Treating nephrotic IMN in Japanese patients with low-dose cyclophosphamide and prednisolone is beneficial for long-term renal prognosis with relatively few adverse effects.

There have been several reports of cases of renal amyloidosis with glomerular crescents. However, it is not clear whether the association is fortuitous or pathogenic related. The present study analyzed 105 cases of renal amyloidosis (61 autopsy cases and 44 biopsy cases) and found glomerular crescents in 14 (13.3%) cases. Among the 14 cases with crescents, a female predominance was noted (male: female, 3: 11) and rheumatoid arthritis was the most common primary disease of amyloidosis. Immunohistochemical analysis demonstrated amyloid protein of AA type in 12 cases. According to the histologic classification, there were 11 cases of mesangial nodular type, which was almost exclusively accompanied by AA amyloid deposition. Of note, the incidence of crescents neither correlated with the extent of amyloid deposition nor the presence of nephrotic syndrome. By contrast, localization of amyloid deposition was closely related to crescent formation. Moreover, electron microscopic observation displayed rupture of the glomerular basement membrane at the site of amyloid deposition. Our results indicated that glomerular crescents were more frequently associated with renal amyloidosis than previously appreciated. Rupture of the fragile glomerular basement membrane by amyloid deposition, as revealed by immunostaining and electron microscopy, may be the mechanism of crescent formation. We suggest that glomerular crescents are a distinct pathology associated with renal amyloidosis, not fortuitous conditions.

Dissecting aortic aneurysm, leading frequently to stroke as a cause of sudden death in chronic dialysis patients, at least in Japan, should be carefully differentiated from other cardiac diseases in chronic dialysis patients, such as severe atherosclerosis.

A case of renal amyloidosis coincidentally associated with crescentic glomerulonephritis is described. A 59-year-old female with 30 years’ history of rheumatoid arthritis developed nephrotic syndrome followed by rapid deterioration of renal function. Among 28 glomeruli in a kidney biopsy specimen, glomerular amyloid deposition was present in 17 and crescent formation in 20. Only one glomerulus was free from amyloid deposition or crescent. The amyloid deposition was clearly demonstrated by congo red, thioflavin-T staining as well as electron-microscopic examination. Glomerular deposition of immunoglobulins and/or complements were not noted. While cyclophosphamide, dipyridamole, and heparin followed by pulse methylprednisolone were given, the renal function deteriorated progressively and dialysis was initiated. Renal function, however, recovered partially without medication after peritoneal dialysis of 3 months’ duration. The second renal biopsy revealed the progression of glomerular amyloid deposition and the increase in fibrous component of crescent.

Background: Eldecalcitol (ELD) is an active vitamin D 3 analog that is widely used in Japan for the treatment of osteoporosis. The most common adverse drug reaction of ELD is hypercalcemia. However, few reports have focused on acute kidney injury (AKI) associated with ELD-induced hypercalcemia. Materials and methods: We retrospectively reviewed the medical records at our hospital for cases of hypercalcemia-induced AKI between April 2013 and February 2018. Among them, we focused on patients who developed AKI secondary to ELD-induced hypercalcemia. Results: Among 69 patients who developed hypercalcemia-induced AKI, 32 patients (46.4%) developed AKI associated with ELD-induced hypercalcemia. Their mean age was 82 ± 5 years, 97% of them were female, mean corrected serum calcium level was 12.2 ± 1.5 mg/dL, serum creatinine level was 2.5 ± 2.2 mg/dL, and estimated glomerular filtration rate was 23.9 ± 14.4 ml/min/1.73 m 2 on admission. ELD administration was discontinued in all patients and some of them were treated with hydration with or without calcitonin, which was followed by a normalization of serum calcium level. Corrected serum calcium level on admission was significantly higher ( p < .05) in patients treated with magnesium oxide. Although there were no significant differences, serum calcium and creatine levels on admission tended to be higher in patients who were treated with other drugs that affect renal hemodynamics and renal calcium metabolism than those not taking these drugs. Conclusions: Prescribers of ELD should regularly monitor serum calcium levels and kidney function to prevent hypercalcemia and AKI associated with ELD and pay more attention to concomitant drugs especially magnesium oxide.