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Year : 2010  |  Volume : 56  |  Issue : 3  |  Page : 216-217

Renal hemosiderosis: A case of black kidneys causing renal failure

1 Department of Internal Medicine, University of Arkansas for Medical Sciences, 4301 West Markham Street, Suite # 634, Little Rock, AR 72205, USA
2 Department of Radiology, University of Arkansas for Medical Sciences, 4301 West Markham Street, Suite # 634, Little Rock, AR 72205, USA

Date of Web Publication23-Aug-2010

Correspondence Address:
N Relia
Department of Internal Medicine, University of Arkansas for Medical Sciences, 4301 West Markham Street, Suite # 634, Little Rock, AR 72205
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0022-3859.68635

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How to cite this article:
Relia N, Kaushik C. Renal hemosiderosis: A case of black kidneys causing renal failure. J Postgrad Med 2010;56:216-7

How to cite this URL:
Relia N, Kaushik C. Renal hemosiderosis: A case of black kidneys causing renal failure. J Postgrad Med [serial online] 2010 [cited 2022 Nov 27];56:216-7. Available from:

A 68-year-old non-diabetic male with history of metastatic colon cancer was referred for evaluation of rising serum creatinine. Past medical history was significant for hypertension well controlled on medications and a remote history of valvular heart disease requiring valve replacement. Patient records indicated a slowly rising serum creatinine level, for the last two years as shown in [Table 1]. Physical examination was remarkable for a loud click on cardiovascular examination and somewhat tender to palpation right upper abdominal quadrant. Laboratory analysis showed hemoglobin of 9.2 mg/dl, hematocrit of 28%, white cell count of 11000/μl and platelet of 210000/μl. Total bilirubin was 1.8 mg/dl, aspartate aminotransferase 80 IU/L, alanine aminotransferase 88 IU/L, alkaline phosphatase 170 IU/L and an elevated lactate dehydrogenase of 468 IU/L. Urinalysis was unremarkable and ultrasonography (USG) showed normal-sized bilateral kidneys with no evidence of obstructive uropathy. Twenty-four-hour urine protein was 0.5 gm. In the absence of a readily available explanation for slowly rising creatinine despite an adequate control of blood pressure, it was decided to perform a kidney biopsy. However, prior to kidney biopsy, an abdominal magnetic resonance imaging (MRI) was done to evaluate the extent of abdominal spread and liver metastases from colon cancer. Incidentally, both T1 [Figure 1]a and T2 [Figure 1]b weighted MRI showed reversal of the normal MRI characteristics of the kidney with markedly hypointense renal cortex (arrowheads in [Figure 1]) compared to the medulla consistent with iron deposition in the kidney suggestive of hemosiderosis. [1] Serum haptoglobin was then obtained and was low at 9.1 mg/dl (N: 27-139 mg/dl) with an elevated reticulocyte count of 4%. In the absence of a recognizable cause of renal dysfunction in our patient, a diagnosis of renal hemosiderosis resulting from chronic mechanical hemolysis from prosthetic cardiac valve leading to chronic kidney disease was made. [2] The decision to perform kidney biopsy was abandoned.
Table 1 :Serum creatinine trend

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Figure 1 :T1-weighted (a) T2-weighted (b) axial images through kidneys reveal markedly hypointense renal cortex as compared to medulla

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Renal hemosiderosis is a known complication of chronic intravascular hemolytic states such as hemolytic anemias, paroxysmal nocturnal hemoglobinuria (PNH) and mechanical hemolysis from prosthetic cardiac valve. The spectrum of renal involvement in renal hemosiderosis has only been scarcely addressed in the literature and is limited to case reports and small case series. Renal hemosiderosis is usually considered a benign and incidental radiologic finding and rarely results in clinically apparent renal dysfunction. [2] A recent review of the literature on PNH describes three cases of renal hemosiderosis presenting with renal failure. [2] Nephrologists routinely recommend and are content with a renal USG before undertaking a renal biopsy. Our patient had an MRI for an unrelated reason that showed evidence of renal hemosiderosis and led to further workup that elucidated the cause of renal failure in our patient. Also, this patient had a valve replacement in the distant past but the elevation in creatinine started only two years back reflecting that a critical level of iron deposition in the kidney heralds the onset of renal dysfunction. Our case underscores the importance of recognizing renal hemosiderosis as a cause of renal failure in an appropriate clinical setting and that advanced imaging beyond renal USG such as MRI can clinch the diagnosis, rendering an invasive procedure like renal biopsy unnecessary.

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1.Rimola J, Martin J, Puig J, Darnell A, Massuet A. The kidney in paroxysmal nocturnal hemoglobinuria: MRI findings. Br J Radiol 2004;77:953-6.  Back to cited text no. 1      
2.Nair RK, Khaira A, Sharma A, Mahajan S, Dinda AK. Spectrum of renal involvement in paroxysmal nocturnal hemoglobinuria: Report of three cases and a brief review of the literature. Int Urol Nephrol 2008;40:471-5.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  


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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
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