Risk factors for chronic kidney disease following acute kidney injury in pediatric allogeneic hematopoietic cell transplantation

Prasad, Malavika; Jain, Namrata G.; Jin, Zhezhen; Satwani, Prakash

doi:10.1038/s41409-021-01228-7

Cited by 3 publications

(2 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Representative studies that focus on the association of AKI with transplant outcomes are shown in Table 2. In pediatric HCT recipient, the incidence of AKI is similar to adults (44,48,49,(56)(57)(58), AKI worsens mortality after HCT (49,57), and the 1-year survival rate is less than 10% in patients with renal failure requiring renal replacement therapy (56). Fortunately, HCT-related AKI has decreased in recent years due to the increased use of less toxic conditioning regimens, decreased rates of SOS, modified infection prophylaxis, less amphotericin B use, and declining rates of severe aGVHD (59,60).…”

Section: Kidney Disease After Hctmentioning

confidence: 99%

Recent Advances of Acute Kidney Injury in Hematopoietic Cell Transplantation

et al. 2022

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a common complication of allogeneic hematopoietic cell transplantation (allo-HCT) and is associated with non-relapse mortality (NRM) and quality of life (QOL). Multiple factors may contribute to AKI during allo-HCT and are often present at the same time making it difficult to determine the cause of AKI in each patient. Nephrotoxic drugs, infections, thrombotic microangiopathy (TMA), and sinusoidal obstruction syndrome (SOS) are well described causes of AKI during allo-HCT. Acute graft-versus-host disease (aGVHD) is a major complication of allo-HCT that mainly targets the intestines, liver, and skin. However, recent studies suggest aGVHD may also attack the kidney and contribute to AKI following allo-HCT. For example, severe aGVHD is associated with AKI, suggesting a link between the two. In addition, animal models have shown donor immune cell infiltration and increased expression of inflammatory cytokines in recipient kidneys after allo-HCT. Therefore, aGVHD may also target the kidney and contribute to AKI following allo-HCT. Herein, we describe the etiology, diagnosis, risk factors, pathophysiology, prevention, and treatment of renal injury after allo-HCT. In addition, we highlight emerging evidence that aGVHD may contribute to the development of AKI after allo-HCT.

show abstract

Section: Kidney Disease After Hctmentioning

confidence: 99%

Recent Advances of Acute Kidney Injury in Hematopoietic Cell Transplantation

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Estimated GFR at the time of AKI is an important risk factor for the development of CKD. In a cohort of 275 children post allogeneic HCT, CKD developed in 69.5% and 69.8% at 1 and 3 years if GFR was < 80 mL/min/1.73 m 2 at the initial AKI episode [ 66 ]. Therefore, renal function in these higher-risk children who developed AKI with GFR <80 mL/min/1.73 m 2 must be monitored closely for early detection of CKD.…”

Section: Chronic Kidney Diseasementioning

confidence: 99%

Kidney Injury in Children after Hematopoietic Stem Cell Transplant

2023

View full text Add to dashboard Cite

Hematopoietic cell transplant (HCT), used for treatment of many malignant and non-malignant pediatric diseases, is associated with serious complications, limiting this therapy’s benefit. Acute kidney injury (AKI), seen often after HCT, can occur at different stages of the transplant process and contributes to morbidity and mortality after HCT. The etiology of AKI is often multifactorial, including kidney hypoperfusion, nephrotoxicity from immunosuppressive and antimicrobial agents, and other transplant-related complications such as transplant-associated thrombotic microangiopathy and sinusoidal obstructive syndrome. Early recognition of AKI is crucial to prevent further AKI and associated complications. Initial management includes identifying the etiology of AKI, preventing further kidney hypoperfusion, adjusting nephrotoxic medications, and preventing fluid overload. Some patients will require further support with kidney replacement therapy to manage fluid overload and AKI. Biomarkers of AKI, such as neutrophil gelatinase-associated lipocalin can aid in detecting AKI before a rise in serum creatinine, allowing earlier intervention. Long-term kidney dysfunction is also prominent in this population. Therefore, long-term follow-up and monitoring of renal function (glomerular filtration rate, microalbuminuria) is required along with management of hypertension, which can contribute to chronic kidney disease.

show abstract