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Many anticancer drugs have been reported to damage the kidneys. Olaparib (ORB) is known not to largely affect renal function due to its specific pharmacological mechanism, and there are no reports on renal dysfunction associated with the drug. The patient was found to have diagnosed with recurrent ovarian cancer. She started therapy with Bevacizumab (BEV). Unfortunately, BEV was discontinued due to development of progressive renal dysfunction with proteinuria. Therefore, she started administration of ORB. However, after switching to ORB, her renal dysfunction progressed. Renal histopathology revealed membranoproliferative glomerulonephritis (MPGN) and thrombotic microangiopathy (TMA). During the clinical course, her renal function deteriorated after administration of ORB and improved after the drug was discontinued because of bone marrow suppression. Moreover, sustained improvement of renal function was observed after complete discontinuation of the drug. This case is considered to be the first report of renal dysfunction due to ORB. Although ORB is not considered to cause renal damage when administered alone, it can be considered to further exacerbate the preceding BEV-induced renal dysfunction. Since switching of anticancer drugs is common, clinicians should be aware of the risk of developing renal dysfunction.

Introduction We previously reported that fibroblast growth factor 23 (FGF23)‐klotho signaling plays a role in B cell immunity. Despite high serum levels of FGF23, a decline in immunity is frequently observed in patients on hemodialysis (HD); thus, abnormalities in the FGF23‐klotho signaling pathway in immune cells may occur in these patients. Methods We analyzed the number of klotho‐positive cells in peripheral blood mononuclear cells from 10 male and 6 female patients on HD and 5 healthy male subjects using flow cytometry. We analyzed the abundance of cleaved klotho protein in the murine B cell line, A20, and in the serum of HD patients and healthy subjects (HS) using flow cytometry and Western blotting. The serum level of A disintegrin and metalloprotease 17 (ADAM17) was measured in HD patients and HS using enzyme‐linked immunosorbent assay. Results The number of klotho‐positive B cells was reduced in HD patients. Serum ADAM17 was responsible for the reduction in klotho, as a specific ADAM17 inhibitor reversed this change. The total serum levels of ADAM17 were similar in HD patients and HS; however, activated ADAM17 was increased in the serum of HD patients. Conclusions We concluded that abnormal ADAM17 activation could contribute to the immunocompromised status in patients on HD, in line with the reported role of ADAM17 as an anti‐inflammatory and immunosuppressive factor., Klotho expression of lymphocyte was lower in the uremic patients (hemodialysis patient) than in healthy subjects, which was one of the causes for a decrease in a number of lymphocyte and immunocompromised status in uremic patients. It was one of the causes for the lower expression of klotho in lymphocyte of the patient that activated A disintegrin and metalloprotease 17 cleavaged klotho in lymphocyte.

A 74-year-old man underwent intravesical bacillus Calmette-Guerin (BCG) therapy for bladder cancer and later presented with lower left back pain. Magnetic resonance imaging of the spine showed high signal intensity, diagnosed as a cystic lesion in the epidural and bilateral intestinal psoas muscle. A computed tomography-guided needle biopsy and histological examination revealed bacteria from the family Mycobacteriaceae, and Mycobacterium bovis was identified using multiplex polymerase chain reaction. If lower back pain appears in a patient who has undergone BCG therapy, it is necessary to test for tuberculous spondylitis. In addition, QuantiFERON is useful for the differential diagnosis of M. bovis BCG infection.

Vascular calcification is significant because of the close association between the degree of vascular calcification and cardiovascular mortality in chronic kidney disease (CKD) patients.There are 2 types of vascular calcification in CKD patients. One is endothelial vascular calcification, a common type of vascular calcification. Another is medial vascular calcification, a specific type that is common in CKD patients. The former is mainly associated with atherosclerosis due to hyperlipidemia, especially hypercholesterolemia. The latter CKD-specific type is called Moenckeberg's arteriosclerosis. A known risk factor for this type of vascular calcification is hyperphosphatemia. In this review article, we mainly discuss a preventive strategy for Moenckeberg type vascular calcification in CKD, primarily involving the treatment of hyperphosphatemia. Several possible modalities are considered. However, at present, dietary restriction of phosphate is not recommended so as to avoid malnutrition in CKD patients. The first consideration is the enhancement of phosphate removal by renal replacement therapy in dialysis patients. Various phosphate binder therapies can be beneficial and effective. Surgical and pharmacological parathyroidectomies are also useful for treating secondary hyperparathyroidism. Good quality bone provides a good pool of calcium and phosphate. Thus, bone protection is another option for preventing vascular calcification. Several therapeutic agents have been developed to manage osteoporosis. These trial agents may be reasonably effective in impeding the progression of vascular calcification in CKD patients. Key Messages: We should make full use of several modalities so as to completely prevent vascular calcification.

Background: Vascular calcification is significant because of the close association between the degree of vascular calcification and cardiovascular mortality in chronic kidney disease (CKD) patients. Summary: There are 2 types of vascular calcification in CKD patients. One is endothelial vascular calcification, a common type of vascular calcification. Another is medial vascular calcification, a specific type that is common in CKD patients. The former is mainly associated with atherosclerosis due to hyperlipidemia, especially hypercholesterolemia. The latter CKD-specific type is called Moenckeberg's arteriosclerosis. A known risk factor for this type of vascular calcification is hyperphosphatemia. In this review article, we mainly discuss a preventive strategy for Moenckeberg type vascular calcification in CKD, primarily involving the treatment of hyperphosphatemia. Several possible modalities are considered. However, at present, dietary restriction of phosphate is not recommended so as to avoid malnutrition in CKD patients. The first consideration is the enhancement of phosphate removal by renal replacement therapy in dialysis patients. Various phosphate binder therapies can be beneficial and effective. Surgical and pharmacological parathyroidectomies are also useful for treating secondary hyperparathyroidism. Good quality bone provides a good pool of calcium and phosphate. Thus, bone protection is another option for preventing vascular calcification. Several therapeutic agents have been developed to manage osteoporosis. These trial agents may be reasonably effective in impeding the progression of vascular calcification in CKD patients. Key Messages: We should make full use of several modalities so as to completely prevent vascular calcification.