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Acute renal failure: common occurrence of preservation of corticomedullary differentiation on MR images
Magnetic Resonance Imaging 19 (2001) 789 –793
Acute renal failure: common occurrence of preservation of corticomedullary differentiation on MR images Jae-Joon Chunga, Richard C. Semelkaa,*, Diego R. Martina,b a
Department of Radiology, University of North Carolina, Chapel Hill, NC 27599-7510, USA Department of Radiology, Robert C. Byrd Health Sciences Center, Morgantown, WV 26506-9235, USA
b
Received 21 September 2000; accepted 8 June 2001
Abstract The purpose of this study was to evaluate the relationship between renal corticomedullary differentiation (CMD) on MR imaging and serum creatinine (sCr) level in patients with acute renal failure (ARF). Twenty-one patients with ARF were retrospectively investigated. In all 21 patients, sCr levels were obtained on the same date as the MR study, and within 8 days before and after the MR study. CMD was assessed on non-contrast T1-weighted images and immediate post-gadolinium spoiled gradient echo (Gd-SGE) images. Presence of CMD was graded into 3 groups as ‘preserved’, ‘intermediate’, or ‘loss’. On non-contrast T1-weighted images, 12/21 (57%) showed loss of CMD and 9/21 (43%) showed preserved CMD. On immediate Gd-SGE images, 5/21 (24%) showed loss of CMD, 12/21 (57%) preserved CMD, and 4/21 (19%) intermediate CMD. The sCr levels of 9 patients with preserved CMD on non-contrast T1-weighted images ranged from 1.4 to 10.5 mg/dl (mean 4.6 mg/dl), while those of 12 patients with loss of CMD ranged from 1.6 to 7.6 mg/dl (mean 4.8 mg/dl), which was not statistically significant (p ⬎ 0.2). Renal CMD can remain preserved on non-contrast T1-weighted or immediate Gd-SGE images in patients with acute presentation of ARF, independent of sCr level. © 2001 Elsevier Science Inc. All rights reserved. Keywords: Kidney, failure; Kidney, function; Kidney, MR; Magnetic resonance (MR), pulse sequences
1. Introduction Acute renal failure (ARF) is a syndrome characterized by rapid decline in glomerular filtration rate (GFR) and retention of water, crystalloid solutes, and nitrogenous metabolites in the body [1,2]. Clinically significant ARF is usually associated with progressively increasing serum creatinine (sCr) and urea nitrogen levels (azotemia) greater than 1.5 mg/dl and 10 mg/dl, respectively [1]. Acute tubular necrosis (ATN), resulting from ischemia or nephrotoxins, is the most common cause of ARF [1,2]. Approximately 20% of patients with ARF with a sCr greater than 2.5 mg/dl may require dialysis [3]. On T1-weighted MR images of the normal healthy kidney, the cortex appears hyperintense with respect to the medulla, resulting in easily visualized corticomedullary differentiation (CMD) [3,4]. Demonstration of CMD is best made on non-contrast T1-weighted fat-suppressed (T1FS) * Corresponding author. Tel.: ⫹1-919-966-6777; fax: ⫹1-919-9665934. E-mail address: [email protected] (R.C. Semelka).
spin echo or spoiled gradient echo (SGE) images [5]. Diminished CMD and globular enlargement of kidneys on T1-weighted MR imaging have been described in patients with ARF, although these findings may be nonspecific [3]. Contrast enhanced CT and fluoroscopic techniques using iodinated contrast agents are contraindicated in patients with ARF due to contrast nephrotoxicity [3]. However, no significant nephrotoxicity has been reported for paramagnetic contrast agents, either ionic or non-ionic, with concentrations used commonly in clinical practice [6]. Loss of CMD has been observed in renal insufficiency of a variety of etiologies, such as glomerulonephritis, acute tubular necrosis, end-stage chronic renal failure, obstructive hydronephrosis, and acute allograft rejection [3]. Although it is well known that CMD is lost in various causes of chronic renal failure, this has not been ascertained in ARF. Preservation of CMD may be construed as reflecting normal renal function. The purpose of this study was to determine the frequency of preservation of CMD on noncontrast T1-weighted images, in patients with ARF during the acute presentation defined as within 2 weeks from the onset of the disease process. The loss or preservation of
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J.-J. Chung et al. / Magnetic Resonance Imaging 19 (2001) 789 –793
CMD on immediate post gadolinium T1-weighted SGE images was also examined.
