Acute kidney injury (AKI) is a clinical syndrome caused by a multitude of hemodynamic, toxic, and structural insults to the kidney, and portends worse patient outcomes. Despite careful history taking, physical examination, and analysis of laboratory data, a void is evident in the diagnostic process and clinical monitoring of AKI. Point-of-care ultrasonography (POCUS) is a limited ultrasound study performed by the clinician at bedside as an adjunct to physical examination. Growing body of evidence points to POCUS as a powerful tool in a variety of clinical settings. Herein, we discuss how nephrologist-performed POCUS has the potential to provide answers to focused questions that we encounter in diagnosis and management of patients with AKI. From excluding hydronephrosis to providing real-time insights into hemodynamics, incorporation of POCUS helps integrate all the pieces of patient data and formulate individualized treatment plans. Future studies are needed to evaluate the impact of multi-organ POCUS on AKI-related pragmatic patient outcomes, the potential of this technique to stratify the risk and to identify patients with different levels of severity of AKI and different pathophysiological signatures.

Point-of-care ultrasonography (POCUS) is a limited bedside ultrasound (US) examination performed by the clinician to answer focused clinical questions and guide patient management. Once confined to procedural guidance, the utility of diagnostic POCUS is being increasingly recognized in the field of nephrology as an adjunct to physical examination [1, 2]. In fact, some institutions have formally integrated POCUS training into their nephrology fellowship curricula [3]. While the role of POCUS has been discussed in a variety of clinical settings, its role in acute kidney injury (AKI) remains less well explored.

AKI is frequently encountered in hospitalized patients and is a clinical manifestation of several pathophysiologic processes that acutely affect the renal function [4]. It is associated with high mortality rates ranging from 16 to 50% depending on the severity, etiology, comorbidity burden, as well as socioeconomic factors [5, 6], which underscores the importance of timely diagnosis and appropriate treatment. The etiology of AKI can be broadly divided into hemodynamic causes (i.e., impaired renal perfusion), obstruction of the urinary tract, and intrinsic renal diseases including glomerulonephritis and tubulointerstitial pathology. This classification is rather simplistic; in clinical practice, multiple pathologies can coexist, and syndrome-based nomenclature might be more suitable such as cardiorenal, hepatorenal, hepatocardiorenal, and sepsis-associated AKI depending on the context [7, 8]. In patients presenting with AKI, urinary tract obstruction must be excluded as a readily treatable etiology. As such, a renal sonogram is often obtained as a part of initial diagnostic work up to rule out hydronephrosis. POCUS allows this binary yes-or-no question to be answered within minutes. Moreover, having first-hand knowledge of the patient’s history and clinical course is an added advantage for the clinician compared to a radiologist. In one study, general internist-performed POCUS had a sensitivity of 90% and specificity of 96% for detection of hydronephrosis [9]. Similarly, bladder-related causes of obstruction such as blocked Foley catheter, stone, mass, and prostatomegaly can be identified at the bedside by nephrologist using ultrasonography [10].

The utility of POCUS in discerning the cause of intrinsic AKI is limited. Parameters such as cortical echogenicity, kidney size, and arterial resistive index (RI) are useful when interpreted in the right clinical context but are nonspecific [11]. For example, enlarged kidneys with preserved parenchymal thickness and altered cortical echogenicity may prompt the nephrologist to pursue work up for infiltrative diseases such as amyloidosis and malignancy although these findings are not diagnostic per se [10, 12]. On the other hand, in instances where baseline serum creatinine is not available, the likelihood of treatable disease can be deemed low if the kidney size is small and cortical echogenicity is increased [13].

