Atypical Antiglomerular Basement Membrane Disease in a Pregnant Patient with Systemic Lupus Erythematosus.

Antiglomerular basement membrane disease (anti-GBM) is an unusual cause of glomerulonephritis. Patients usually present with rapidly progressive glomerulonephritis with or without pulmonary hemorrhage. The diagnosis is based on linear deposits of IgG along the GBM and the presence of anti-GBM antibodies. However, cases with atypical anti-GBM disease in which an anti-GBM antibody was not detected have been reported. We report a 29-year-old pregnant woman with underlying systemic lupus erythematosus (SLE) who presented with severe glomerulonephritis due to atypical antiglomerular basement membrane disease. She was initially diagnosed with active lupus nephritis and her renal function gradually worsened after steroid treatment, so the pregnancy was terminated due to the high maternal and fetal risks. A kidney biopsy showed linear capillary wall staining with fibrous crescents without endocapillary proliferation. The anti-GBM antibody showed negative results two times, so she was diagnosed with atypical anti-GBM disease. Treatment began with intravenous pulse methylprednisolone and continued with mycophenolate mofetil and prednisolone. Due to the intolerability of side effects, the treatment regimen was subsequently changed to intravenous cyclophosphamide. Although she had a significant improvement in clinical edema, serum albumin, and hematuria, her renal function gradually decreased during the 12 months of treatment. A review of the literature showed that the atypical anti-GBM is less aggressive than the typical anti-GBM disease. However, several patients had persistent renal dysfunction and 20-30% of patients had progression to ERSD. To the best of our knowledge, this is the first case of atypical anti-GBM disease in pregnant patients with suspected SLE reported in the literature.

Clinicopathological Correlation of Polyomavirus Nephropathy in Renal Allograft Recipients According to the Banff 2018 Classification.

BACKGROUND: Polyomavirus nephropathy (PVN) is a rare kidney disease caused by the BK virus, a strain of polyomavirus. The disease primarily affects transplant recipients, which is related to intensive immunosuppression protocol and can lead to kidney allograft failure. OBJECTIVES: The objective of this study is to analyze histopathological features of PVN using the Banff 2018 PVN classification and to determine clinical features and outcomes of patients with PVN in each histologic class. MATERIALS AND METHODS: The study included 44 patients who had been diagnosed with PVN by renal allograft biopsy in a large tertiary care hospital in Thailand from January 2011 to January 2020. The kidney biopsy slides were reviewed for Banff 2018 PVN classification and other histologic features. Patient demographic information, clinical data, and laboratory results were retrospectively collected. RESULTS: Nine (20.45%), 27 (61.36%), and eight (18.18%) cases of PVN were Class I, Class II, and Class III, respectively. The time from transplant to PVN diagnosis for Classes I, II, and III was four, 19, and 33.5 months, respectively. Class III had the worst clinical outcomes in terms of deterioration of allograft function, the lowest rate of resolution, and the highest rate of graft failure. CONCLUSIONS: PVN classification provides prognostic information in renal allograft biopsy. Our study confirmed the validity of the three-tier histologic PVN classification put forward by the Banff Working Group in 2018.

Color Doppler Guided in Early Renal Allograft Biopsy: A Safer and Non-Inferior Technique.

BACKGROUND: This study compared a novel technique for renal allograft biopsy, color Doppler ultrasound-guided biopsy (CDUS-Bx), with routine ultrasound-guided biopsy (RUS-Bx). METHODS: A retrospective review was conducted on 111 patients, with 42 undergoing CDUS-Bx and 69 undergoing RUS-Bx. Urologists used an 18-gauge automatic spring-loaded biopsy needle for all procedures. CDUS-Bx tissue collection was guided by identifying renal vessels with color Doppler mode. RESULTS: Overall, the adequacy rate was 90.1%, with a higher number of glomeruli obtained in the CDUS-Bx group (25.6 ± 10.3 vs. 20.6 ± 11.3, P = .008). Acute tubular necrosis was the most frequent pathological diagnosis, with a higher prevalence in the CDUS-Bx group (69% vs 40.6%). T cell-mediated rejection had a lower incidence in the CDUS-Bx group (4.8% vs 21.7%), and antibody-mediated rejection was comparable between the 2 groups. The most common complication was microscopic hematuria, which was significantly less frequent in the CDUS-Bx group (48.7% vs 70.1%, P = .028), but there was no significant difference in the rate of gross hematuria between CDUS-Bx and RUS-Bx (11.9% vs 11.6%, P = .961). The number of cores was the only predictor of adequate biopsy, with a 93.2% adequacy rate after 3 cores of allograft biopsy. Multivariate analysis revealed that only the guiding type, CDUS-Bx, was associated with less microscopic hematuria (adjusted odds ratio 0.325, P = .018). CONCLUSIONS: Color Doppler ultrasound-guided biopsy had comparable tissue adequacy to RUS-Bx, with a lower incidence of microscopic hematuria. These findings suggest that CDUS-Bx may be a safe and effective alternative to RUS-Bx for allograft biopsy.