2. Materials and methods 2.1. Patients A total of 21 consecutive patients (9 men, 12 women), ranging from 13 to 64 years in age (mean, 40 years), with a clinical diagnosis of ARF were assessed retrospectively, based upon a review of our MR records. Inclusion criteria for all 21 patients were that the sCr level was obtained on the MR examination date and within 8 days before and 8 days after the MR examination. No follow-up MR study was available in any of the patients. At our institution, a sCr level less than 1.2 mg/dl is within normal limits. No patient was on an established hemodialysis regimen prior to the MR study. Five patients underwent initial hemodialysis between 2 to 3 days before the MR examination. Five patients underwent percutaneous or open renal biopsy within 5 days after the MR scan. The underlying causes of ARF included exogenous agent induced ATN (n ⫽ 7), rhabdomyolysis (n ⫽ 4), Grampositive cocci bacteremia (n ⫽ 2), sepsis (n ⫽ 2), postinfectious glomerulonephritis (n ⫽ 1), bacterial endocarditis (n ⫽ 1), malakoplakia (n ⫽ 1), pancreatitis (n ⫽ 1), cocaine overdose (n ⫽ 1), and Klippel-Trenaunay-Weber syndrome (n ⫽ 1). The histopathological assessment of renal biopsies in 5 patients were ATN (n ⫽ 2), post-infectious glomerulonephritis (n ⫽ 1), malakoplakia (n ⫽ 1), and chronic glomerulonephritis with advanced glomerular sclerosis in a patient with Klippel-Trenaunay-Weber syndrome (n ⫽ 1). Indications for the MR studies in 21 patients were determined from the requisition data submitted in each patient’s electronic medical file, including: suspected abdominal abscess (n ⫽ 8), questionable hepatic or pancreatic lesion (n ⫽ 6), suspected renal lesion (n ⫽ 3), retroperitoneal hemorrhage (n ⫽ 2), bowel ischemia (n ⫽ 1), and malignant lymphoma (n ⫽ 1). 2.2. MR technique MR studies were performed on a 1.5 Tesla superconducting magnet (SP 4000 or VISION, Siemens Medical Systems, Iselin, NJ) using the following sequences: non-contrast T1-weighted spoiled gradient echo (SGE) (17 patients) (TR ⫽ 150 msec/TE ⫽ 4 msec/Flip angle ⫽ 80°/section thickness ⫽ 8 –10 mm/intersection gap ⫽ 20%/FOV ⫽ 350 ⫻ 400 mm/effective matrix ⫽ 128 ⫻ 256/number of signal averages ⫽ 1/22 section in a 20-s breath hold) and T1-weighted fat-suppressed SGE (T1FS-SGE) (4 patients) images. Images were acquired in the transverse and coronal planes, and images encompassing the entire kidneys were obtained in one acquisition. SGE was performed before
contrast administration and immediately post-gadolinium administration (Gd-SGE) in all patients. Gadolinium (Magnevist, Berlex, Wayne, NJ or Omniscan, Nycomed, NY, NY) was administrated in a dosage of 0.1 mmol/kg at 2 cc/sec followed by an injection of 10 cc normal saline at 2 cc/sec. Immediate Gd-SGE scanning was initiated 18-s after initiation of the gadolinium administration. All patients fasted for 6 h prior to MR scanning. 2.3. Image interpretation Visual assessments for presence of CMD on non-contrast T1-weighted SGE or T1FS-SGE images, and on immediate Gd-SGE images, were performed independently by two radiologists. Readers were blinded to the underlying cause of renal disease or the sCr level of the patients. Presence of CMD was graded into three categories according to the following criteria: ‘preserved’ (clearly visualized throughout all segments of both kidneys), ‘intermediate’ (present but less conspicuous or with absence of CMD in portions of the kidneys), and ‘loss’ (not visualized anywhere throughout both kidneys). Agreement on the presence or absence of CMD was found in all cases. In 3 cases, there was disagreement of classification between preserved and intermediate CMD, but all cases were resolved by consensus reassessment. The sCr levels were correlated with MR imaging findings, and the trend (increasing, decreasing, or stable) in sCr was also determined.
