Increased renal cortical echogenicity does not always indicate chronic kidney disease
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 7-11 mm, being thicker at the poles. Following is an infographic illustrating hyperechoic cortex in a patient with lupus nephritis.
Here is another example from a patient with AKI stage III secondary to ethylene glycol poisoning. Note normal sized kidneys with bright cortex, likely secondary to calcium oxalate deposition.
Another example of hyperechoic kidney obtained from a patient with CKD stage IV. Note the loss of cortico-medullary differentiation, typically seen in CKD (not always).
1-minute video showing another example: