Home About us Current issue Ahead of Print Back issues Submission Instructions Advertise Contact Login   

Search Article 
Advanced search 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 1546 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 

Table of Contents   
Year : 2014  |  Volume : 25  |  Issue : 1  |  Page : 170-171
Inverted cortico-medullary differentiation of renal hemosiderosis

1 Department of Nephrology, Max Super-speciality, Shalimar Bagh, New Delhi, India
2 Department of Radiology, University of Ottawa, Ottawa, Canada
3 SP Medical College, Bikaner, India

Click here for correspondence address and email

Date of Web Publication7-Jan-2014

How to cite this article:
Gupta A, Khandelwal A, Khandelwal K. Inverted cortico-medullary differentiation of renal hemosiderosis. Saudi J Kidney Dis Transpl 2014;25:170-1

How to cite this URL:
Gupta A, Khandelwal A, Khandelwal K. Inverted cortico-medullary differentiation of renal hemosiderosis. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2021 Jun 18];25:170-1. Available from: https://www.sjkdt.org/text.asp?2014/25/1/170/124559
To the Editor,

A 26-year-old woman suffering from hemo­globin (Hb) SS disease underwent magnetic resonance imaging (MRI) liver for quantifica­tion of iron overload. She had been receiving red cell exchange transfusions for the past 12 months. Her transfusion schedule was 16 mL transfusions every five weeks targeted to maintain Hb S levels below 50% so as to reduce any severe acute sickle crisis. Her phy­sical examination was essentially normal. Her recent blood work showed Hb 104 g/L, hematocrit 0.307 L/L, Hb S 38.3%, Hb F 1.6%, Hb A2 3.3%, few sickle cells, target cells and iregularly contracted red blood cells. Bioche­mistry profile revealed lactate dehydrogenase 494 U/L, total bilirubin 37 μmol/L, alanine aminotransferase 36 U/L, aspartate aminotransferase 34 U/L, urea 5.5 mmol/L, creatinine 41 μmol/L, iron 16 μmol/L, iron binding capa­city 43 μmol/L, transferrin saturation 37%, ferritin 805 μg/L and random urine albumin/ creatinine ratio 0.8 g/mol (normal <2.8).

MRI liver revealed estimated liver iron con­centration 110 μmol/g (normal <30 μmol/g) as calculated by the method described by Gandon et al. [1] This corresponds to a moderate degree of iron overload. Liver was normal in size and shape and appeared mildly hypointense on longer echo time in-phase sequence compared with out of phase sequence, suggesting suscep­tibility effect due to iron overload. The bila­teral kidneys were normal in size and revealed T2 hypointense signal of renal cortices with "reverse corticomedullary differentiation," suggesting iron overload of kidneys [Figure 1]a. The renal cortex on the sequential increasing TE sequences (Time to repeat, TR-120, Time to echo, TE-20) showed increasingly hypo-intense signal [Figure 1]b. Bone marrow of the visualized vertebra also showed mild iron deposition.
Figure 1: (a) Coronal true FISP (Fast Imaging with Steady State Precession) and (b) axial gradient echo (GRE) sequence images show diffuse hypointense signal of renal cortices (arrows) with "reverse corticomedullary differentiation." The spleen (S) and liver (L) also show diffuse hypointense signals on GRE sequences due to the susceptibility effect of deposited iron.

Click here to view

The renal cortices contain highest concen­trations of glomeruli and proximal tubules. The iron deposits likely localize to the tubular system as proximal tubules contain avid heme transport molecules. Specifically, megalin and cubulin bind to and internalize free circulating hemoglobin. The elevated circulating free hemoglobin from chronic hemolysis is the dominant cause for renal iron deposition in transfused sickle cell disease patients. How­ever, patients with mild sickle cell disease who have not undergone transfusion do not develop iron overload in the renal cortex because extravascular hemolysis in the reticulo-endo-thelial system by the defective red blood cells is the main pathophysiology. [2],[3] In our case, hemosiderin and ferritin storage in renal tubules, due to frequent transfusions leading to iron overload, explains the low intensity of renal cortex on MR images, giving the cha­racteristic appearance.

   References Top

1.Gandon Y, Olivié D, Guyader D, et al. Non-invasive assessment of hepatic iron stores by MRI. Lancet 2004;363:357-62.  Back to cited text no. 1
2.Schein A, Enriquez C, Coates TD, Wood JC. Magnetic resonance detection of kidney iron deposition in sickle cell disease: A marker of chronic hemolysis. J Magn Reson Imaging 2008;28:698-704.  Back to cited text no. 2
3.Jeong JY, Kim SH, Lee HJ, Sim JS. Atypical low-signal-intensity renal parenchyma: Causes and patterns. Radiographics 2002;22:833-46.  Back to cited text no. 3

Correspondence Address:
Ankur Gupta
Department of Nephrology, Max Super-speciality, Shalimar Bagh, New Delhi
Login to access the Email id

DOI: 10.4103/1319-2442.124559

PMID: 24434406

Rights and Permissions


  [Figure 1]


    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  

    Article Figures

 Article Access Statistics
    PDF Downloaded294    
    Comments [Add]    

Recommend this journal