In our opinion, hemodynamic AKI is where nephrologist-performed POCUS could prove the most helpful. This type of AKI encompasses various insults that result in renal hypoperfusion (e.g., hypovolemia, systemic vasodilatation, and increased intra-abdominal pressure) and renal venous congestion. It must be noted that renal perfusion is determined by the difference between forward flow/mean arterial pressure and venous outflow/right atrial pressure (RAP). However, clinical assessment had traditionally revolved around the adequacy of forward flow, ignoring the deleterious effect of venous congestion/iatrogenic fluid overload on the kidney. Accumulating data, however, suggests that fluid overload portends worse outcomes [14]. Adding to the problem, the diagnostic accuracy of conventional physical examination findings is often limited for detecting clinically significant aberrations in fluid status [1]. Multi-organ POCUS aids in the objective volume status assessment by facilitating comprehensive evaluation of the hemodynamic circuit at the bedside. This involves Pump, Pipes, and Leaks approach where pump represents focused cardiac US (FoCUS), pipes represent inferior vena cava (IVC) US and Doppler evaluation of the systemic veins, and the leaks indicate assessment of extravascular lung water and ascites [15]. In other words, one can assess the forward arterial inflow, venous outflow, as well as tissue congestion, and instantaneously integrate this data with overall clinical picture to formulate an individualized management plan for the patient. For instance, in a patient suspected to have hepatorenal syndrome, there is no reason to administer intravenous albumin if the lung US demonstrates congestion, RAP is elevated, or FoCUS reveals high cardiac output indicating a vasodilatory state rather than volume depletion [16]. FoCUS also allows detection of abnormalities such as cardiac chamber enlargement, gross valvular dysfunction, and pericardial effusion prompting appropriate intervention and/or specialist consultation. Further, POCUS may provide clues to raised intra-abdominal pressure by revealing large ascites, bowel obstruction or gaseous distension, small IVC discordant with internal jugular vein, and diminished hepatic vein flow. Figure 1 illustrates the common sonographic findings and parameters used in the evaluation of AKI.

Fig. 1.

Common sonographic parameters and findings assessed using POCUS in AKI. Red and blue arrows indicate blood blow; yellow arrows indicate backward transmission of cardiac pressures. Illustration made using Biorender®. IVC, inferior vena cava; IJV, internal jugular vein; US, ultrasound.

Fig. 1.

Common sonographic parameters and findings assessed using POCUS in AKI. Red and blue arrows indicate blood blow; yellow arrows indicate backward transmission of cardiac pressures. Illustration made using Biorender®. IVC, inferior vena cava; IJV, internal jugular vein; US, ultrasound.

Close modal

In addition, serial POCUS examinations can aid in assessing the efficacy and adequacy of therapy. For example, in a patient with hypovolemic AKI and/or hyponatremia, bedside stroke volume assessment can be used to monitor improvement in hemodynamics along with laboratory data [17]. In a recent case series, Argaiz et al. [18] showed that portal vein pulsatility improves in parallel with serum creatinine with decongestive therapy in patients with acute heart failure outperforming isolated IVC US. In fact, severe flow alterations on hepatic, portal, and renal parenchymal venous Doppler (VExUS) together with a dilated IVC have shown to predict congestive kidney injury better than IVC alone [19]. Figure 2 illustrates a case of AKI and hyponatremia where serial monitoring of venous waveforms as a part of daily clinical examination showed consistent improvement with diuretic therapy. This patient neither had pedal edema nor obvious jugular venous distention; thought to be hypovolemic prior to POCUS, and he was found with elevated RAP and severe venous congestion (top panel). Of note, the patient had heart failure with reduced ejection fraction and the IVC was chronically dilated, which renders isolated use of this parameter inadequate for follow-up.

Fig. 2.

