infections (HBV/HCV) (for Switch Cohort andswitching C5 SNP Pretreated Cohort participants who recently received C5 inhibitortreatment).

• Cryoglobulinemia at screening (for Switch Cohort and C5 SNP Cohort participants whorecently received C5 inhibitor treatment).

• Diagnosis of a condition leading to non-aHUS TMA: Thrombotic ThrombocytopenicPurpura (TTP), Shiga Toxin producing Escherichia Coli (STEC)-TMA, Pneumococcal HUS,TMA secondary to cobalamin C defect (as demonstrated by either increased total bloodhomocysteine levels or MMACHC gene mutation) and TMA related to Diacylglycerolkinase ε (DGKE) nephropathy.