Ferras Alashkar

To the Editor, Sickle cell nephropathy (SCN) is a major determinant of morbidity and mortality in sickle cell disease (SCD), yet early injury remains difficult to recognize with conventional laboratory markers alone. Creatinine-based assessment is problematic in SCD because low muscle mass, increased tubular secretion, and glomerular hyperfiltration may keep serum creatinine (SCr) deceptively low even in the presence of evolving nephropathy.

1 Introduction Cold agglutinin disease (CAD) is a low-grade lymphoproliferative disorder of clonal B cells that produce cold agglutinin, usually of the immunoglobulin M (IgM)-κ class [1-3]. CAD is a member of the autoimmune hemolytic anemia family (AIHA) accounting for 15%–30% of all AIHA cases [1, 2, 4, 5]. As the name implies, the cold agglutinin can lead to agglutination of red blood cells (RBC) at ≤ 37°C after recognizing the “I” antigen on the surface of RBCs [5, 6].

Die Sichelzellkrankheit (SCD) stellt eine seltene, aber äußerst komplexe, multisystemische Erkrankung dar, die eine umfassende interdisziplinäre und spezialisierte Versorgung und daher neue strukturelle Voraussetzungen erfordert. Neben der Versorgung dieser chronisch kranken Patienten stellt insbesondere der Transitionsprozess eine vulnerable Phase, mit maßgebendem Einfluss auf die weitere Behandlung, dar.