Barriers to conservative kidney management for Japanese healthcare professionals involved in the treatment of end-stage renal disease.

BACKGROUND: Conservative kidney management (CKM) is a treatment alternative for patients with end-stage kidney disease (ESKD). Despite the increasing population of elderly dialysis patients in Japan, CKM is not as readily available compared with that in North America and Europe. Therefore, it is important to clarify the barriers to CKM in Japan. METHODS: We interviewed 11 experts to explore their beliefs and issues regarding CKM. Based on the interviews, we categorized the CKM barriers into eight categories and created a 24-item questionnaire. A questionnaire survey was conducted among 112 medical professionals involved in ESKD management. To investigate the types of barriers, we conducted an exploratory factor analysis using the questionnaire results. RESULTS: Responses were obtained from 53 (47.3%) of 112 subjects (18 doctors, 29 nurses, 6 clinical engineers), with 94.3% considering CKM as a treatment option for ESKD. Factor analysis categorized the questions into the following: (1) Lack of palliative care experience, (2) Ethics and responsibility, (3) Patient's problem, (4) Dialog with patients and families, and (5) Lack of support system. Regarding barriers to CKM, "lack of experience in palliative care" and "lack of support system" scored the highest, and "ethics and responsibility" scored the lowest. CONCLUSIONS: Barriers to CKM may be classified into five factors, with "lack of experience in palliative care" and "lack of support system" being the important barriers to overcome. Additionally, most healthcare professionals consider CKM as the fourth option for renal replacement therapy.

Severe lactic acidosis with euglycemic diabetic ketoacidosis due to metformin overdose.

Metformin-associated lactic acidosis is a well-known metformin treatment complication; however, the development of euglycemic diabetic ketoacidosis (euDKA) has rarely been reported. Here we report a case of lactic acidosis and euDKA after metformin overdose. A 57-year-old female patient was transferred to our hospital with severe metabolic acidosis and acute kidney injury. She had type 2 diabetes mellitus and was on oral antidiabetic therapy of vildagliptin metformin hydrochloride daily. On the admission day, she had committed suicide by overdosing 50 tablets of vildagliptin metformin hydrochloride, which was equivalent to 25,000 mg of metformin and 2500 mg of vildagliptin. She had severe lactic acidosis 5 h after overdosing. However, after 34 h of overdosing, serum lactate levels decreased while serum anion gap levels increased. She received single hemodialysis treatment. Serum total ketone bodies, ß-hydroxybutyrate acetoacetic acid, and acetone were increased even after hemodialysis treatment. Her blood glucose levels have never exceeded 250 mg/dL since admission. Therefore, we considered that the cause of metabolic acidosis in this patient was not only lactic acidosis but also euDKA. The causes of euDKA in our patient might be hepatic production of ketone bodies due to metformin overdose in addition to type 2 diabetes mellitus, starvation, infection, and stressful physical conditions such as vomiting and diarrhea. We propose that not only lactic acidosis but also ketoacidosis is one of the important pathological conditions in patients with metformin overdose.

A case of systemic sarcoidosis with mesangial proliferative glomerulonephritis showing predominant deposition of IgG in the mesangial region.

A 37-year-old African-British man was referred to our hospital for detailed examination because of persistent fever, swelling and pain in both ankle joints, and blurred vision for two months. Inguinal lymph node biopsy showed a large number of epithelioid granulomas without necrosis. Granulomatous anterior uveitis, nephropathy, high serum angiotensin-converting enzyme activity, and high serum-soluble interleukin-2 receptor were observed, and the diagnosis of systemic sarcoidosis was made. His serum creatinine was 1.4 mg/dL and hematuria, leukocyturia, and urine protein were also seen. The renal biopsy finding was mesangial proliferative glomerulonephritis, with no findings of granuloma formation or tubular interstitial nephritis. Immunofluorescence staining showed deposition of IgG, C3, and C1q in the mesangial region. IgG3 was dominant in subclass staining. There was no monoclonality on kappa and lambda staining. Electron microscopy showed predominant deposition in the mesangial region with some subepithelial and endothelial deposition. His hematuria and leukocyturia disappeared with steroid therapy, suggesting sarcoidosis-related nephropathy. A case of systemic sarcoidosis with mesangial proliferative glomerulonephritis showing predominant deposition of IgG in the mesangial region is presented. No cases of such histological findings have been reported so far, and it is necessary to analyze further cases to clarify the pathogenic significance of the renal biopsy findings observed in this case.