Acute kidney injury triggered by excessive alcohol intake was described for the first time by Japanese researchers in a patient with cold agglutinin disease (CAD).
The case was reported in the study “Acute Kidney Injury by Renal Hemosiderosis Secondary to Primary Cold Agglutinin Disease Associated with an Excessive Alcohol Intake,” published in the journal Internal Medicine.
CAD is a rare disease in which the immune system starts to attack its own red blood cells, causing them to form clumps and leading to hemolysis (red blood cell destruction). Cold is a common trigger of CAD attacks, which are mediated by components of the immune system that commonly fight infections, including immunoglobulin M and complement proteins.
If hemolysis occurs in the kidney, it can cause accumulation of hemosiderin (a component of red blood cells) in the tissues and impairment of the organ’s normal function.
Hemolysis, although a common manifestation of CAD, is usually mild and has not been reported up until now to cause renal hemosiderosis, a consequence of severe hemolysis.
Japanese researchers have described for the first time the case of a patient with CAD who developed acute kidney injury (AKI) caused by renal hemosiderosis.
The 67-year-old man was admitted to the hospital with a general feeling of discomfort and yellowish skin. He said he was a heavy drinker and had been drinking much more than usual previous week.
For the past three years, he had small blood vessel constriction in the extremities (also known as Raynaud’s phenomenon) and dark urine after exposure to cold. A previous clinical evaluation did not find any significant alterations except for the levels of bilirubin, which were 1.7-2.9 times higher than normal.
On admission, he had a fever and severely yellow skin. Physical examination did not find any alterations within the abdominal organs that could explain these symptoms. Still, lab results revealed that he had liver dysfunction, renal dysfunction, and hemolytic anemia.
He was found to be positive for antibodies targeting red blood cells and immune complement proteins. He also had high amounts of cold agglutinin, consistent with primary CAD diagnosis. Still, this diagnosis did not explain all his symptoms, such as the renal manifestations.
Analysis of the bone marrow revealed that he had some abnormal white blood cells consistent with a diagnosis of lymphoplasmacytic lymphoma/Waldenstrom’s macroglobulinemia (LPL/WM).
This finding was in accordance with previous reports that suggested LPL/WM is the underlying cause of autoimmune hemolytic anemia in half of the CAD patients who develop this complication.
Evaluation of the kidney by computed tomography did not reveal any significant alterations of the organ’s size or appearance. Further analysis of a kidney tissue sample showed some structural changes, as well as significant accumulation of hemosiderin deposits, which further confirmed the diagnosis of CAD with secondary renal hemosiderosis.
He started taking dexamethasone to block the production of autoantibodies, and received plasma infusions to help remove the harmful antibodies. However, his kidneys continued to deteriorate and he had to undergo three sessions of hemodialysis. To manage his LPL/WM, he received four doses of Rituxan (rituximab).
After this, his health improved significantly, and remained stable for at least the next four years with no signs of CAD recurrence. He reduced alcohol intake and started to avoid exposure to cold.
“In conclusion, primary CAD can be associated with severe hemolysis, resulting in [acute kidney injury] due to renal hemosiderosis, especially in patients with an excessive alcohol intake,” researchers stated.
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