A 15-year-old boy developed abdominal pain and melena two weeks after COVID-19 infection, which was followed by gross hematuria and proteinuria. Laboratory studies revealed significantly elevated inflammatory markers. Endoscopic examinations showed multiple jejunal and ileal ulcers. Renal biopsy suggested mesangial proliferative glomerulonephritis with crescent formation, necrosis of capillary loops, and mesangial IgA deposits. IgA vasculitis without purpura was considered as a possible diagnosis, and the treatment with prednisone led to remission of both gastrointestinal and renal diseases.

Cervical chondrocutaneous branchial remnants (CCBRs) are a rare congenital benign abnormality resulting from branchial arch dysplasia, characterized primarily by the presence of ectopic exophytic cartilaginous tissue in the neck present at birth. In July 2024, a case of CCBRs was treated at Plastic Surgery Hospital, Chinese Academy of Medical Sciences, involving a 7-year-and-10-month-old female patient. At birth, a bean-sized, rod-shaped, firm mass was noted on the left side of her neck, which progressively grew to the size of a corn kernel, measuring approximately 1.0 cm×1.2 cm. No significant local tenderness, redness, swelling, or ulceration was observed. Comprehensive examinations revealed no associated comorbidities. The patient underwent surgical excision of the neck mass. Postoperative pathological examination with hematoxylin-eosin (HE) staining revealed elastic cartilage in the central region of the lesion. The neck incision healed primarily, and no subsequent reappearance of the lesion was observed during the four-month follow-up. This article summarized the diagnostic and therapeutic process of this patient with CCBRs, and through a comprehensive literature review, highlighted that CCBRs represent one of the superficial markers of branchial arch dysplasia, with surgical excision being the primary treatment. Given that branchial arch abnormalities may be associated with structural or functional anomalies in other organs, a thorough systemic evaluation is recommended prior to surgery. Notwithstanding the absence of concomitant malformations detected on initial evaluation, continuous long-term follow-up monitoring is recommended to mitigate the risk of potential diagnoses being overlooked.

Cervical chondrocutaneous branchial remnants (CCBRs) are a rare congenital benign abnormality resulting from branchial arch dysplasia, characterized primarily by the presence of ectopic exophytic cartilaginous tissue in the neck present at birth. In July 2024, a case of CCBRs was treated at Plastic Surgery Hospital, Chinese Academy of Medical Sciences, involving a 7-year-and-10-month-old female patient. At birth, a bean-sized, rod-shaped, firm mass was noted on the left side of her neck, which progressively grew to the size of a corn kernel, measuring approximately 1.0 cm×1.2 cm. No significant local tenderness, redness, swelling, or ulceration was observed. Comprehensive examinations revealed no associated comorbidities. The patient underwent surgical excision of the neck mass. Postoperative pathological examination with hematoxylin-eosin (HE) staining revealed elastic cartilage in the central region of the lesion. The neck incision healed primarily, and no subsequent reappearance of the lesion was observed during the four-month follow-up. This article summarized the diagnostic and therapeutic process of this patient with CCBRs, and through a comprehensive literature review, highlighted that CCBRs represent one of the superficial markers of branchial arch dysplasia, with surgical excision being the primary treatment. Given that branchial arch abnormalities may be associated with structural or functional anomalies in other organs, a thorough systemic evaluation is recommended prior to surgery. Notwithstanding the absence of concomitant malformations detected on initial evaluation, continuous long-term follow-up monitoring is recommended to mitigate the risk of potential diagnoses being overlooked.

A 15-year-old boy developed abdominal pain and melena two weeks after COVID-19 infection, which was followed by gross hematuria and proteinuria. Laboratory studies revealed significantly elevated inflammatory markers. Endoscopic examinations showed multiple jejunal and ileal ulcers. Renal biopsy suggested mesangial proliferative glomerulonephritis with crescent formation, necrosis of capillary loops, and mesangial IgA deposits. IgA vasculitis without purpura was considered as a possible diagnosis, and the treatment with prednisone led to remission of both gastrointestinal and renal diseases.

A 31-year-old man sought medical evaluation for a 2-year history of edema and proteinuria, with prior pathology suggesting atypical membranous nephropathy (MN). Despite treatment with a combination of steroids, calcineurin inhibitors, and four courses of rituximab (1 g, intravenous injection), the patient′s nephrotic syndrome showed no relief (24 h urine protein peaked at 31.18 g/d), indicating refractory nephrotic syndrome. Later in the disease course, a sudden surge of creatinine level (322.5 μmol/L) prompted a renal biopsy, which revealed concurrent acute interstitial nephritis. Further treatment involving steroids, cyclophosphamide, and a fifth rituximab infusion (1 g, intravenous injection) resulted in improvement in renal function (serum creatinine: 322.5?147 μmol/L), but the MN failed to achieve partial relief. Subsequent treatment with the novel humanized CD20 monoclonal antibody obinutuzumab (1 g, intravenous injection) was initiated. In the latest follow-up, anti-phospholipase-A2-receptor antibody (PLA2R) antibody were negative, B cells were eliminated, serum albumin was 36 g/L, urine protein-to-creatinine ratio was 4 810 mg/g, and serum creatinine was 162 μmol/L. This case underscores the potential efficacy of obinutuzumab in refractory MN. For advanced MN cases, prompt identification of the cause of acute kidney injury is crucial, emphasizing the need for targeted interventions to potentially stall renal function decline.