Doppler venous waveforms demonstrating improvement (from top to bottom) in a patient with AKI and hyponatremia. In physiologic state, hepatic vein Doppler resembles central venous trace, and S-wave is larger than the D-wave. As the RAP increases, S-wave reduces in amplitude and finally reverses leaving only D-wave below the baseline. Portal vein is normally continuous (<30% pulsatile) and the pulsatility increases with increasing RAP eventually with late-systolic flow reversal (below-the-baseline flow). Pulsatile portal vein might indicate gut congestion, which potentially influences diuretic absorption. Renal parenchymal vein is normally continuous (similar to portal but below-the-baseline) and with increasing RAP, becomes pulsatile with distinct S- and D-waves, with S-reversal ultimately like that of hepatic vein. Generally, improvement in portal vein precedes that of hepatic and renal veins as seen above. Renal interstitial edema may delay the recovery of venous waveform. Na, serum sodium; AP, assessment and plan; S-wave, systolic wave; D-wave, diastolic wave.

Fig. 2.

Doppler venous waveforms demonstrating improvement (from top to bottom) in a patient with AKI and hyponatremia. In physiologic state, hepatic vein Doppler resembles central venous trace, and S-wave is larger than the D-wave. As the RAP increases, S-wave reduces in amplitude and finally reverses leaving only D-wave below the baseline. Portal vein is normally continuous (<30% pulsatile) and the pulsatility increases with increasing RAP eventually with late-systolic flow reversal (below-the-baseline flow). Pulsatile portal vein might indicate gut congestion, which potentially influences diuretic absorption. Renal parenchymal vein is normally continuous (similar to portal but below-the-baseline) and with increasing RAP, becomes pulsatile with distinct S- and D-waves, with S-reversal ultimately like that of hepatic vein. Generally, improvement in portal vein precedes that of hepatic and renal veins as seen above. Renal interstitial edema may delay the recovery of venous waveform. Na, serum sodium; AP, assessment and plan; S-wave, systolic wave; D-wave, diastolic wave.

Close modal

Conceptually, measuring intrarenal arterial RI is an attractive means to assess renal perfusion, which has been studied in multiple clinical scenarios including heart failure, septic shock, and hepatorenal syndrome demonstrating some usefulness [20-23]. It is calculated by the formula (peak systolic velocity – end diastolic velocity)/peak systolic velocity in a given cardiac cycle. However, RI is influenced by several variables including pulse pressure, heart rate, arteriosclerosis, vasoconstriction, venous congestion, underlying chronic kidney disease, valvular diseases such as aortic stenosis as well as drugs limiting its utility in the point-of-care settings [24]. Moreover, in our experience, the inter- and intra-operator variability in reporting RI is high precluding reliable monitoring of response to therapeutic intervention. On the other hand, we find intrarenal venous Doppler more reliable and technically easier due to its qualitative nature i.e., waveform analysis without the need for precise measurements. Venous congestion could very well be the explanation for elevated RI in patients with volume overload as it increases the resistance to flow. Interestingly enough, RAP has shown to be a strong independent determinant of RI in patients with shock [25]. Finally, even when a patient has acute tubular necrosis diagnosed by urine sediment analysis, it would be prudent to identify and address superimposed volume disorders; such ongoing insults impede renal recovery and might lead to relapses, portending worse outcome [26].

In summary, multi-organ POCUS is a valuable addition to nephrologists’ toolkit, which enhances the diagnostic accuracy and guides therapy when properly integrated with clinical and laboratory parameters. Future research is needed to evaluate whether adoption of such an integrative approach, as opposed to individual sonographic parameters, would portend salutary impact on the outcomes. We also need to explore whether this approach can successfully risk stratify the patients with various levels of severity of AKI in distinct clinical settings.

In the last 3 years, Dr. Claudio Ronco has been consulting or part of advisory boards for ASAHI, Astute, Baxter, Biomerieux, B. Braun, Cytosorbents, ESTOR, FMC, GE, Jafron, Medtronic, and Toray. Dr. Amir Kazory has been consulting or part of advisory boards for Elsevier, Inc. and NuWellis, Inc. Dr. Abhilash Koratala has no conflicts of interest.

No funding was received for this study.

A.Ko. drafted the initial version of the manuscript, performed point-of-care US studies. C.R. and A.Kz. reviewed and revised the manuscript for critical intellectual content.

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