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Is Fat Deposition of Renal Sinus a Concomitant Finding to Fatty Liver Disease? The First Study Regarding the Relationship Between Kidney and Liver Fat Content with Non-Contrast Computed Tomography

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Introduction: It has been established that abnormal fat deposits are associated with fat deposition in other abdominal regions and linked to obesity, diabetes mellitus, hypertension, vascular and metabolic diseases. This study aimed to determine whether there was a relationship between fat deposition of the renal (i.e., kidney) sinus (FRS) and fatty liver disease (FLD) in a sample of adults. The authors hypothesized that FRS could be a diagnostic finding associated with Hepatosteatosis (HS) in a sample of younger patients. This study was the first apparent investigation of this possible phenomenon. Methods: A convenience sample of 92 adult patients of which 19 (20.7%) were females and 73 (79.3%) were males, and with a mean age of 30.19 (SD = 6.00) were included. The authors calculated Hounsfield Units (HU) (i.e., relative quantitative measurement of radio density) of patients' livers and spleens on non-contrast computed tomography (CT). Liver and spleen differences < 10 HU were considered steatosis (FLD). The authors stratified sample patients into two analytic subgroups according to the presence of FLD or not and compared them based on their FRS widths. Results: In the FLD subgroup (N = 48), the difference of HU values between liver and spleen was -5.19 (SD = 11.32), with a range of -38 - 8 HU, while, in the non-steatosis subgroup (N = 44), the mean difference was 16.36 (SD = 3.90), range of 11 - 26 HU. The average diameter of FRS width was 12.5 mm in those patients with steatosis (FLD subgroup) although 9.3 mm in non-FLD patients. (p = 0.02). Conclusions: Based on these results, FRS may be able to be used by radiologists as an ancillary method in the detection of hepatic steatosis in younger adults. The effectiveness of premedical processes (e.g., exercise and diet modification) can also be increased by non-radiologists after detection of lower-grade HS.
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Is Fat Deposition of Renal Sinus a Concomitant Finding to Fatty
Liver Disease? The First Study Regarding the Relationship Between
Kidney and Liver Fat Content with Non-Contrast Computed
Tomography
Emrah Doğan, MD
1 a , Ferda Bacaksızlar Sarı, MD
2
1 Radiology, Mugla Sıtkı Kocman University, 2 Mugla Sıtkı Kocman University Education of Research Hospital
Keywords: Renal fat deposition, Fatty liver disease, Computed tomography, Hepatic steatosis
https://doi.org/10.51894/001c.32411
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INTRODUCTION
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METHODS
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RESULTS
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CONCLUSIONS
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Corresponding author:
Emrah Doğan MD, emrahdogan@mu.edu.tr
a
Doğan E, Bacaksızlar Sarı F. Is Fat Deposition of Renal Sinus a Concomitant Finding to
Fatty Liver Disease? The First Study Regarding the Relationship Between Kidney and
Liver Fat Content with Non-Contrast Computed Tomography. SMRJ. 7(1).