Vancomycin Nephrotoxicity Causing Renal Transplant Acute Kidney Injury.

Nephrotoxicity is a rather frequent side effect of vancomycin treatment. Attributes of vancomycin nephrotoxicity (VN) are well documented, including its clinical manifestations and renal morphologic changes. However, VN has not been emphasized as the cause of acute kidney injury (AKI) in the renal transplant setting. We report the first 3 such cases. In each of these cases, AKI developed concurrently with vancomycin treatment and resolved after its cessation. As compared with the general population, VN in the renal transplant setting displayed some unusual clinical behaviors. Its development was rather capricious, being noted in some but not every episode of vancomycin treatment, even in the same individual. AKI developed gradually in conjunction with protracted vancomycin treatment, in contrast to a precipitous course in the nontransplant setting. However, renal transplant biopsies showed typical features of VN in each case. VN is an unusual but now well-documented cause of AKI in renal transplant recipients. VN in this setting may display some atypical features, setting it apart from that in the general population. However, renal transplant biopsy changes are characteristic and are amenable to a definitive diagnosis.

Vancomycin-Associated Tubular Casts and Vancomycin Nephrotoxicity.

INTRODUCTION: Vancomycin nephrotoxicity is frequent and may be due to drug-induced acute tubular necrosis (ATN) or tubulointerstitial nephritis (TIN). Vancomycin-associated tubular cast (VTC) was recently described and may represent a novel cause of vancomycin nephrotoxicity. However, much is still unknown about VTC. MATERIALS AND METHODS: Thirty-seven kidney biopsy specimens from patients who were treated with vancomycin and developed acute kidney injury (AKI) were found among a total of 4673 biopsy samples between 2010 and 2019. These biopsy specimens were subjected to light microscopy, immunofluorescence, electron microscopy, and immunolocalization for vancomycin, uromodulin, myoglobin, tubular segment-specific markers, and examined for VTCs. The findings were correlated with the clinical course. RESULTS: VTCs displayed precipitated vancomycin casts in a background of uromodulin; the casts were limited to the distal tubules, and always associated with a background of more diffuse renal injury (ATN or TIN). The diagnosis of vancomycin nephrotoxicity was made in in 28 of 37 patients. VTC was noted in 25 of 28 biopsy samples from patients diagnosed with vancomycin nephrotoxicity and in one of nine biopsy samples from patients without this diagnosis. Vancomycin nephrotoxicity was diagnosed in 25 of 26 patients whose biopsy specimens showed VTC, but in only 3 of 11 patients without VTC in the biopsy samples. CONCLUSIONS: VTC displays a characteristic morphologic profile amenable to ready recognition in biopsy specimens. It results from coprecipitation of vancomycin and uromodulin. It facilitates the biopsy diagnosis of vancomycin nephrotoxicity. It may have a nephrotoxic effect superimposing on and independent from the ATN or interstitial nephritis in the pathogenesis of vancomycin nephrotoxicity.

18F-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography for preoperative planning in a rare case of hyperfunctional bilateral adrenocortical carcinoma and review of literatures.

Adrenal cortical carcinoma (ACC) is a rare aggressive endocrine tumor with poor prognosis. About 60% of ACC are functional tumors. Bilateral ACC is extremely rare, roughly 2%-10% of cases. Diagnosis and staging of ACC by imaging modalities are crucial for preoperative planning and prognostication. Detection of hyperfunctional bilateral adrenocortical carcinoma by 18F-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography (18F- FDG PET/CT) has never been reported. Herein, we report a male patient who presented with Cushing's syndrome, type II diabetes mellitus due to Cushing's syndrome, and hypogonadism with biopsy confirmed left ACC. He underwent 18F-FDG PET/CT to evaluate the contralateral adrenal mass and to plan for laparoscopic adrenalectomy, which subsequently confirmed bilateral ACC. Furthermore, 18F-FDG PET/CT was useful in staging, which revealed paraaortic lymph node and lung metastasis.

Vancomycin nephrotoxicity: Vancomycin tubular casts with characteristic electron microscopic findings.

We herein report a 46-year-old man with diabetes who developed acute kidney injury and oliguria after receiving vancomycin to treat his foot infection. Renal biopsy revealed typical features of advanced diabetic nephropathy as well as features of acute vancomycin nephrotoxicity. Several changes typical for acute vancomycin nephrotoxicity, but hitherto not adequately described, were seen. There was an element of acute tubulointerstitial injury associated with frequent tubular casts consisting of typical hyaline casts, pale glassy material suggestive of uromodulin, and distinctive features suggestive of vancomycin deposition. Coprecipitation of vancomycin and uromodulin was confirmed by immunostain. Electron microscopic study showed features supportive for the diagnosis of diabetic nephropathy and distinctive concentric appearance of vancomycin tubular casts within the fibrillary background of uromodulin. The patient's renal function improved rapidly after cessation of vancomycin and initiation of steroid therapy, suggesting that vancomycin-associated tubular injury is potentially reversible over time with proper management.