Peyronie Disease Caused by Beta-Blocker; Cushing Syndrome Ascribed to High-Dose Topical Corticosteroids; Two Reports of Adverse Drug Reactions Caused by Long-Acting Risperidone Injections; Spontaneous Hematoma Associated with Diclofenac; Bevacizumab-Associated Osteonecrosis of the Jaw; Varenicline-Associated Acute Renal Failure

2009 ◽  
Vol 44 (2) ◽  
pp. 114-117
Author(s):  
Joel Shuster
1971 ◽  
Vol 106 (5) ◽  
pp. 619-621 ◽  
Author(s):  
P.J. Dudzinski ◽  
A.F. Petrone ◽  
M. Persoff ◽  
E.E. Callaghan

Renal Failure ◽  
1995 ◽  
Vol 17 (4) ◽  
pp. 475-478 ◽  
Author(s):  
Shawn J. Marsh ◽  
George M. Dolson

2007 ◽  
Vol 293 (4) ◽  
pp. F994-F1006 ◽  
Author(s):  
Midhun C. Korrapati ◽  
Jaya Chilakapati ◽  
Frank A. Witzmann ◽  
Chundury Rao ◽  
Edward A. Lock ◽  
...  

Previous studies (Vaidya VS, Shankar K, Lock EA, Bucci TJ, Mehendale HM. Toxicol Sci 74: 215–227, 2003; Korrapati MC, Lock EA, Mehendale HM. Am J Physiol Renal Physiol 289: F175–F185, 2005; Korrapati MC, Chilakapati J, Lock EA, Latendresse JR, Warbritton A, Mehendale HM. Am J Physiol Renal Physiol 291: F439–F455, 2006) demonstrated that renal repair stimulated by a low dose of S-(1,2-dichlorovinyl)l-cysteine (DCVC; 15 mg/kg ip) 72 h before administration of a normally lethal dose (75 mg/kg ip) protects mice from acute renal failure (ARF) and death (autoprotection). The present study identified the proteins indicative of DCVC-induced ARF and autoprotection in male Swiss Webster mice. Renal dysfunction and injury were assessed by plasma creatinine and histopathology, respectively. Whole-kidney homogenates were run on two-dimensional gel electrophoresis gels, and the expression of 18 common proteins was maximally changed (≥10-fold) in all the treatment groups and they were conclusively identified by liquid chromatography tandem mass spectrometry. These proteins were mildly downregulated after low dose alone and in autoprotected mice in contrast to severe downregulation with high dose alone. Glucose-regulated protein 75 and proteasome α-subunit type 1 were further investigated by immunohistochemistry for their localization in the kidneys of all the groups. These proteins were substantially higher in the proximal convoluted tubular epithelial cells in the low-dose and autoprotected groups compared with high-dose alone group. Proteins involved in energetics were downregulated in all the three groups of mice, leading to a compromise in cellular energy. However, energy is recovered completely in low-dose and autoprotected mice. This study provides the first report on proteomics of DCVC-induced ARF and autoprotection in mice and reflects the application of proteomics in mechanistic studies as well as biomarker development in a variety of toxicological paradigms.


2005 ◽  
Vol 60 (9) ◽  
pp. 1147-1151 ◽  
Author(s):  
A. Corsonello ◽  
C. Pedone ◽  
F. Corica ◽  
B. Mazzei ◽  
A. Di Iorio ◽  
...  

1995 ◽  
Vol 21 (3) ◽  
pp. 288-289 ◽  
Author(s):  
B. Veber ◽  
I. Mohammedi ◽  
B. Gachot ◽  
J. P. Bédos ◽  
M. Wolff

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 5499-5499
Author(s):  
Shin Yin Lee ◽  
Robert Meehan ◽  
John Mark Sloan ◽  
Karen Quillen ◽  
Dina Brauneis ◽  
...  

Abstract Background: High-dose melphalan with autologous peripheral blood stem cell transplantation (HDM/SCT) has been shown to extend survival as well as to induce hematologic and clinical responses in selected patients with light chain (AL) amyloidosis. The most frequent toxicities of HDM are profound myelosuppression and gastrointestinal (GI) side effects. Studies have shown that 80% of melphalan is bound to plasma proteins (60% albumin bound) with ~20% free. We hypothesized that AL amyloidosis patients with severe nephrotic syndrome and profound hypoalbuminemia might have greater free melphalan fraction and more treatment-related toxicity. Methods: Patients with AL amyloidosis treated with HDM/SCT between 2011 and 2014 with severe hypoalbuminemia (SH), defined as a pre-transplant serum albumin of ≤2g/dL, were studied retrospectively. The stem cell transplant database was queried for patient demographic information, pre-transplant albumin level, HDM dose, renal function, pre-transplant 24-hour urine protein level, time to neutrophil and platelet engraftment, and treatment-related complications. Patients with AL amyloidosis treated between 2011 and 2012 without severe hypoalbuminemia, defined as serum albumin level of > 2g/dL (WSH), served as a control group. Results: Of the 84 patients with AL amyloidosis treated with HDM/SCT in this 4 year period, 16 (19%) with SH were identified. 41 patients were identified in the control group (WSH). There was no difference in the proportion of patients with all non-hematologic grade 3 or 4 adverse events between the groups. All patients suffered from expected grade 4 myelosuppression. The only statistically different non-hematologic grade 4 toxicity in SH was acute renal failure requiring temporary hemodialysis (n=4/16, 25% SH vs n=2/41, 5% WSH; p=0.05), with 1 subject eventually needing long term dialysis. There were no grade 4 mucositis or GI toxicities in either groups. The only statistically different grade 3 non-hematologic toxicity was lightheadedness (n=3/16, 19% SH vs n=0/41, 0% WSH; p=0.02). Conclusion: These data suggest that patients with severe hypoalbuminemia do not have more prolonged myelosuppression or GI toxicities when treated with HDM/SCT compared to those with higher serum albumin levels in AL amyloidosis. Grade 4 renal toxicity with acute renal failure requiring temporary hemodialysis (p=0.05) and grade 3 lightheadedness (p=0.02) occurred more commonly in SH than WSH group. In this retrospective study, we did not measure free melphalan concentrations in the blood. However, these data suggest that patients with severe hypoalbuminemia do not require adjustment of melphalan dosing. Figure 1. Figure 1. Disclosures No relevant conflicts of interest to declare.


2001 ◽  
Vol 47 (6) ◽  
pp. 537-540 ◽  
Author(s):  
Desirée van den Bongard ◽  
Ron Mathôt ◽  
Willem Boogerd ◽  
Jan Schornagel ◽  
Marcel Soesan ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document