Acute interstitial nephritis is a common cause of acute kidney injury (AKI). The granulomatous inflammation is rarely but often manifests as a form of a granulomatous interstitial nephritis (GIN) in the kidney. Acute granulomatous interstitial nephritis is mainly associated with drugs, infection and autoimmune diseases. A 44-year-old-male visited our out-patient department with symptoms of nausea, vomiting, and general weakness that had developed over the previous 2 weeks. He had history of medication, nonsteroidal anti-inflammatory drugs. On admission to the general ward, his serum creatinine level was markedly elevated. GIN was confirmed by renal biopsy and 30 mg of corticosteroid per day was immediately initiated. Subsequently, his serum creatinine level and uremic symptoms dramatically decreased. Acute granulomatous interstitial nephritis is a rare but important disease on AKI. As long as we can carefully exclude infectious diseases as the cause of granulomatous lesion, acute granulomatous interstitial nephritis can be treated with steroid regardless of the etiologies. Since there is no proven treatment for the GIN yet, we can carefully suggest that moderate to high dosage corticosteroid can be helpful for prognosis in case of acute granulomatous interstitial nephritis of patients with AKI.

Background: Larger middle molecules are important substances associated with cardiovascular complications in end- stage renal disease. Unfortunately, larger middle molecules are not reliably removed by a high-flux dialyzer. A medium cut-off (MCO) membrane could effectively remove larger middle molecules. This study aimed to identify the long -term effect of the MCO membrane for changes of larger middle molecules. Methods: Thirty-four patients were prospectively analyzed for 12 months. The enrolled patients were divided into control and MCO groups. We measured the plasma levels of growth differentiation factor 15, sclerostin, and fibroblast growth factor 23 in larger middle molecules and those of biomarkers including small solutes. Single-pool Kt/V (spKt/V) and reduction ratios also were evaluated. Results: Plasma sclerostin did not increase significantly in patients using the MCO dialyzer (135.3 [-637.7 to 908.3], p = 0.715). And there was a significant difference in change of plasma sclerostin level between the two groups (-1,646.9 [-3,015.2 to -278.7], p = 0.033). Furthermore, a negative association between calcium and sclerostin was not observed in the MCO group (r = -0.142, p = 0.587). Solute clearance of larger middle molecules in the MCO group was significantly higher. Moreover, spKt/V values for patients in the MCO group were significantly increased without albumin loss. Values are presented as mean (95% confidence interval [CI]) or adjusted mean (95% CI). Conclusion: The MCO dialyzer can increase dialytic adequacy and suppress the increase in plasma sclerostin level without significant albumin loss in patients with end-stage renal disease.

Jung JH, et al. J Korean Med Sci. 2020 Jan;35(9):e44. https://doi.org/10.3346/jkms.2020.35.e44

Jung JH. Chonnam Med J. 2017 May;53(2):170-170. https://doi.org/10.4068/cmj.2017.53.2.170

Chronic kidney disease–mineral bone disorder (CKD‐MBD) is the most common complication in CKD patients. Although there is a consensus on treatment guidelines for CKD‐MBD, it remains uncertain whether these treatment recommendations reflect actual practice. Therefore, the aim of this study was to investigate the CKD‐MBD medication trend in real‐world practice. This was a retrospective and observational study using a 12‐year period database transformed into a common data model from three tertiary university hospitals. Study populations were subjects initially diagnosed as CKD. The date of diagnosis was designated as the index date. New patients were categorized year to year from 2008 to 2019 with a fixed observation period of 365 days to check the prescription of CKD‐MBD medications including calcium‐containing phosphate binder, noncalcium‐containing phosphate binder, aluminium hydroxide, vitamin D receptor activator (VDRA), and cinacalcet. The numbers of CKD patients in the three hospitals were 7555, 2424, and 5351, respectively. The proportion for patients with CKD‐MBD medication prescription decreased yearly regardless of hospital and CKD stage (p for trend < 0.05). The use of aluminium hydroxide disappeared steadily while the use of VDRA increased annually in all settings. Despite these changes in prescription patterns, the mean value for CKD‐MBD‐related serologic markers was almost within target range. The proportion of the population within the target value was not significantly changed. Irrespective of hospital and CKD stage, similar trends of prescription for CKD‐MBD medications were observed in real‐world practice. Further research with a distributed network study may be helpful to understand medication trends in CKD‐MBD treatment.