Those with a chronic disease, whether in remission or not, remain mindful or minding what clinical tests are telling them about what is happening in their body. It did not matter before their illness. No need to be minding or mindful then.
The diabetes patient did not know their glucose level before diagnosis and they lived with the fluctuations from high to low unaware. They are mindful and minding because they need to act to stop glucose levels going too high or low.
Similarly in aHUS patients did not know how normal or abnormal; their blood measures were, they lived with what they had.
During an aHUS onset that changed and quickly.
Among the symptoms of aHUS is anaemia. The key measure for detecting anaemia is Hgb or Hb , Haemoglobin, it falls to low levels despite the efforts of the bone marrow going into hyper production to replace the lost red blood cells , RBCs, because of shear stress trying to pass the blood clots in the blood vessels.
They are haemolytic and restoration of Hb level to normal range is the key measure of complement inhibitor effectiveness in clinical trials, along with LDH, platelets and EGFR.
But in subsequent monitoring some patients may become minding or mindful of other parameter such as Mean Corpuscular Hemoglobin (MCH) and Mean Corpuscular Hemoglobin Concentration (MCHC). Most aHUS patients will not have heard of them. They were not important for treatment trials. They measure the density and quality of the RBCs produced by the bone marrow. aHUS does not alter the RBCs produced. It just destroys them. Density ( MCH) should be low if Hb is low. Quality stays the same in the surviving RBCs and new ones produced .
So why would these parameters matter long after the acute aHUS process has stopped.
MCH and MCHC can change from pre-aHUS baseline to post-resolution values, even after the acute episode has resolved. Bone marrow function is typically not permanently altered in most cases of resolved aHUS, but temporary effects or secondary factors can influence RBC measures long-term.
aHUS causes thrombotic microangiopathy (TMA): complement overactivation damages small blood vessels, leading to RBC fragmentation (schistocytes), hemolytic anemia, and consumption of platelets. This often results in:
• Lower hemoglobin.
• Abnormal RBC morphology.
• Potentially altered MCH (average hemoglobin per RBC) and MCHC (hemoglobin concentration in RBCs) due to mechanical shearing and accelerated RBC turnover.
During active disease, these measures indices reflect the hemolytic process rather than primary bone marrow failure.
With successful treatment (e.g., eculizumab or supportive care), hemolysis typically stops, and RBC production normalizes. Many patients see hematologic recovery, including normalization of hemoglobin, platelets, and LDH.
However, MCH and MCHC can still differ from pre-illness baselines due to:
Residual or secondary effects, there could be mild ongoing low-grade hemolysis. Or depending on the level of kidney function damage , kidney function could change. There could be inflammation, or nutritional deficiencies (e.g., iron, B12, folate).
RBC turnover and recovery of the new RBCs produced after the crisis may have slightly different levels in the recovery phase.
And of course individual factors in each patient, like age, genetics, or other concurrent conditions influence the return to “normal.”
These changes are often subtle and not necessarily indicative of active disease if other TMA markers (schistocytes, LDH, platelets are normal.
So what about the bone marrow, its function is rarely altered . More likely is its interaction with the kidney, particularly erythropoietin production which the bone marrow needs.
Post-resolution shifts in MCH/MCHC are possible and often benign if trends are stable and patients feel well. They do not automatically mean bone marrow dysfunction or relapse.
But most aHUS are not even mindful of these measures and minding what is happening.
Of the two measures it is the poor quality RBC measure which may need minding because there can be other conditions affecting and revealing another non aHUS reason for any anaemia. This is something for the treating physician to be mindful of.
aHUS alliance Global Action is not medically qualified neither are aHUS peers in social media platforms. Always interpret results in full clinical context with your hematologist/nephrologist—trends matter more than single values. Regular monitoring helps distinguish normal variation from any new issues. If concerned, discuss specific pre- and post-lab comparisons with your doctor. This is not personalized medical advice.
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