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:E H2D :>A@CE2?E E@ @3E2:? DA=66? G2=F6D 2=@?8 H:E9 E96
=:G6C)68:@?@7:?E6C6DE)& H2DD6=64E652D2AAC@I:>2E6=J
F?:ED#:G6C+H:?5@HH:5E9.@F?DX6=5F?:ED
,=6?8E9#,H2DFD655FC:?8E96>62DFC6>6?ED
:8FC6D2?5
+96=:G6CD2?5DA=66?D@7D2>A=6A2E:6?EDH6C62=D@6G2=
F2E65:?E96 235@>:?2=H:?5@H.,# ,+96
>62DFC6>6?EA@:?EDH6C649@D6?7C@> 5:776C6?E=:G6C D68
>6?ED$62DFC6>6?EDH6C6?@E E2<6?7C@>C68:@?DH96C6
7@42=72E56A@D:E:@?H2D@3D6CG6568A6C:A@CE2=2C62D2?5
2C@F?5 E96 82==3=2556C '6C:A96C2= 2C62 >62DFC6>6?ED
H6C6AC676CC653642FD6@79:=2CG2D4F=2C:EJH96?>62DFC:?8
DA=66?,
7 E96 5:776C6?46 :? + 2EE6?F2E:@? 36EH66? =:G6C 2?5
DA=66?H2D=6DDE92?,E96A2E:6?EH2D:?4=F565:?E96
*8C@FA&E96CH:D6E96JH6C625565E@E96?@?DE62E@D:D
8C@FA7E6C56E6C>:?:?86249D2>A=6A2E:6?EUDDF38C@FA
E96)*H:5E9 H2D2=D@42=4F=2E65 :?3@E9<:5?6JD -2=F6D
36EH66?2?5 ,2C@F?5 92G6366? 2446AE65
7@C72E56?D:EJ
+96=2C86DE5:2>6E6C:?E96 2I:2=A=2?6H2D4@?D:56C65
52E2D42=64@?E2:?:?8E96,G2=F6D @7E96=:G6CDA=66?
E96,5:776C6?46@7EH@@C82?D2?5E96=2C86DE5:2>6E6C@7
)*4>H2D42=4F=2E65249:>286H2D:?56A6?56?E=J
2DD6DD652?5=:G6C2?5DA=66?,F?:EDH6C6:?56A6?56?E=J
42=4F=2E653JEH@6IA6C:6?465C25:@=@8:DED ?42D6 @74@?
EC25:4E@CJ C6DF=ED DF49 :>286D H6C6 C66G2=F2E65 3J 3@E9
C25:@=@8:DEDE@86E96C
+962?2=JE:4D2>A=6H2DDEC2E:X65:?E@EH@:?56A6?56?E
DF38C@FAD :6 A2E:6?ED H:E9 * 2?5 A2E:6?ED H:E9@FE
DE62E@D:DAC62?2=JD:D>:?:>2=D2>A=6D:K6A@H6C2?2=J
D:D 925 366? 4@?5F4E65 FD:?8 G-power 3 software
9EEADHHHADJ49@=@8:699F562C36:ED8CFAA6?2==86
>6:?6ADJ49@=@8:6F?52C36:EDADJ49@=@8:68A@H6C :?5:
42E:?8E92E2E@E2=2?2=JE:4D2>A=6@7:6A6CD2>A=6
DF38C@FAH@F=5AC@G:56E962FE9@CDH:E9βA@H6C
E@56E64E>62?:?87F=D2>A=6DF38C@FA5:776C6?46D
2E2H6C6DE@C65@?2$:4C@D@7E&7X46I46=DAC625D966E
X=6I46= $:4C@D@7E2?52 DE2E:DE:42=2?2=JE:4D@7E
H2C6:6*'**G6CD:@? $H2DFD65E@4@?5F4E2?
2=JE:4AC@465FC6D@?E:?F@FD G2C:23=6DH6C66IAC6DD65 2D
>62? L * *E2?52C5 6G:2E:@? G2=F6D 2E68@C:42= G2C:
23=6DH6C66IAC6DD65 2D4@F?ED2?5 A6C46?E286D+96*EF
56?EUD+E6DEH2D4@?5F4E65E@ 4@>A2C6>62?D@74@?E:?
