Renal damage in cryoglobulinemia

　　The main cause of cold agglutinin disease is that under cold conditions, various diseases may cause abnormal immunoglobulins to appear in the circulation of patients, including SLE, poststreptococcal glomerulonephritis, systemic vasculitis, leukemia, hepatitis C, and other acute and chronic infections, Sjögren's syndrome, Waldenstrom's macroglobulinemia, and multiple myeloma. The factors that cause the progression of glomerulonephritis depend on the activity of cold agglutinins, while skin vasculitis requires the activity of cold agglutinins and rheumatoid factors. This suggests that skin and renal vasculitis have different pathogenic mechanisms. However, the common feature is that under the stimulation of cold conditions, immunoglobulins coagulate and deposit in the small and medium-sized blood vessels throughout the body, causing vasculitis diseases.

　　Renal damage caused by cold agglutinins is relatively rare. With the progression of the disease, it often complicates systemic skin vasculitis syndrome and chronic renal uremia, and in severe cases, it can complicate acute renal failure.

　　Primary cold agglutinin disease is more common in young and middle-aged people, with women slightly more than men. When patients encounter cold weather and the body surface temperature decreases, the cold agglutinins in the extremity blood vessels precipitate or become gelatinous, blocking the capillaries, and causing ischemic necrosis of the vascular wall and vascular spasm. Purpura and cold urticaria are the most common skin manifestations. Some patients may have Raynaud's phenomenon, joint pain, enlargement of the liver and spleen, enlargement of lymph nodes, peripheral neuritis (such as sensory abnormalities and numbness), and vasculitis syndrome. Some patients may have cold agglutinin disease-related leg ulcers, mainly due to cutaneous vasculitis.

　　Prevention is important to reduce the occurrence of diseases, and this is no exception for cold agglutinin disease-related renal damage. The following is a specific introduction to the prevention measures for this disease, which can be referred to.

　　1. Do not ignore the common cold: Most chronic kidney diseases are immune diseases, and colds or infections can induce the body's immune system, thereby accelerating the progression of the disease.

　　2. Combine work and rest, emphasize rest: After people are tired, the metabolism products in the body increase, and increasing the workload of the kidneys can worsen the condition. Therefore, avoiding fatigue and taking appropriate rest is beneficial to the recovery of kidney function.

　　3. Adjust diet to assist in nutrition: Patients with chronic kidney disease should have a light taste, avoid smoking and drinking, and spicy foods. When renal function damage occurs, dietary protein intake should be restricted, mainly from animal proteins such as eggs, milk, and lean meat, and oral essential amino acid agents should be taken to prevent malnutrition.

　　Cold environments can lead to the occurrence of this disease. To make an accurate diagnosis, the following examinations are generally required:

　　1. Serum Protein Electrophoresis

　　Examination shows increased gamma globulin, increased immunoglobulins (especially IgG, IgM), positive rheumatoid factor, decreased C3, and rapid blood sedimentation.

　　2. Cold Agglutinin Determination

　　According to the characteristics of cold agglutinins precipitating at 4°C, polymerizing at 25-30°C, and dissolving at 37°C, anticoagulate with EDTA or sodium oxalate, use a syringe at 37°C to draw blood, separate the plasma after centrifugal precipitation, add a small amount of sodium azide as a preservative, and transfer the plasma into 2 Wintrobe tubes, place the test tube in a 4°C refrigerator, and the control tube in a 37°C incubator for 72 hours. The presence of precipitation in the test tube and no precipitation in the control tube indicates a positive result, and then the cold precipitate is quantitatively determined.

　　3. Optical Microscopy

　　In patients with acute renal failure, the optical microscope of renal biopsy usually shows extensive capillary hyperplasia or glomerular capillary damage with crescent formation and a large amount of subendothelial deposits in the glomeruli, as well as large, round thrombi in the lumens.

　　4. Immunofluorescence Microscopy

　　Examination can find granular deposits on the capillary wall, glomerular basement membrane, and C3, IgG, and IgM aggregates in the lumen, which are similar to circulating cold agglutinins in immunology, with only a small amount of C1q deposition, and IgM deposition may be present in the stroma.

　　5. Electron Microscopy

　　Electron microscopy can be found in large deposits on the capillary wall and electron-dense deposits with crystalline structures.

　　Patients with this disease should pay attention to a low-salt diet, eat light, avoid alcohol and spicy foods, and eat less greasy and animal protein-rich foods (such as fatty meat, shrimp, crabs, etc.). Avoid eating beans and their products (such as tofu, sprouts, bean powder, etc.), and those with edema, hypertension, and heart failure should pay more attention.

　　Glucocorticoid therapy can control the symptoms of polyarteritis nodosa and the progression of renal lesions, and cyclophosphamide, anticoagulants can be commonly used with glucocorticoids. Early treatment and control of blood pressure should be active. For patients with rapidly progressive nephritis, it is advocated to use high-dose glucocorticoids and plasma exchange therapy.