FATTY KIDNEY (FKD)

 

RECOGNIZING FKD CLINICALLY ‐ THE NEED FOR RADIOGRAPHIC IMAGING

NASH and NAFLD were not reported on abdominal imaging until their clinical importance was recognized. Since then, imaging characteristics of NASH and NAFLD have helped to develop the understanding of fatty liver disease and have led to important innovations.

FKD is currently in the same situation that NASH and NAFLD were 20 years ago. Radiologic reports of MRI and CT scans of the abdomen typically do not elaborate on the presence of ectopic renal hilar or sinus fat, presumably being unaware of its clinical significance. It would help the understanding and recognition of FKD as a distinct entity if radiologists can help define the imaging criteria for FKD.

Currently, renal cortical fat deposits are difficult to measure except with Proton MRI. There are issues of the boundary of the renal capsule and perirenal fat and the paucity of intrarenal fat normally. Advances in renal ultrasound, CT, and MRI may be able to overcome these obstacles and allow a radiographic diagnosis and better characterization.

MRI and CT are presently able to delineate only perirenal fat, hilar fat, and RSF. Hilar fat and RSF should perhaps be considered a combined “entity” because a demarcation is not possible. The assessment of renal triglyceride content by Dutch groups is encouraging. 43 , 44

Noninvasive molecular imaging of kidney disease is progressing and, it is hoped, can measure renal triglyceride/fat as well. 45 , 46

In a weight loss study, MRI was able to assess fat loss in RSF but could not detect any change in renal parenchymal fat. 47

Ultrasound elastography of the kidney may be a technique to measure renal fat content. 48 Sonographic evaluation of para‐ and perirenal fat thickness has been used as a predictor of early kidney damage in obese patients. 35 B‐mode renal ultrasound targeting perirenal fat thickness in specific locations is showing promise. 49 “Para and peri‐renal fat ultrasonographic thickness may be … a useful tool for the assessment of visceral fat and early kidney damage in obese adults”. 35

Much might be learned from such imaging and some centers are beginning the radiographic exploration of FKD. 43 , 46

Because visceral obesity affects multiple organs, it is plausible that FKD occurs whenever NAFLD occurs, as suggested by human 50 , 51 and animal studies. 46

If this is confirmed by imaging studies, it may be possible to infer the presence of FKD whenever NASH is identified, thus obviating the need for specific renal imaging. To the extent that imaging can quantify the degree and location of ectopic fat, there may a quantifiable threshold of visceral obesity that initiates the pathological consequences in the kidney as it appears to do in the liver.

Similarly, there may be implications for recognizing that the location and amount of fat accumulation in other organs, such as the epicardium, determines the extent of pathological consequences, both systemically and to the organ itself.

Pig data show a 100% correlation between the presence of NAFLD and fatty kidney by renal biopsies and triglyceride measured by MRI 7‐Tesla. 46 We postulate that this coexistence also is present in humans, mainly because of many parallel associated factors (metabolic syndrome, insulin resistance, dyslipidemia, proinflammatory state, etc.). No specific type of renal disease has been described when NAFLD and CKD are both present as there are no data published on renal biopsies in that setting. No causal link between NAFLD and CKD has been established, but the relationship has been reviewed in detail. 9

It is certainly possible that the time course and nature of progression of NAFLD to NASH differs from that of FKD to CKD, but they both would be expected to reflect the toxicity of ectopic fat deposits.

FKD (ie, all three stated components: ORG, hilar/renal sinus fat, and intrarenal ectopic fat deposits) has been shown to be a major risk factor for CKD initiation and progression for CKD and hypertension in multiple publications. 7 , 10 , 11 , 24

One key feature of renal cortical lipid deposition (triglyceride and lipid droplets) is podocyte toxicity with albuminuria and CKD development. 23