F@FD G2C:23=6D '62CD@? 49:DBF2C6 χ AC@465FC6D H6C6
4@>A=6E65E@6G2=F2E6E96C6=2E:@?D9:A36EH66?42E68@C:42=
G2C:23=6D4@67X4:6?E=A92AG2=F6@7=6DDE92?G2=F6
H2D@3D6CG652DDE2E:DE:42==JD:8?:X42?E
)*,#+*
E@E2=@7A2E:6?EDH6C6XCDE6G2=F2E65:?E6C>D@7*
+962FE9@CD 6I4=F5652DF3D6E@7A2E:6?ED7C@>
E96 DEF5J D2>A=6 7@C E96 7@==@H:?8 >65:42= C62D@?D 
 A2E:6?ED 925 <:5?6J DE@?6D D6G6?  925
A2C6?49J>2=2EC@A9JEH@92529:DE@CJ@74@CE:4@D
E6C@:5FD6=D@EH@  255:E:@?2=A2E:6?EDH6C66I
4=F5657C@>E96DEF5J5F6 E@<?@H?DA=6?:45:D62D6D:6
4@>A2C:D@? @7 =:G6C 2?5 DA=66? H2D @?6 @7 E96 >2:? A2
C2>6E6CD@7E96 DEF5J2?5DA=6?:4 5:D62D6DH@F=592G627
764E65DEF5JC6DF=ED ?255:E:@?@?6A2E:6?E+
925 :>28:?8 >@E:@? 2CE6724ED E92E AC6G6?E65 6G2=F2E:@?
@FC  @E96C 6I4=F565 A2E:6?ED 925 >@D2:47@42=
DE62E@D:D +9:D =67E 2 E@E2= @7  A2E:6?ED 7@C E96 2?2=JE:4
D2>A=6  AC65@>:?2?46 @7 >2=6D   :? E96 E@E2=
D2>A=6H2D?@E65H9:=6H6C676>2=6
D2E6A@D:E:@?@7)6?2=*:?FD2@?4@>:E2?E:?5:?8E@2EEJ#:G6C:D62D6+96:CDE*EF5J)682C5:?8E96)6=2E:@?D9:A
Spartan Medical Research Journal 2
Figure 1. Calculation of HU values of liver and spleen as well as FRS diameter in patient with steatosis
(Arrowhead). Pay attention to the difference between the liver and the spleen HU.
Figure 2. Calculation of the HU values of the liver and spleen as well as the FRS diameter in the patient
without steatosis. Pay attention to the difference between the liver and the spleen HU.
**,)&,'
+9:DDF38C@FAH2D4@>AC:D65@7A2E:6?ED4@?D:DE:?8@7
>2=6D2?576>2=6D+96>62?286@7E96
*DF38C@FAH2D *2?5 C2?865 7C@>S
J62CD@7286$62?=:G6C,G2=F6D2G6C2865*
2?5C2?8657C@>S+96>62?DA=6?:4,G2=F6
H2D* 2?5C2?8657C@>  +96>62?
5:776C6?46D36EH66?=:G6C2?5DA=66?,G2=F6DH6C6
*2?5C2?8657C@>
D2E6A@D:E:@?@7)6?2=*:?FD2@?4@>:E2?E:?5:?8E@2EEJ#:G6C:D62D6+96:CDE*EF5J)682C5:?8E96)6=2E:@?D9:A
Spartan Medical Research Journal 3
Table 1. The number of patients and rates in the HS and non-steatosis groups according to criterion I and II
(comparison)
Criteria I/II Liver value (< 40 HU) Liver value (> 40 HU) Spleen (30 - 60 HU)
Steatosis (N = 44) 29.55% (N = 13) 70.45% (N = 31) 100% (N = 44)
Non-steatosis (N= 48) - 100% (N = 48) 100% (N = 48)
Table 2. Statistical values of FRS width in the HS and Non-HS subgroups.
Subgroup Mean (cm) SD Variance
Steatosis (N = 44) 12.54 6.00 36.01
Non-steatosis (N= 48) 9.35 6.36 40.46
%&%**,)&,'
+9:DDF38C@FAH2D4@>AC:D65@7A2E:6?EDH:E9
>2=6D2?576>2=6D+96>62? 2867@CE96%@?
*DF38C@FAH2D *2?5 C2?865 7C@>S
J62CD@7286$62?=:G6C,G2=F6D2G6C2865*
2?5C2?8657C@>+96>62?DA=6?:4,G2=F6
H2D* 2?5C2?8657C@>  +96>62?
