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13 pages, 303 KiB

Open AccessReview

Acute Kidney Injury (AKI) before and after Kidney Transplantation: Causes, Medical Approach, and Implications for the Long-Term Outcomes

by Alessandra Palmisano, Ilaria Gandolfini, Marco Delsante, Chiara Cantarelli, Enrico Fiaccadori, Paolo Cravedi and Umberto Maggiore

J. Clin. Med. 2021, 10(7), 1484; https://doi.org/10.3390/jcm10071484 - 2 Apr 2021

Cited by 25 | Viewed by 5416

Abstract

Acute kidney injury (AKI) is a common finding in kidney donors and recipients. AKI in kidney donor, which increases the risk of delayed graft function (DGF), may not by itself jeopardize the short- and long-term outcome of transplantation. However, some forms of AKI may induce graft rejection, fibrosis, and eventually graft dysfunction. Therefore, various strategies have been proposed to identify conditions at highest risk of AKI-induced DGF, that can be treated by targeting the donor, the recipient, or even the graft itself with the use of perfusion machines. AKI that occurs early post-transplant after a period of initial recovery of graft function may reflect serious and often occult systemic complications that may require prompt intervention to prevent graft loss. AKI that develops long after transplantation is often related to nephrotoxic drug reactions. In symptomatic patients, AKI is usually associated with various systemic medical complications and could represent a risk of mortality. Electronic systems have been developed to alert transplant physicians that AKI has occurred in a transplant recipient during long-term outpatient follow-up. Herein, we will review most recent understandings of pathophysiology, diagnosis, therapeutic approach, and short- and long-term consequences of AKI occurring in both the donor and in the kidney transplant recipient. Full article

(This article belongs to the Special Issue New Pathogenetic Mechanisms and Therapeutic Challenges in Acute Kidney Injury)

18 pages, 337 KiB

Open AccessReview

COVID-19 and the Kidney: A Worrisome Scenario of Acute and Chronic Consequences

by Luis Sanchez-Russo, Marzuq Billah, Jorge Chancay, Judy Hindi and Paolo Cravedi

J. Clin. Med. 2021, 10(5), 900; https://doi.org/10.3390/jcm10050900 - 25 Feb 2021

Cited by 7 | Viewed by 3032

Abstract

Acute kidney injury (AKI) is a common finding in patients with coronavirus disease 2019 (COVID-19) and has been associated with higher rates of death when compared to COVID-19 patients without kidney injury. Whereas the definitive pathogenesis of COVID-19-related AKI (CoV-AKI) is not clear, histopathologic evidence seems to point at multiple etiologies for the disease, including indirect and direct viral kidney injury. The high incidence of CoV-AKI, along with the aggressive clinical presentation of this entity, have increased the demands for kidney replacement therapies, rapidly overwhelming the supplies of healthcare systems even in major tertiary care centers. As a result, nephrologists have come up with alternatives to maximize the efficiency of treatments and have developed non-conventional therapeutic alternatives such as the implementation of acute peritoneal dialysis for critically ill patients. The long-term implications of CoV-AKI are yet unknown, though early studies suggest that around one third of the patients who survive will remain dependent on kidney replacement therapy. Nephrologists and healthcare workers need to be familiar with the clinical presentation and therapeutic challenges of CoV-AKI in order to develop strategies to mitigate the burden of the disease for patients, and for services providing kidney replacement therapies. Full article

(This article belongs to the Special Issue New Pathogenetic Mechanisms and Therapeutic Challenges in Acute Kidney Injury)

21 pages, 1038 KiB

Open AccessReview

Review: Ischemia Reperfusion Injury—A Translational Perspective in Organ Transplantation

by André Renaldo Fernández, Rodrigo Sánchez-Tarjuelo, Paolo Cravedi, Jordi Ochando and Marcos López-Hoyos