3. Results On non-contrast T1-weighted images, 12 (57%) of 21 patients demonstrated loss of CMD and 9 (43%) demonstrated preserved CMD. The sCr levels of 9 patients with preserved CMD on non-contrast T1-weighted images ranged from 1.4 to 10.5 mg/dl (mean 4.6 mg/dl), while those of 12 patients with loss of CMD ranged from 1.6 to 7.6 mg/dl (mean 4.8 mg/dl), which was statistically not significant (p ⬎ 0.2). On immediate Gd-SGE images, 5 (24%) of 21 patients showed loss of CMD, 12 (57%) showed preserved CMD, and 4 (19%) showed intermediate CMD. The sCr levels of 16 patients with preserved CMD on immediate Gd-SGE images ranged from 1.4 to 10.5 mg/dl (mean 4.6 mg/dl), while those of 5 patients with loss of CMD ranged from 2.9 to 7.5 mg/dl (mean 5.2 mg/dl), which was statistically not significant (p ⬎ 0.2). Of 12 patients with loss of CMD on non-contrast T1weighted images, 5 patients (42%) had loss of CMD on immediate Gd-SGE images. Of the remaining 7 patients, 3 patients (25%) showed intermediate CMD and 4 (33%) showed preserved CMD (Fig. 1) on immediate Gd-SGE images. Of 9 patients with preserved CMD on non-contrast T1-weighted images, 8 patients (89%) showed preserved CMD (Fig. 2) and 1 (11%) showed intermediate CMD on
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Fig. 1. Acute renal failure with acute tubular necrosis (sCr level ⫽ 7.6 mg/dl). Non-contrast SGE image (TR/TE ⫽ 150/4 msec) (a) shows intermediate loss of CMD in both kidneys with globular enlargement. On Gd-SGE image (TR/TE ⫽ 150/4 msec) (b), CMD is intermediately demonstrated in both kidneys. This patient had worsening renal function at the time of MR imaging.
immediate Gd-SGE images. Table 1 summarizes the correlation of CMD on non-contrast T1-weighted or Gd-SGE images relative to sCr level. Of 5 patients with biopsy-proven histopathology, 2 patients with ATN (see Fig. 1) and 1 patient with KlippelTrenaunay-Weber syndrome showed preserved CMD on either non-contrast T1-weighted images or immediate GdSGE images. One patient with malakoplakia showed loss of CMD on both non-contrast T1-weighted images and immediate Gd-SGE images. One patient with post-infectious glomerulonephritis showed loss of CMD on non-contrast T1weighted images and preserved CMD on immediate GdSGE images. Fourteen patients (67%) had worsening renal function and 7 patients (33%) had abnormal but progressively improving renal function at the time of MR imaging. Table 2 summarizes the CMD relative to worsening or improving phase on MR study date. Within 8 days after MR study, 16 patients (76%) showed decrease of sCr value and 5 patients (24%) showed persistent or increased elevation of sCr value.
Comparing the trend in sCr, either increasing or decreasing during the time of MR imaging, revealed that a greater fraction of patients with improving sCr level had preserved CMD (Fig. 2). Conversely, a greater fraction of patients with worsening sCr demonstrated loss of CMD. However, these differences were not statistically different. Similar observation of CMD preservation based upon Gd-SGE images was also observed, despite the fact that the physiology for CMD is based upon a different mechanism. Our study showed that CMD was preserved in a large fraction (43%) of patients with ARF on both non-contrast T1-weighted and Gd-SGE images. There was no statistically significant difference between the sCr levels of the ARF group showing preserved CMD versus the group with loss of CMD.
4. Discussion It is presumed that renal CMD on non-contrast T1FS images correlates with differences in water content between
Fig. 2. Acute renal failure with acute tubular necrosis (sCr level ⫽ 6.0 mg/dl). Non-contrast SGE image (TR/TE ⫽ 150/4 msec) (a) shows intermediate loss of CMD in both kidneys with mild globular enlargement. Diffuse low signal intensity of both kidneys on this image results from iron deposition. On Gd-SGE image (TR/TE ⫽ 150/4 msec) (b), CMD is well demonstrated in both kidneys. This patient had improving renal function at the time of MR imaging.