5:776C6?46D36EH66?=:G6C2?5DA=66?,G2=F6DH6C6
*2?5C2?8657C@>
+96EH@7@==@H:?8>2:?+6G2=F2E:@?4C:E6C:2H6C6E2<6?
:?E@244@F?E2?54@>A2C65
Criterion I:+96>62DFC65,G2=F6H2D=6DDE92?
Criterion II:+965:776C6?4636EH66?=:G6C2?5DA=66?,
G2=F6DH2D=6DDE92?
@?D:56C:?82==D2>A=6A2E:6?ED,G2=F6D@7E96=:G
6CDH6C6*2?5C2?8657C@>,G2=
F6D@7 E96DA=66?DH6C6*2?5C2?8657C@>
S @H6G6C @7E96A2E:6?ED :?E96*
8C@FA9252=:G6C,G2=F6+96C6H2D5:D4C6A2?4J36
EH66?E96EH@4C:E6C:2+9:D4@>A2C:D@?:DD9@H?:?+23=6
:8FC656A:4EDE96?@E23=65:776C6?46D36EH66?,G2=
F6D@7E96=:G6C2?5E96DA=66?:?E96*2?5?@?DE62E@D:D
D2>A=6DF38C@FAD
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Figure 3. The box plot graphic shows difference
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Figure 4. Scatter plot of FRS of HS and non-HS
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Spartan Medical Research Journal 7
... Because conventional anthropometric measures of adiposity fail to capture the organ-specific fat deposition, advanced imaging techniques are indispensable for exploring the plausible implications of RSF accumulation on human health. Volumetric analysis of RSF by computed tomography (CT) and magnetic resonance imaging (MRI) and assessment of its association with metabolic and cardiovascular risks have been previously reported (6)(7)(8)(9)(10). ...
... Nevertheless, we addressed the associations of and RSF volume and FF values with VAT area, SAT area, hepatic fat fraction, and pancreatic fat fraction. Previous studies have shown that RSF deposition was related to other deleterious fat depots, such as VAT and hepatic fat (8,10,20,31). In our study, we further extended these findings and found that there were correlations of the RSF volumes and FFs in both kidneys with VAT area, hepatic fat fraction and pancreatic fat fraction in the overall subjects. ...
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Purpose To determine the renal sinus fat (RSF) volume and fat fraction (FF) in normal Chinese subjects using MRI fat fraction mapping and to explore their associations with age, gender, body mass index (BMI) and ectopic fat deposition. Methods A total of 126 subjects were included in the analysis. RSF volume and FF, visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) area, and hepatic and pancreatic FFs were measured for each subject. The comparisons in gender were determined using two-tailed t-tests or the nonparametric Mann-Whitney U-test for normally or non-normally distributed data for continuous variables and the chi-square test for categorical variables. Comparisons of RFS volume and FF between right and left kidneys were determined using paired sample t-tests. Multivariable logistic models were performed to confirm whether RSF differences between men and women are independent of VAT or SAT area. When parameters were normally distributed, the Pearson correlation coefficient was used; otherwise, the Spearman correlation coefficient was applied. Results The RSF volumes (cm ³ ) of both kidneys in men (26.86 ± 8.81 for right and 31.62 ± 10.32 for left kidneys) were significantly bigger than those of women (21.47 ± 6.90 for right and 26.03 ± 8.55 for left kidneys) (P < 0.05). The RSF FFs (%) of both kidneys in men (28.33 ± 6.73 for right and 31.21 ± 6.29 for left kidneys) were significantly higher than those of the women (23.82 ± 7.74 for right and 27.92 ± 8.15 for left kidneys) (P < 0.05). The RSF differences between men and women are independent of SAT area and dependent of VAT area (except for right RSF volume). In addition, the RSF volumes and FFs in both kidneys in the overall subjects show significant correlations with age, BMI, VAT area, hepatic fat fraction and pancreatic fat fraction (P < 0.05). However, the patterns of these correlations varied by gender. The RSF volume and FF of left kidney were significantly larger than those of the right kidney (P < 0.05). Conclusion The association between renal sinus fat and ectopic fat deposition explored in this study may help establish a consensus on the normal values of RSF volume and FF for the Chinese population. This will facilitate the identification of clinicopathological changes and aid in the investigation of whether RSF volume and FF can serve as early biomarkers for metabolic diseases and renal dysfunction in future studies.
