Acute Kidney Injury in Immunoglobulin A Nephropathy: Potential Role of Macroscopic Hematuria and Acute Tubulointerstitial Injury

2009 ◽  
Vol 13 (4) ◽  
pp. 273-277 ◽  
Author(s):  
Radoslav Kveder ◽  
Jelka Lindič ◽  
Andreja Aleš ◽  
Damjan Kovač ◽  
Alenka Vizjak ◽  
...  
2012 ◽  
Vol 38 (3) ◽  
pp. 467-473 ◽  
Author(s):  
Perrine Hoet ◽  
Vincent Haufroid ◽  
Gladys Deumer ◽  
Xavier Dumont ◽  
Dominique Lison ◽  
...  

Author(s):  
Norbert Lameire

This chapter summarizes the pharmacological interventions that can be used in the prevention of acute kidney injury (AKI). These following interventions are discussed: the use and selection of vasopressors; the administration of loop diuretics and mannitol; vasodilating drugs including dopamine, atrial natriuretic peptide, nesiritide, fenoldopam, and adenosine antagonists. The role of N-acetylcysteine in the prevention of contrast-induced AKI and cardiac surgery is discussed. The chapter concludes with a summary of the potential role of insulin-like growth factor and erythropoietin in the prevention of AKI.


2018 ◽  
Vol 7 (2) ◽  
pp. 198-203 ◽  
Author(s):  
Hiroki Ishii ◽  
Keiji Hirai ◽  
Katsunori Yanai ◽  
Taisuke Kitano ◽  
Mitsutoshi Shindo ◽  
...  

2014 ◽  
Vol 33 (3) ◽  
pp. 139-143 ◽  
Author(s):  
Yu Ho Lee ◽  
Yang-Gyun Kim ◽  
Sang-Ho Lee ◽  
Ju-Young Moon ◽  
Kyung-Hwan Jeong ◽  
...  

2020 ◽  
pp. 4909-4917
Author(s):  
Jonathan Barratt ◽  
John Feehally

Immunoglobulin A nephropathy (IgAN) is the commonest pattern of glomerulonephritis identified in areas of the world where renal biopsy is widely practised. It is defined pathologically by IgA deposition in the glomerular mesangium accompanied by a mesangial proliferative glomerulonephritis which may vary greatly in severity. Aetiology is uncertain, but abnormalities of IgA1 hinge-region O-glycosylation are consistently found. Clinical features—IgAN can present with (1) visible haematuria, typically in children and young adults, developing within a day or two of upper respiratory tract infection (‘synpharyngitic’); (2) asymptomatic nonvisible haematuria/proteinuria; (3) nephrotic syndrome (<5% of cases); (4) acute kidney injury (uncommon); and (5) chronic renal failure with up to 25% of patients reaching endstage renal failure within 20 years of diagnosis. Henoch–Schönlein purpura (HSP) is a small vessel systemic vasculitis characterized by small blood vessel deposition of IgA that predominantly affects the skin, joints, gut, and kidney, with nephritis that may be histologically indistinguishable from IgA nephropathy. Management—there is no treatment known to modify mesangial deposition of IgA. Treatment options are mostly directed at controlling blood pressure and limiting proteinuria through blockade of the renin–angiotensin–aldosterone axis. In the rare patient presenting with acute kidney injury in whom biopsy shows crescentic IgA nephropathy, a regimen such as those used for renal vasculitis and other forms of crescentic glomerulonephritis should be considered, for example, oral prednisolone in combination with cyclophosphamide.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shinya Taguchi ◽  
Sumi Hidaka ◽  
Mitsuru Yanai ◽  
Kunihiro Ishioka ◽  
Kenji Matsui ◽  
...  

Abstract Background Macroscopic hematuria-associated acute kidney injury (AKI) is a well-known complication of immunoglobulin A (IgA) nephropathy. In such cases, intratubular obstruction by red blood cell (RBC) casts and acute tubular necrosis are mainly observed pathologically. Herein, we report the case of a patient with IgA nephropathy presenting with AKI following an episode of macrohematuria. The patient presented with severe renal tubular hemosiderosis and acute tubular necrosis and without any obvious obstructive RBC casts. Case presentation A 68-year-old woman, who was diagnosed with IgA nephropathy on renal biopsy 6 years ago, was admitted to our hospital after an episode of macroscopic glomerular hematuria and AKI following upper respiratory tract infection. Renal biopsy showed mesangial proliferation of the glomeruli, including crescent formation in 17 % of the glomeruli, and acute tubular necrosis without obvious hemorrhage or obstructive RBC casts. The application of Perls’ Prussian blue stain showed hemosiderin deposition in the renal proximal tubular cells. Immunofluorescence showed granular mesangial deposits of IgA and C3. Based on these findings, she was diagnosed with acute tubular necrosis with a concurrent IgA nephropathy flare-up. Moreover, direct tubular injury by heme and iron was considered to be the cause of AKI. She was treated with intravenous pulse methylprednisolone followed by oral prednisolone. Thereafter, the gross hematuria gradually faded, and her serum creatinine levels decreased. Conclusions IgA nephropathy presenting with acute kidney injury accompanied by macrohematuria may cause renal hemosiderosis and acute tubular necrosis without obstructive RBC casts. Hemosiderosis may be a useful indicator for determining the pathophysiology of macroscopic hematuria-associated AKI. However, renal hemosiderosis may remain undiagnosed. Thus, Perls’ Prussian blue iron staining should be more widely used in patients presenting with hematuria.


2018 ◽  
Vol 31 (3) ◽  
pp. 321-323 ◽  
Author(s):  
Laurie Jansky ◽  
Pallavi Mukkamala ◽  
Deborah Jebakumar ◽  
Arundhati Rao ◽  
Tove M. Goldson ◽  
...  

2021 ◽  
Vol 7 ◽  
Author(s):  
Spyridon Graidis ◽  
Theodosios S. Papavramidis ◽  
Maria Papaioannou

Background: Acute kidney injury (AKI) constitutes a multi-factorially caused condition, which significantly affects kidney function and can lead to elevated risk of morbidity and mortality. Given the rising scientific evidence regarding vitamin D's (VitD's) multisystemic role, the connection between AKI and VitD is currently being studied, and the complex relation between them has started to be unraveled.Methods: A systematic review had been conducted to identify the pathogenetic relation of VitD and AKI and the potential role of VitD as a biomarker and therapeutic–renoprotective factor.Results: From 792 articles, 74 articles were identified that fulfilled the inclusion criteria. Based on these articles, it has been found that not only can VitD disorders (VitD deficiency or toxicity) cause AKI but, also, AKI can lead to great disruption in the metabolism of VitD. Moreover, it has been found that VitD serves as a novel biomarker for prediction of the risk of developing AKI and for the prognosis of AKI's severity. Finally, animal models showed that VitD can both ameliorate AKI and prevent its onset, suggesting its renoprotective effect.Conclusion: There is a complex two-way pathogenetic relation between VitD disorders and AKI, while, concomitantly, VitD serves as a potential novel predictive–prognostic biomarker and a treatment agent in AKI therapy.


Nephron ◽  
2017 ◽  
Vol 137 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Meric Oruc ◽  
Haydar Durak ◽  
Serkan Feyyaz Yalin ◽  
Nurhan Seyahi ◽  
Mehmet Rıza Altıparmak ◽  
...  

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