New Ultrasound Techniques Promise Further Advances in AKI and CKD

Abstract

AKI and CKD are important clinical problems because they affect many patients and the associated diagnostic and treatment paradigms are imperfect. Ultrasound is a cost-effective, noninvasive, and simple imaging modality that offers a multitude of means to improve the diagnosis, monitoring, and treatment of both AKI and CKD, especially considering recent advances in this technique. Ultrasound alone can attenuate AKI and prevent CKD by stimulating the splenic cholinergic anti-inflammatory pathway. Additionally, microbubble contrast agents are improving the sensitivity and specificity of ultrasound for diagnosing kidney disease, especially when these agents are conjugated to ligand-specific mAbs or peptides, which make the dynamic assessment of disease progression and response to treatment possible. More recently, drug-loaded microbubbles have been developed and the load release by ultrasound exposure has been shown to be a highly specific treatment modality, making the potential applications of ultrasound even more promising. This review focuses on the multiple strategies for using ultrasound with and without microbubble technology for enhancing our understanding of the pathophysiology of AKI and CKD.

Keywords: acute kidney injury; chronic kidney disease; ultrasound.

Figure 1.

Targeted MBs for the diagnosis and monitoring of AKI and its progression. (A) Schematic representation of MB contrast agent and a targeting strategy using an mAb. MBs comprise a gas core surrounded by a lipid shell, which can be targeted to specific anatomic compartments or disease-specific antigens by conjugation to an mAb, such as anti–P-selectin, which is upregulated in the vasculature after injury. (B) Grayscale renal US image overlaid with molecular US signal color-coded image of P-selectin–targeted MBs injected before or after 4 or 24 hours of IRI in rats. Note significant signal enhancement at 4 hours, concomitant with renal tissue inflammation, followed by subsequent signal reduction at 24 hours secondary to recovery from the short ischemic conditions. Anti–P-selectin antibody is targeted to areas of vascular activation, such as those which occur after AKI. Modified from reference , with permission.