Acute and Chronic Nephropathy

Fig. 2.1

Grayscale image of normal kidney size and echogenicity. Elementary information given by B-mode includes kidney size, parenchymal thickness, cortical echogenicity, corticomedullary differentiation, and renal profiles. (a) Coronal section is considered the most accurate scan to estimate kidney’s longitudinal length. (b) Oblique cross section allows measurement of renal width and thickness for renal volume estimation through the ellipsoid formula

Kidney’s length is the most clinically useful measurement of kidney size because it is simple to obtain and shows only minimal intra- and inter-observer variations. Normal kidneys are approximately 10–12 cm in length, with the left kidney slightly longer than the right. Size also varies with sex and age: women and elderly, respectively, have kidneys smaller than men and young.

Length is especially important in differential diagnosis between AKI and CKD: small kidneys suggest the diagnosis of CKD, although in early diabetic nephropathy, kidney size is normal or increased. Indeed increased kidney size is often a feature of AKI: large kidney may result from infiltrative diseases (amyloidosis, multiple myeloma, lymphoma), edema and inflammation (acute glomerulonephritis, acute interstitial nephritis), and vascular injury (renal vein thrombosis) [2].

Echogenicity is a main criterion to evaluate kidney diseases. Normal parenchyma, including the cortex and medulla, is isoechoic or slightly hypoechoic compared with the liver or spleen. But in the case of bright liver due to steatosis, the evaluation of renal echogenicity may result more difficult and is based principally on operator’s experience (Fig. 2.2).

Fig. 2.2

Grayscale ultrasonographic image demonstrating normal kidney compared to a bright liver

Increased parenchymal echogenicity in CKD is a consequence of fibrous tissue that reflects sound waves back. Hyperechogenicity may occur in AKI by acute interstitial nephritis and glomerulonephritis because of inflammatory infiltrates. Proteinaceous casts are thought to cause increased echogenicity that occurs in ATN. Hypoechogenic renal cortex may be the ultrasonographic feature of cortical necrosis, a rare cause of AKI, and consequence of severe ischemia due to hemolytic–uremic syndrome, eclampsia, or sepsis, which results in necrosis of tubular cells of the cortex and increase in interstitial fluid.

The measure of renal resistive index (RI) is one of the most sensitive parameters in the study of disease-derived alterations of renal plasma flow, providing quantitative hemodynamic information about the intrarenal and extrarenal vasculature [3]. A standardized protocol is required to perform a correct measurement of RI, with color Doppler focused on interlobar arteries and low pulse repetition frequency (PRF) of 1–1.5 kHz. When pulsed wave Doppler module is activated, the sample volume should be placed in the lumen of interlobar arteries with a size of 1–2 mm in order to avoid artifacts. Renal RI is the arithmetic average obtained from at least three different samplings in different areas of the kidney (Fig. 2.3).

Fig. 2.3

Duplex ultrasound with normal RI finding. The renal RI is calculated through the measure of peak systolic velocity (PSV) and the telediastolic velocity (TDV) according to the formula RI = (PSV – TDV)/PSV

In adult a value <0.70 is considered normal, but many confounding factors, such as severe hypotension, heart rhythm disorders, renal compressions for perirenal or subcapsular fluid collections, and extrarenal causes of impaired vascular elasticity, should be always kept in account.

2.3 Acute Kidney Injury (AKI)

Acute kidney injury is a clinical syndrome including all renal physiopathology. AKI may be determined by renal hypoperfusion (prerenal), renal parenchymal diseases (renal), or acute obstruction of the urinary tract (postrenal). Differential diagnosis between prerenal, renal, and postrenal AKI is necessary, because the therapy is different [4].

2.3.1 Prerenal AKI

Prerenal AKI (30–60 %) is essentially the functional and reversible syndrome that results from kidney hypoperfusion due to hypovolemia, low cardiac output, systemic vasodilatation, or intrarenal vasoconstriction. Classic urinary biomarkers, including urinary sodium (Na) and fractional excretion of sodium (FENa), cannot be used in anuric patients and are unreliable after diuretics or hemodialysis administration. New proposed biomarkers, as NGAL and KIM-1, have still limited clinical value because of low specificity and high costs. In this setting DUS with calculation of intrarenal RI can play a crucial role in the differential diagnosis between two most common types of AKI: functional (prerenal) and organic (renal) AKI. The former is characterized by a reduction in renal perfusion and is rapidly reversible if promptly treated, whereas the latter is caused by a direct damage of the renal parenchyma or by the evolution of a prerenal form in ATN and tends to be persistent (Fig. 2.4).

