Parenchymal Signal Intensity Changes

T1-weighted (T1w) spin-echo and gradient-echo sequences show a CMD in normal kidneys, with lower signal intensity (SI) within the medulla, which is enhanced by fat suppression. On T2-weighted (T2w) sequences, CMD is reversed with a higher SI within the medulla. These effects are presumably due to higher water content per unit of tissue mass within pyramids. CMD is decreased on T1w images, nonspecifically, when serum creatinine is increased (Fig. 1) (1). Proposed mechanisms are either owing to a decreased cortical SI caused by edema or to an increased medullary SI caused by a decreased tubular flow or deposition of proteinaceous or bloody materials. The intensity of CMD decrease was initially shown to be correlated with


Figure 1 CMD on T1w MR images: examples of (A) normal and (B) absent CMD. These changes are not specific and independent of renal function. Abbreviations: MR, magnetic resonance; CMD, corticomedullary differentiation; T1w, T1-weighted.

the degree of renal failure and was supposedly absent when serum creatinine reached 3.0mg/dL (1). However, in acute renal failure (ARF), CMD may remain preserved at least within two weeks of developing ARF, and its degree independent of serum creatinine level (2).

Other types of parenchymal SI changes have been described in some specific diseases. These changes essentially concern cases of decrease of cortical or medullary SI on T2w images (3). Ischemia and hemosiderin deposition are the most frequent causes of such changes. Where hemosiderin is concerned, hemolysis is the first mechanism to be proposed. It may occur either within the cortex or within the medulla (Fig. 2). The three main causes of cortical decrease of SI on T2w images related to hemosiderin deposition are: paroxysmal nocturnal hemoglobinuria (Fig. 2A), sickle-cell disease, and causes of mechanical hemolysis (e.g., patients with certain types of artificial heart valves). Within the medulla, hemosiderin deposition may occur after episodes of hemorrhagic congestion, mainly within the outer medulla, which is more sensitive to hypoxic injury. The main causes of these MR features are hemorrhagic fever with renal syndrome, ischemic ARF (Fig. 2B), and renal vein thrombosis. Besides hemosiderin, a decrease of SI on T2w images may also be due to ischemia, as shown in infarction and in cortical necrosis. In this case, no enhancement is noted on post-gadolinium (Gd) contrast administration using T1w sequences.

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