Int. J. Mol. Sci. 2020, 21(22), 8549; https://doi.org/10.3390/ijms21228549 - 13 Nov 2020

Cited by 87 | Viewed by 8455

Abstract

Thanks to the development of new, more potent and selective immunosuppressive drugs together with advances in surgical techniques, organ transplantation has emerged from an experimental surgery over fifty years ago to being the treatment of choice for many end-stage organ diseases, with over 139,000 organ transplants performed worldwide in 2019. Inherent to the transplantation procedure is the fact that the donor organ is subjected to blood flow cessation and ischemia during harvesting, which is followed by preservation and reperfusion of the organ once transplanted into the recipient. Consequently, ischemia/reperfusion induces a significant injury to the graft with activation of the immune response in the recipient and deleterious effect on the graft. The purpose of this review is to discuss and shed new light on the pathways involved in ischemia/reperfusion injury (IRI) that act at different stages during the donation process, surgery, and immediate post-transplant period. Here, we present strategies that combine various treatments targeted at different mechanistic pathways during several time points to prevent graft loss secondary to the inflammation caused by IRI. Full article

(This article belongs to the Special Issue Molecular Aspects of Renal Immunology: Current Status and Future Perspectives)

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15 pages, 1244 KiB

Open AccessReview

Complement and Complement Targeting Therapies in Glomerular Diseases

by Sofia Andrighetto, Jeremy Leventhal, Gianluigi Zaza and Paolo Cravedi

Int. J. Mol. Sci. 2019, 20(24), 6336; https://doi.org/10.3390/ijms20246336 - 16 Dec 2019

Cited by 22 | Viewed by 7421

Abstract

The complement cascade is part of the innate immune system whose actions protect hosts from pathogens. Recent research shows complement involvement in a wide spectrum of renal disease pathogenesis including antibody-related glomerulopathies and non-antibody-mediated kidney diseases, such as C3 glomerular disease, atypical hemolytic uremic syndrome, and focal segmental glomerulosclerosis. A pivotal role in renal pathogenesis makes targeting complement activation an attractive therapeutic strategy. Over the last decade, a growing number of anti-complement agents have been developed; some are approved for clinical use and many others are in the pipeline. Herein, we review the pathways of complement activation and regulation, illustrate its role instigating or amplifying glomerular injury, and discuss the most promising novel complement-targeting therapies. Full article

(This article belongs to the Special Issue Rare Kidney Diseases: New Translational Research Approach to Improve Diagnosis and Therapy)

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9 pages, 86 KiB

Open AccessArticle

Spironolactone Plus Full-Dose ACE Inhibition in Patients with Idiopathic Membranous Nephropathy and Nephrotic Syndrome: Does It Really Work?

by Paolo Cravedi, Varusca Brusegan, Piero Ruggenenti, Ruth Campbell and Giuseppe Remuzzi

Pharmaceuticals 2010, 3(1), 1-9; https://doi.org/10.3390/ph3010001 - 5 Jan 2010

Cited by 10 | Viewed by 12533

Abstract

We have studied the effects of add-on spironolactone treatment (100 mg/day) in 11 patients with idiopathic membranous nephropathy (IMN) and > 3 gm proteinuria/day despite angiotensin converting enzyme (ACE) inhibitor therapy titrated to a systolic/diastolic blood pressure < 120/80 mmHg. Blood pressure, 24-hour urinary protein excretion, and creatinine clearance were measured prior to, after two months of combined therapy, and after a 2-month withdrawal period of spironolactone. While systolic and diastolic blood pressure decreased significantly after spironolactone therapy, proteinuria did not improve. Serum potassium increased significantly as well, with three patients requiring resin-binding therapy. Thus, spironolactone seems to have no additional antiproteinuric effects over ACE inhibitor therapy in patients with IMN and nephrotic syndrome and carries the risk of significant hyperkalemia. Full article

(This article belongs to the Special Issue Antihypertensive Drugs)

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