Fig. 2.4

Two cases of AKI followed through RI variation. (a) On the left side of the image, a patient treated for transient AKI showed a clinical worsening to persistent AKI despite medical therapy with progressive elevation of RI from 0.53 to 0.87. (b) On the right side of the image, an oliguric patient with a remarkable urea and resistive index increase (RI = 0.78) responsive to medical therapy with significative intrarenal hemodynamic improvement (final RI = 0.59)

While B-mode echogenicity and parenchymal thickness are nonspecific, a RI value > 0.75 is reported as optimal in attempting differential diagnosis between prerenal AKI and ATN. An RI > 0.80 is even a more reliable indicator of persistent AKI than the common urinary markers and could be a promising tool to predict the reversibility of AKI in critically ill patients [5].

Appraisal of the inferior vena cava collapsibility index (IVC-CI), lung B-lines, and pleural or peritoneal fluid effusions can give an idea of the patient’s global hydration status, supporting or confuting the diagnosis of prerenal AKI and eventually directing effective therapy (Fig. 2.5) [6–8].

Fig. 2.5

Hydration assessment is important to establish the correct diagnosis and the right therapy for patient with renal injury: (a) echo B-mode with longitudinal scan of IVC may give a gross idea of patient hydration status; (b) better estimation comes from the measurement of the IVC collapsibility index in M-mode with the following formula: (D _max–D _min)/(D _max). The patient should always be checked for (c) lung ring-down artifacts and (d) pleural and peritoneal effusions to complete the clinical picture and administrate the right fluid therapy

2.3.2 Renal AKI

Renal AKI (20–50 %) is caused mostly by ATN, acute interstitial nephritis due to ischemia or nephrotoxic agents (i.e., radiologic contrast agents), glomerulonephritis, and vasculitis.

In acute primitive or secondary glomerulonephritis, kidneys are usually symmetrically involved, sometimes showing a globular appearance with renal sinus compression (Fig. 2.6a). More often they are near normal in size and morphology, with hyperechogenic parenchyma and marked differentiation between the cortex and medulla (Fig. 2.6b) [9].

Fig. 2.6

AKI arising from acute glomerulonephritis or systemic vasculitis involving the kidneys. Renal morphology on ultrasound sometimes shows (a) a specific globular pattern with central sinus compression and increased volume with width/length ratio >0.5; more often (b) kidney’s appearance is near normal with hypoechogenic pyramids and marked differentiation between the cortex and medulla

Color Doppler signals may reveal parenchymal hypervascularization, while RI value is usually normal. In tubulointerstitial diseases instead, parenchymal perfusion is reduced and RI increased. In hemolytic–uremic syndrome, the renal cortex is hyperechogenic with increased corticomedullary differentiation, and DUS shows RI >0.80 with low diastolic flux [10]. In acute lupus nephritis, kidneys may present reduced or increased dimensions and an increased cortical echogenicity with reduced corticomedullary differentiation.

Anyway echo-guided renal biopsy is imperative to diagnose AKI derived by acute glomerular diseases or vasculitis, such as Wegener’s granulomatosis or polyarteritis nodosa.

Acute pyelonephritis and renal infarction can both lead to AKI [11]. In the right clinical context, renal ultrasound implemented with microbubble contrast enhancement ultrasound (CEUS) may help in the diagnosis of both, depicting one or more hypovascularized areas into the renal parenchyma, whereas echo B-mode and ECD alone show less sensibility and specificity (Fig. 2.7) [12].

Fig. 2.7

Effectiveness of CEUS as diagnostic tool. (a) In acute pyelonephritis microbubbles indentify hypoenhanced areas due to inflammation, edema, and pus collection with performances comparable to CT. (b) Renal infarcts appear as triangular or wedge-shaped areas without contrast uptake. Although a high grade of clinical suspicion is necessary, in both renal diseases, CEUS represents an effective diagnostic tool

ECD has a central role in the diagnosis of AKI of vascular origin. DUS is essential to diagnose renal artery stenosis (RAS) demonstrating the well-known direct and indirect criteria (Fig. 2.8) [13].