... Our study showed that the renal sinus fat volume of the left kidney was somewhat larger than that of the right kidney (2.83 cm 2 vs. 2.56 cm 2 ), and this result was consistent with previous studies [33][34][35]. Previous studies have shown that renal fat sinus deposition was related to other deleterious fat depots, such as liver steatosis and visceral fat [33,[36][37][38][39], similar to our results. Zhang et al. [33] found that there were correlations between the renal sinus fat in both kidneys with visceral adipose fat, hepatic fat fraction, and pancreatic fat fraction. ...
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The vascular risk associated with obesity is particularly associated with visceral adiposity, but recent studies suggest that ectopic fat might contribute to the increased risk of atherosclerotic cardiovascular disease. Our study aimed to explore the connection between arterial calcification of the aorta and renal arteries with visceral and ectopic fat deposits, including liver, pancreatic, and renal sinus fat. Retrospective analysis of thoracoabdominal multi-slice computed tomography (MSCT) scans of 302 patients included measurements of calcification volumes of thoracic and abdominal aorta, and of both renal arteries. On the same scans, the visceral fat volume, liver-to-spleen ratio, pancreatic-to-spleen ratio, and both renal sinus fat areas were retrieved. Logistic regression showed the left kidney sinus fat area to be the most strongly associated with calcifications in the aorta and both renal arteries (coef. from 0.578 to 0.913, p < 0.05). The visceral fat positively predicted aortic calcification (coef. = 0.462, p = 0.008), and on the contrary, the pancreatic fat accumulation even showed protective effects on thoracic and abdominal aorta calcification (coef. = −0.611 and −0.761, p < 0.001, respectively). The results suggest that ectopic fat locations differently impact the calcification of arteries, which should be further explored.
... No association was observed between NAFLD and disease severity and prognosis in acute PE disease. Detection rates of hepatic steatosis by evaluation of the liver and spleen with CT vary according to the radiological criteria used [18]. According to the hepatosteatosis definition criteria in the literature, fatty liver rates vary and reach 80% [19,20]. ...
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Objectives: Pulmonary embolism (PE) is an important disease due to its mortality and morbidity-related clinical conditions. Patients with a high risk of death within 30 days are discriminated against with the help of various clinical scores. Non-alcoholic fatty liver disease (NAFLD) has been found to be associated with atherosclerosis. We aimed to investigate the effect of NAFLD on disease severity and early death rate in patients with pulmonary embolism. Methods: This retrospective study includes patients who applied to the emergency department with suspected pulmonary embolism and whose diagnosis was confirmed according to the results of the examination. In addition to confirming the diagnosis of PE, hepatic steatosis was detected and graded by tomographic examination of the liver and spleen. Disease severity was stratified by Simplified Pulmonary Embolism Severity Index (sPESI). Results: A total of 165 patients (105 with sPESI≥1 and 60 with sPESI<1 controls) were included. The rate of mortality was 12% (n=13) in the sPESI≥1 group. The prevalence of NAFLD was 64% and the prevalence of hepatosteatosis was similar according to disease severity and prognosis (67% vs. 58%; P=0.28 and 69% vs. 63%; P=0.77). Besides the effect of disease severity; chronic lung disease (CLD) and chronic kidney disease (CKD) were independently associated with poor prognosis by multivariate analysis [3.71 (1.02-13.46); P=0.04 and 15.89 (2.57-98.35); P=0.003]. Conclusion: No association between disease severity and prognosis was observed with NAFLD in acute PE disease.
