scholarly journals Acute Kidney Injury Following Exposure to Calcineurin Inhibitors in a Patient with Idiopathic Membranous Nephropathy

2019 ◽  
Vol 6 (1) ◽  
Author(s):  
Maciej Goździk ◽  
Agnieszka Płuciennik ◽  
Anna Zawiasa-Bryszewska ◽  
Maja Nowicka ◽  
Zuzanna Nowicka ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Membranous Nephropathy ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Idiopathic Membranous Nephropathy

scholarly journals Acute kidney injury in idiopathic membranous nephropathy with nephrotic syndrome

Renal Failure ◽  
2021 ◽  
Vol 43 (1) ◽  
pp. 1004-1011
Author(s):  
Tianxin Chen ◽  
Ying Zhou ◽  
Xinxin Chen ◽  
Bo Chen ◽  
Jingye Pan
Keyword(s):  
Acute Kidney Injury ◽  
Nephrotic Syndrome ◽  
Membranous Nephropathy ◽  
Kidney Injury ◽  
Idiopathic Membranous Nephropathy

Serial Quantification of Urinary Protein Biomarkers to Predict Drug-induced Acute Kidney Injury

2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
Author(s):  
Yi Da ◽  
K. Akalya ◽  
Tanusya Murali ◽  
Anantharaman Vathsala ◽  
Chuen-Seng Tan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cystatin C ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Protein Biomarkers ◽  
Drug Induced ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.

scholarly journals Thrombotic thrombocytopenic purpura developed during the conservative treatment of anti-phospholipase A2 receptor antibody-positive idiopathic membranous nephropathy: a case report

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Rei Iio ◽  
Shin’ichi Akiyama ◽  
Kensuke Mitsumoto ◽  
Yukimasa Iwata ◽  
Hiroki Okushima ◽  
...  
Keyword(s):  
Conservative Treatment ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Hemolytic Anemia ◽  
Membranous Nephropathy ◽  
Kidney Injury ◽  
Idiopathic Membranous Nephropathy ◽  
Thrombocytopenic Purpura ◽  
Disturbance Of Consciousness ◽  
Phospholipase A2 Receptor ◽  
Adamts13 Deficiency

Abstract Background Idiopathic membranous nephropathy (MN) is one of the major glomerulonephritis that cause nephrotic syndrome. The phospholipase A2 receptor (PLA2R) has recently been identified as an endogenous antigen of idiopathic MN. Thrombotic thrombocytopenic purpura (TTP) is a disorder characterized by schistocytes, hemolytic anemia, thrombocytopenia, and organ dysfunction which occurs as a result of thrombi. Patients with acquired TTP have autoantibodies against a disintegrin and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13). These autoantibodies act as an inhibitor and cause ADAMTS13 deficiency. Idiopathic MN and acquired TTP are usually considered as independent autoimmune diseases. We experienced a patient who developed TTP during the conservative treatment of idiopathic MN, with the coexistence of ADAMTS13 inhibitor and anti-PLA2R antibody. Case presentation A 73-year-old man presented with thrombocytopenia, hemolytic anemia, disturbance of consciousness, and acute kidney injury after 4-year course of biopsy-proven idiopathic MN. ADAMTS13 activity was undetectable and the ADAMTS13 inhibitor was identified. Additionally, he was positive for anti-PLA2R antibody. The patient did not have any diseases that could cause secondary thrombotic microangiopathy, and he was diagnosed with acquired TTP. Steroid therapy and plasma exchange were initiated and the acquired TTP resolved. MN achieved remission 3 months after the anti-PLA2R antibody disappeared. Conclusions This is the first reported case of acquired TTP developed during conservative treatment of idiopathic MN, with both ADAMTS13 inhibitor and anti-PLA2R antibody positive at the onset of the TTP. The present case suggests that idiopathic MN might be associated with the development of some cases of acquired TTP.

scholarly journals ACUTE TACROLIMUS-INDUCED KIDNEY INSUFFICIENCY IN PATIENT AFTER HEART TRANSPLANTATION

2016 ◽  
Vol 18 (1) ◽  
pp. 53-57
Author(s):  
D. V. Doronin ◽  
A. M. Chernyavskiy ◽  
A. V. Fomichev ◽  
M. N. Deryagin ◽  
V. N. Gorbatykh
Keyword(s):  
Acute Kidney Injury ◽  
Side Effects ◽  
Heart Transplantation ◽  
Immunosuppressive Therapy ◽  
Clinical Case ◽  
Standard Dose ◽  
Transplant Rejection ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Kidney Insufficiency

In recent years the success of transplantation is associated primarily with extensive use of calcineurin inhibitors (CNIs) – cyclosporine and tacrolimus which became the basis of the various immunosuppressive therapy protocols. These drugs despite their effectiveness in the prevention of transplant rejection have serious side effects. Nephrosclerosis due to chronic nephrotoxic effect is recognized as the most important of them. But along with chronic nephrotoxic effects there are cases of acute kidney injury on the background of calcineurin inhibitors usage. The article presents a clinical case demonstrating the development of severe reversible nephropathy in a patient after heart transplantation receiving tacrolimus in standard dose.

Subtoxic doses of calcineurin inhibitors induce predisposition to acute kidney injury

2015 ◽  
Vol 238 (2) ◽  
pp. S258
Author(s):  
M. Prieto ◽  
A.G. Casanova ◽  
M.T. Hernández-Sánchez ◽  
L. Vicente-Vicente ◽  
M. Pescador ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Calcineurin Inhibitors ◽  
Kidney Injury

scholarly journals Urinary Matrix Metalloproteinase-9 and Nephrin in Idiopathic Membranous Nephropathy: A Cross-Sectional Study

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Akankwasa Gilbert ◽  
An Changjuan ◽  
Cheng Guixue ◽  
Liu Jianhua ◽  
Qin Xiaosong
Keyword(s):  
Matrix Metalloproteinase ◽  
Membranous Nephropathy ◽  
Healthy Subjects ◽  
Kidney Injury ◽  
Matrix Metalloproteinase 9 ◽  
Idiopathic Membranous Nephropathy ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cross Sectional ◽  
Glomerular Diseases ◽  
Metalloproteinase 9

Aim. Idiopathic membranous nephropathy (IMN) has a varied clinical course that requires accurate prediction as a prerequisite for treatment administration. Currently, its prognosis relies on proteinuria, a clinical parameter whose onset lags behind kidney injury. Increased urinary excretion of matrix metalloproteinase-9 (MMP-9) and nephrin has been reported in a number of IMN-like glomerular diseases in which they reflected disease severity. However, little or nothing is known of the importance of these biomarkers in IMN, a major cause of adult nephrotic syndrome. To highlight their potential, we measured both biomarkers and assessed their relationships with key parameters of renal function in IMN. Methods. We quantified urinary MMP-9 and nephrin in 107 biopsy-proven IMN patients and 70 healthy subjects by enzyme-linked immunosorbent assay (ELISA). We then compared biomarker levels between patients and healthy subjects and among patients with different clinical features. We also determined the relationship of each biomarker with proteinuria and the estimated glomerular filtration rate (eGFR). Results. Urinary MMP-9 and nephrin were significantly higher in IMN compared to healthy controls. Unlike nephrin, MMP-9 correlated significantly with proteinuria and was significantly higher among patients with nephrotic range proteinuria. Both biomarkers were correlated with eGFR, but only MMP-9 was significantly higher in patients with eGFR less than 90 ml/min/1.73 m2. Conclusion. Our findings suggest that urinary MMP-9 holds a greater potential than urinary nephrin in monitoring the severity of IMN.

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