Objective To prepare and identify rabbit anti-cyclin dependent kinase 6 (CDK6) antibody. Methods The recombinant pET21a (+)/CDK6 was successfully constructed, then the recombinant plasmid was transformed into E.coli BL21 (DE3) competent cells and was induced by isopropyl-β-D-thiogalactopyranoside (IPTG) for protein expression, which was detected by SDS-PAGE and Western blot analysis. The expressed protein was purified by nickel-chelating nitrilotriacetic acid (Ni-NTA) agarose and then analyzed by SDS-PAGE. Japanese white rabbits were immunized with purified CDK6 protein for many times every two weeks. The blood was collected at 0, 2, 4 and 6 weeks after immunization, and serum was separated from blood. The titer was detected by indirect ELISA. Western blot analysis, immunofluorescence assay and immunohistochemistry were employed to determine the specificity. Results High purity CDK6 protein and high specificity of rabbit anti-CDK6 antibody were successfully prepared. The titer of CDK6 rabbit serum antibody reached 1:30 000 after immunization, which could specifically recognize the CDK6 protein expressed in cervical cancer cell line and cervical cancer tissues. Conclusion The high titer and specificity of rabbit anti-CDK6 antibody is successfully prepared.
Animals ; Female ; Humans ; Rabbits ; Antibodies ; Antibody Specificity ; Blotting, Western ; Cyclin-Dependent Kinase 6 ; Enzyme-Linked Immunosorbent Assay ; Uterine Cervical Neoplasms

Primary biliary cirrhosis/cholangitis is an autoimmune disease. Renal tubular acidosis is a common form in PBC cases, but Fanconi syndrome is rarely reported. The paper reported a 66-year-old female patient with fatigue, renal insufficiency and elevated bile duct enzymes. The patient presented with type 2 proximal renal tubular acidosis and complete Fanconi syndrome. Laboratory examinations showed high-titer-positive anti-mitochondrial antibodies, elevated serum IgM, and type 3 cryoglobulinemia. Renal biopsy revealed interstitial nephritis, and electron micrographs showed abnormal mitochondria in proximal tubular epithelial cells. The patient's renal function ameliorated, and acid-base imbalance and electrolyte disturbances were corrected after high-dose glucocorticoid treatment.

The article reported one case of renal damage caused by lenvatinib in the treatment of advanced primary liver cancer. The patient was a 63-year-old male who was admitted to the hospital due to "liver cancer for 4 years, blood pressure elevation for nearly 2 years, and edema for 7 months". During the treatment of liver tumors with atezolizumab combined with lenvatinib, blood pressure increased and renal insufficiency aggravated progressively. Pathological light microscopy of renal biopsy showed endothelial cell lesion and tubulointerstitial damage, and electron microscopy showed moderate proliferation of mesangial cells and deposition of mesangial matrix. There were many agglomerated low-electron density deposits in the mesangial area, and a small amount of electron dense deposits in the subendothelium. The pathological diagnosis was endothelial cell disease (thrombotic microangiopathy) and secondary focal segmental glomerulosclerosis. Renal injury was considered as secondary to lenvatinib. After discontinuing lenvatinib and giving angiotensin receptor antagonist treatment, blood pressure was normal, urine protein turned negative, and renal function improved significantly after 8 months of outpatient follow-up.

A 67-year-old female patient with lymph node metastasis from lung adenocarcinoma received the treatment of chemotherapy, immunotherapy, and targeted therapy (cisplatin, pemetrexed, pembrolizumab, and lenvatinib) at the same time. After the end of the third cycle of treatment, the patient developed elevated blood pressure (160/100 mmHg), blood creatinine increase (from 90 μmol/L to 160 μmol/L), anemia (hemoglobin 90 g/L), and metabolic acidosis (total carbon dioxide 18 mmol/L). Renal histopathological examination showed tubulointerstitial damage. Excluding kidney injury caused by other drugs, it was considered to be the immune adverse reaction caused by pembrolizumab. The drug was discontinued and hormone, antihypertensive, and symptomatic treatments were given. After 5 months, the patient′s blood pressure was 110-120/70-80 mmHg, serum creatinine decreased to 130 μmol/L, hemoglobin was 117 g/L, and total carbon dioxide was 26 mmol/L.

A 67-year-old female patient with lymph node metastasis from lung adenocarcinoma received the treatment of chemotherapy, immunotherapy, and targeted therapy (cisplatin, pemetrexed, pembrolizumab, and lenvatinib) at the same time. After the end of the third cycle of treatment, the patient developed elevated blood pressure (160/100 mmHg), blood creatinine increase (from 90 μmol/L to 160 μmol/L), anemia (hemoglobin 90 g/L), and metabolic acidosis (total carbon dioxide 18 mmol/L). Renal histopathological examination showed tubulointerstitial damage. Excluding kidney injury caused by other drugs, it was considered to be the immune adverse reaction caused by pembrolizumab. The drug was discontinued and hormone, antihypertensive, and symptomatic treatments were given. After 5 months, the patient′s blood pressure was 110-120/70-80 mmHg, serum creatinine decreased to 130 μmol/L, hemoglobin was 117 g/L, and total carbon dioxide was 26 mmol/L.