... Contrast computed tomography (CT) is used to further clarify the diagnosis. Nevertheless, during this technique, the radiation is relatively high, and a number of undesirable effects may arise as a result of the injection of contrast material [3,7]. ...
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Introduction: Gas accumulation in human joint spaces has been generally described as the vacuum phenomenon (VP). To date, the sacroiliac joint VP has been associated mostly with pathological, particularly degenerative conditions (e.g., arthritis, obesity, discal degenerations, fractures, dislocations, avascular necrosis). Objective: The study aimed to examine the characteristics of the physiological form of VP and its radiological patterns in a sample of pediatric patients. Methods: A sample of seventy patients between 0 and 17 years old (mean age, 11.4 ± 5.54) were included in the study. Sample VP cases was evaluated according to types, age group, anatomic localization, gender, and sides. RESULTS: Two (2.9%) of sample children had degenerative VP, with 24 (34.2%) of patients demonstrating physiological VP in the sacroiliac joints. VP rates significantly increased after nine years of age (p < 0.01) and 83% of physiological VP cases were determined to be bilateral. Conclusions: Although degenerative VP is a rare entity in children, non-pathological VP can be a more common aspect of sacroiliac anatomy. Although sacroiliac VP is frequently an underreported or omitted finding in imaging studies, this condition may be clinically important as a clue for other degenerative diagnoses. Normal variants of VP may be clinically important in children since they may mimic inflammatory and infectious pathologies during magnetic resonance imaging and computed tomography images.
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Introduction and Objectives Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver abnormalities including steatosis, steatohepatitis, fibrosis, and cirrhosis. Liver biopsy remains the gold standard method to determine the disease stage in NAFLD but is an invasive and risky procedure. Studies have previously reported that changes in intrahepatic fatty acids (FA) composition are related to the progression of NAFLD, mainly in its early stages. The aim of this study was to characterize the liver FA composition in mice fed a Choline-deficient L-amino-defined (CDAA) diet at different stages of NAFLD using magnetic resonance spectroscopy (MRS). Methods We used in-vivo MRS to perform a longitudinal characterization of hepatic FA changes in NAFLD mice for 10 weeks. We validated our findings with ex-vivo MRS, gas chromatography-mass spectrometry and histology. Results In-vivo and ex-vivo results showed that livers from CDAA-fed mice exhibit a significant increase in liver FA content as well as a change in FA composition compared with control mice. After 4 weeks of CDAA diet, a decrease in polyunsaturated and an increase in monounsaturated FA were observed. These changes were associated with the appearance of early stages of steatohepatitis, confirmed by histology (NAFLD Activity Score (NAS) = 4.5). After 10 weeks of CDAA-diet, the liver FA composition remained stable while the NAS increased until 6 showing a combination of early and late stages of steatohepatitis. Conclusion Our results suggest that monitoring lipid composition in addition to total water/fat with MRS may yield additional insights that can be translated to non-invasively stratification of high-risk NAFLD patients.
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An increasing percentage of people have or are at risk to develop non-alcoholic fatty liver disease (NAFLD) worldwide. NAFLD comprises different stadia going from isolated steatosis to non-alcoholic steatohepatitis (NASH). NASH is a chronic state of liver inflammation that leads to the transformation of hepatic stellate cells to myofibroblasts. These cells produce extra-cellular matrix that results in liver fibrosis. In a normal situation, fibrogenesis is a wound healing process that preserves tissue integrity. However, sustained and progressive fibrosis can become pathogenic. This process takes many years and is often asymptomatic. Therefore, patients usually present themselves with end-stage liver disease e.g., liver cirrhosis, decompensated liver disease or even hepatocellular carcinoma. Fibrosis has also been identified as the most important predictor of prognosis in patients with NAFLD. Currently, only a minority of patients with liver fibrosis are identified to be at risk and hence referred for treatment. This is not only because the disease is largely asymptomatic, but also due to the fact that currently liver biopsy is still the golden standard for accurate detection of liver fibrosis. However, performing a liver biopsy harbors some risks and requires resources and expertise, hence is not applicable in every clinical setting and is unsuitable for screening. Consequently, different non-invasive diagnostic tools, mainly based on analysis of blood or other specimens or based on imaging have been developed or are in development. In this review, we will first give an overview of the pathogenic mechanisms of the evolution from isolated steatosis to fibrosis. This serves as the basis for the subsequent discussion of the current and future diagnostic biomarkers and anti-fibrotic drugs.
