Fluid (e.g. blood, urine, serous fluid in cysts) is an excellent transmitter of sound waves and appears black (= anechoic) on a sonogram. On greyscale images, prominent vasculature or vascular malformations can mimic hydronephrosis or cysts depending on the location. We should always obtain a few Doppler images when performing kidney ultrasound irrespective of the suspected etiology.
Dromedary hump is a prominent focal bulge on the lateral border of the left kidney caused by splenic impression, which can mimic renal neoplasm. It is similar in appearance to the hump of a dromedary camel and thus the name. It is a benign anatomic variant and exhibits the same imaging characteristics as adjacent renal cortex with normal blood flow pattern on Doppler sonography. On the other hand, malignant lesions are usually heterogenous in echogenicity (though can be perfectly isoechoic to cortex sometimes) and the blood flow tends to be prominent in the periphery of the lesion.
Following Doppler loop shows that a medullary pyramid is extending into the hump with normal blood supply around it. If it was a tumor, the pyramid wouldn’t extend into the mass and the blood flow, if you see would be ‘around the mass’ and not ‘around the pyramid’.
The diagnosis of a simple benign renal cyst on ultrasound requires the presence of all the following findings: a well-defined, roundish, anechoic structure, imperceptible near wall and thin echogenic far wall, and increased through transmission manifested by acoustic enhancement. Acoustic enhancement refers to the hyperechoic or bright area relative to surrounding tissues, distal to structures that are excellent transmitters of sound waves. This artefact is not restricted to cysts and can be seen with any fluid containing space such as a blood vessel or urinary bladder. Any lesion that does not meet criteria for a simple cyst is considered a complex cyst and may be characterized by findings such as irregular thickened walls, septations, internal echoes, and calcifications.
What is the utility of sonography in Bosniak classification of cysts?
The Bosniak classification system helps in the diagnosis and management of renal cysts. As the detection of neovascularization in malignant lesions, indicated by contrast enhancement (on CT) of solid components, septa or walls, is an essential part of the classification, ultrasound cannot be used instead of CT. However, it is known that ultrasound may demonstrate internal septa better than CT and MRI. Therefore, it has been suggested that simple and minimally complex (Bosniak I and II) cysts may be followed with sonography alone.
Nephrocalcinosis: by default, we apply this term to ‘medullary’ calcification (= medullary nephrocalcinosis), though it can occur in renal cortex (e.g. in renal cortical necrosis of pregnancy or chronic active glomerulonephritis). Nephrocalcinosis is associated with conditions that cause hypercalcemia, hyperphosphatemia, and increased excretion of calcium, phosphate, and/or oxalate in the urine. Hypocitraturia also may contribute, especially in those with distal (type 1) renal tubular acidosis. Citrate normally inhibits crystal formation by forming a complex with calcium.
Important conditions that cause Medullary nephrocalcinosis: With hypercalcemia + hypercalciuria: primary hyperparathyroidism, sarcoidosis, too much vitamin D. Conditions with hypercalciuria but no hypercalcemia: Distal renal tubular acidosis, medullary sponge kidney, too much furosemide.
On a renal sonogram, the medullary pyramids appear bright or white (hyperechoic) instead of anechoic or hypoechoic. Kidney appears like a stretched chrysanthemum flower. Acoustic shadowing may or may not be seen. Sometimes, the whole pyramid becomes hyperechoic while sometimes it’s only the rim (especially in early stages).
Autosomal dominant polycystic kidney disease (ADPKD) is relatively a common genetic disorder, occurring in approximately 1 in every 400 – 1000 live births. It is generally an adult-onset, multisystem disorder characterized by gradually growing renal cysts that can originate from all areas of the kidneys, though they more commonly emerge form distal regions of the nephron and the collecting duct. Mutations in PKD1 or PKD2, which encode polycystin 1 and 2, respectively, are the most common cause of ADPKD. Patients with PKD2 have a less severe phenotype than those with PKD1, though not benign. Cysts occur later in PKD2 disease, as does end-stage renal disease (mean age of ESRD: 74.0 vs 54.3 years in PKD1).
On a renal sonogram, kidneys are usually large with multiple cysts appearing as bunch of grapes. The number of cysts required for diagnosis vary depending on the age of the patient. Simple renal cysts will appear anechoic (black) with well-defined margins and posterior acoustic enhancement (brightness or white area past the cyst). Hemorrhagic or infected cysts will demonstrate echogenic material within the cyst, without internal blood flow. Calcification may be seen in some cases. Presence of liver cysts in addition to renal cysts is a clue to the presence of ADPKD. Polycystic liver disease is characterized by presence of multiple cysts scattered throughout the liver parenchyma, which form owing to overgrowth of the biliary epithelium.
In terms of risk stratification, Magnetic resonance-based, height-adjusted total kidney volume (htTKV) over 600 ml/m predicted the development of CKD stage 3 within 8 years in the Consortium for Radiologic Imaging in Polycystic Kidney Disease (CRISP) cohort. This was a prospective, observational, longitudinal, multicenter study included 241 adults with ADPKD and preserved renal function. In the same cohort, an ultrasound kidney length over 16.5 cm and htTKV over 650 ml/m had the best cut point for predicting the development of CKD stage 3. When MRI is not available, kidney length on ultrasound can be used for risk stratification in these patients.
Parapelvic cysts can mimic hydronephrosis because of their anechoic nature (like urine, clear fluid in the cysts is also black on ultrasound) and close proximity to the collecting system. Hydronephrosis appears as branching, ‘interconnected’ anechoic area, while parapelvic cysts are seen as ‘noncommunicating’ renal sinus cystic masses. In addition, a parapelvic cyst is more spherical as opposed to irregular/cauliflower contour of hydronephrosis and is not connected to the ureter distally. When the sonogram is not clear enough, a CT scan with contrast should be considered to differentiate between these two conditions. On CT, the contrast will not enter the cyst while the collecting system lights up. See one of my previously published case reports for a better idea in addition to below infographic.
Echogenicity of the renal cortex relative to liver or spleen can be evaluated both qualitatively and quantitatively, though qualitative method is commonly used. Normal renal cortex is usually hypoechoic (less bright) or sometimes isoechoic (similar brightness) to that of liver or spleen. Increased cortical echogenicity is commonly attributed to chronic kidney disease (CKD) and has been correlated with interstitial fibrosis, tubular atrophy, and glomerulosclerosis in histologic studies. However, increased echogenicity can also be seen in acute kidney injury (AKI) where inflammatory infiltrates and proteinaceous casts reflect sound waves (e.g. acute glomerulonephritis, acute tubular necrosis).
Note that CKD is usually associated with decreased kidney length and cortical thickness in addition to increased echogenicity (except diabetic nephropathy and infiltrative diseases). If a patient with no significant co-morbidities is found to have elevated serum creatinine and bright renal cortex, think of AKI/glomerulonephritis especially if the length and thickness are preserved. The normal pole-to-pole kidney length in adults is 10-12 cm, and varies with body size. Cortical thickness is measured from the base of the medullary pyramid to the outer margin of the kidney. It is generally around 7-10 mm, being thicker at the poles. Following is an infographic illustrating hyperechoic cortex in a patient with lupus nephritis.