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Renal sinus lipomatosis are condition, seen in the kidneys of elderly patients. Disease is usually unilateral and associated with renal calculi. There is proliferation of excessive lipomatous tissue in the renal sinus, renal hilum, and peri-renal space. presentation of disease is varied, ranging from chronic renal pain to features of renal abscesses or pyonephrosis. Here we report an interesting case of bilateral renal sinus lipomatosis mimicking as emphysematous pyelonephritis.
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Purpose: To investigate the relationship between renal sinus lipomatosis (RSL) and abdominal visceral and subcutaneous fat accumulation and metabolic risk factors. Material and methods: A total 73 subjects were included in the study. The study group consisted of 35 cases with RSL and 38 control cases matched for age and sex. Total, visceral, and subcutaneous abdominal fat areas were measured by abdominal computed tomography (CT). The relationship between RSL and visceral abdominal fat, subcutaneous abdominal fat, total abdominal fat, high total cholesterol level, high low-density lipoprotein (LDL) cholesterol level, high very low-density lipoprotein (VLDL) cholesterol level, high triglyceride level, low high-density lipoprotein (HDL) cholesterol level, impaired fasting glucose level, type 2 diabetes mellitus, hypertension (HT), and metabolic syndrome (MS) were investigated. Results: RSL existence was observed at significantly higher levels statistically in cases with low HDL cholesterol level, high LDL cholesterol level, high VLDL cholesterol level, high triglyceride level, high total cholesterol level, and high glucose levels. In the presence of MS, DM, and HT, the presence of RSL was at a significantly higher level according to the statistics. Logistic regression analysis was performed to examine the factors affecting RSL presence together. It was observed that the model formed as the result of the evaluation using the backward method is statistically significant. Furthermore, the variables of age, high total cholesterol level, high glucose level, and abdominal subcutaneous fat were included in the obtained model. Conclusions: Our study demonstrated an association between the presence of RSL and age, high total cholesterol level, high glucose level, and subcutaneous fat.
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Adipose tissue plays multiple and complex roles not only in mechanical cushioning and energy storage but also as an important secretory organ that regulates energy balance and homeostasis multilaterally. Fat tissue is categorized into subcutaneous fat tissue (SCAT) or visceral fat tissue (VSA) depending on its distribution, with the two having different metabolic functions. Near-total lack of fat in congenital/acquired generalized lipodystrophy, cachexia, or any other severe malnutrition condition induces severe multi-organ dysfunction due to lack of production of leptin and other adipokines. Increased visceral fat tissue secondary to obesity, hypercortisolism, or multiple symmetric lipomatosis raises the risk of insulin resistance, cardiac complications, and airway or spinal canal stenosis, although the fat distribution pattern differs in each condition. Partial abnormal fat distribution conditions such as HIV/HAART therapy-associated lipodystrophy, familial partial lipodystrophies, and acquired partial lipodystrophy frequently show a mixture of lipoatrophy and lipohypertrophy with metabolic dysfunction. Characteristic imaging features in conditions with local abnormal fat distribution can provide information about a patient's co-existent/unrecognized disease(s), past medical history, or lifestyle. Knowledge of characteristic abnormal fat distribution patterns can contribute to proper and timely therapeutic decision-making and patient education.
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Non-alcoholic fatty liver disease (NAFLD) is the leading cause of diffuse liver disease. An accurate estimate of the fat in the liver is important in the diagnostic work-up of patients with NAFLD because the degree of liver steatosis is linked to the metabolic syndrome and the cardiovascular risk. Ultrasound (US) B-mode imaging allows to subjectively estimate the fatty infiltration in the liver; however, it has a low performance for the detection of mild steatosis. Quantitative US is based on the analysis of the radiofrequency echoes detected by an US system, and it allows to calculate a backscatter coefficient or an attenuation coefficient or the sound speed. The estimation of the backscatter coefficient is rather cumbersome and requires the use of a phantom for addressing all sources of variability. Controlled attenuation parameter (CAP) available on the FibroScan® system (Echosens, France) measures the attenuation of the US beam. CAP is accurate in grading fatty infiltration-even though there is an overlap between consecutive grade of liver steatosis-and the values are not influenced by liver fibrosis. Several US manufacturers are developing or have already developed software for quantifying the attenuation of the US beam. Preliminary results show that proprietary technologies implemented in US systems seem more accurate than CAP for grading liver steatosis. Another available method for quantifying liver steatosis is based on the computation of the sound speed and the initial results appear promising.
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Nonalcoholic fatty liver disease (NAFLD) is estimated to afflict approximately 1 billion individuals worldwide. In a subset of NAFLD patients, who have the progressive form of NAFLD termed nonalcoholic steatohepatitis (NASH), it can progress to advanced fibrosis, cirrhosis, hepatocellular carcinoma, and liver-related morbidity and mortality. NASH is typically characterized by a specific pattern on liver histology, including steatosis, lobular inflammation, and ballooning with or without peri-sinusoidal fibrosis. Thus, key issues in NAFLD patients are the differentiation of NASH from simple steatosis and identification of advanced hepatic fibrosis. Until now, liver biopsy has been the gold standard for identifying these 2 critical end points, but has well-known limitations, including invasiveness; rare but potentially life-threatening complications; poor acceptability; sampling variability; and cost. Furthermore, due to the epidemic proportion of individuals with NAFLD worldwide, liver biopsy evaluation is impractical, and noninvasive assessment for the diagnosis of NASH and fibrosis is needed. Although much of the work remains to be done in establishing cost-effective strategies for screening for NASH, advanced fibrosis, and cirrhosis, in this review, we summarize the current state of the noninvasive assessment of liver disease in NAFLD, and we provide an expert synthesis of how these noninvasive tools could be utilized in clinical practice. Finally, we also list the key areas of research priorities in this area to move forward clinical practice.
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Hepatic steatosis is a frequently encountered imaging finding that may indicate chronic liver disease, the most common of which is nonalcoholic fatty liver disease (NAFLD). NAFLD is implicated in the development of systemic diseases and its progressive phenotype, nonalcoholic steatohepatitis (NASH), leads to increased liver-specific morbidity and mortality. With the rising obesity epidemic and advent of novel therapeutics aimed at altering metabolism, there is a growing need to quantify and monitor liver steatosis. Imaging methods for assessing steatosis range from simple and qualitative to complex and highly accurate metrics. Ultrasound may be appropriate in some clinical instances as a screening modality to identify the presence of abnormal liver morphology. However, it lacks sufficient specificity and sensitivity to constitute a diagnostic modality for instigating and monitoring therapy. Newer ultrasound techniques such as quantitative ultrasound show promise in turning qualitative assessment of steatosis on conventional ultrasound into quantitative measurements. Conventional unenhanced computed tomography (CT) is capable of detecting and quantifying moderate to severe steatosis but is inaccurate at diagnosing mild steatosis and involves the use of radiation. Newer CT techniques, like dual-energy CT, show potential in expanding the role of CT in quantifying steatosis. MRI PDFF is currently the most accurate and precise imaging biomarker to quantify liver steatosis. As such, PDFF is the most appropriate noninvasive endpoint for steatosis reduction in clinical trials and therapy response assessment.