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Table 1 Presence of CMD on T1-weighted and Gd-SGE images relative to sCr level sCr level (mg/dl) (n ⫽ 21)
CMD on T1WI & Gd-SGE No CMD on T1WI, CMD on Gd-SGE No CMD on T1WI or Gd-SGE
⬍1.2
1.2⬃1.9
3.0⬃8.5
⬎8.5
1 1
2 1
5 5
1
1
4
Note—Numbers are numbers of patients. CMD: corticomedullary differentiation. T1WI: noncontrast T1-weighted image. Gd-SGE: immediate post-gadolinium spoiled gradient echo image. sCr: serum creatinine.
the renal cortex and medulla [7,8] with the medulla having more water content per unit tissue mass than the cortex [9] resulting in relatively diminished signal. Pathologic processes causing cortical edema leads to prolongation of T1 relaxation with diminution of CMD. Decreased tubular flow, or deposition of proteinaceous or bloody material in the medulla may result in increased SI in the medulla [4], which could also diminish CMD on non-contrast T1weighted images. CMD on Gd-SGE images results from differential blood flow to the renal cortex and medulla, with approximately tenfold greater flow to the cortex [10]. Pathologic processes that alter the differential blood flow or impair delivery and filtration of intravascular gadolinium should diminish CMD on post-gadolinium images. Even though we assessed the visibility of CMD after gadolinium injection, we are not certain that this is also representative of the same process as loss of CMD on non-contrast T1-weighted images, because the appearance after gadolinium injection probably relates to not only water content but also perfusion in renal cortex or medulla. Kettritz et al. [4] and Semelka et al. [5] reported that there was a good correlation between loss of CMD and increasing level of sCr concentration in the majority of patients with renal diseases. It was also shown that the degree of renal dysfunction, rather than the etiology of underlying renal disease, was the more important factor determining loss of CMD [4]. This consistent observation of Table 2 CMD relative to worsening or improving phase on MR study date Worsening
Good CMD Moderate CMD No CMD
Improving
T1WI
Gd-SGE
T1WI
Gd-SGE
5 (36%)
7 (50%) 3 (21%) 4 (29%)
4 (57%)
5 (71%) 1 (14%) 1 (14%)
9 (64%)
3 (43%)
Note—Numbers are numbers of patients. CMD: corticomedullary differentiation. T1WI: noncontrast T1-weighted image. Gd-SGE: immediate post-gadolinium spoiled gradient echo image. sCr: serum creatinine.
loss of CMD was observed in patients with various forms of chronic renal failure [4,5]. These prior studies also found that CMD on non-contrast T1FS images was consistently lost with sCr value ⬎ 3 mg/dl, whereas CMD on Gd-SGE images was not lost until sCr reached a level of 8 mg/dl. This showed that loss of CMD on Gd-SGE images was relatively insensitive to decreased renal function, although the authors postulated that it might reflect irreversible renal damage [4]. We think the state of hydration can affect the CMD on MR images, even though it is difficult to document the state of hydration of patients readily. The prognosis for recovery of renal function after presentation with ARF depends on the etiology of the disorder [1]. ARF due to prerenal causes, as well as certain renal pathologies such as glomerulonephritis, vasculitis, and renal tubular injury, are potentially reversible [1]. Liou et al. [11] found that loss of CMD, identified on non-contrast T1weighted MR scans of patients with ARF due to ATN, was reversible in patients who had successful treatment of ARF with improvement of renal function measured by decreased sCr. Therefore, loss of CMD on non-contrast T1-weighted images does not necessarily indicate a poor prognosis for recovery of renal function [5]. A key difference between these previous studies and the current study is that, here, we selected patients based upon a clinical history of recent onset ARF, while previously, the patients were imaged at least 2 weeks or longer beyond initial clinical presentation of renal insufficiency. It is likely that there is a delay between the initial clinical presentation of ARF, and the MR imaging findings of loss of CMD. The findings in this current study illustrates that CMD on noncontrast images is in fact commonly preserved in the early period (within 2 weeks) of developing ARF. Our belief is that there is a time lag between the renal parenchymal insult and the development of fluid changes in the cortex and medullary compartments. The clinical importance of this observation is that preservation of CMD in ARF should not be misconstrued as reflecting normal renal function, because of the known finding that CMD is invariably lost in chronic renal failure. Patients with ARF and preserved CMD may have severe renal dysfunction, as our results have shown. This study has a few limitations. First, no follow-up MR renal scans were available in any of the patients. This limits the ability to determine a time course relationship between initial presentation and loss of CMD. Based upon previously published reports, it is presumed that there is a delay between onset of ARF and loss of CMD on MR imaging, and that this delay is in the order of at least 2 weeks. A second limitation is that only sCr was available for quantitative assessment of renal function in all patients, and was used to reflect GFR. A more accurate measure such as creatinine clearance was not available. Nevertheless, many studies have previously depended upon sCr as a reasonable estimate of GFR. A third limitation is that the number of patients in this study would not yield robust statistical data
J.-J. Chung et al. / Magnetic Resonance Imaging 19 (2001) 789 –793
for detection of more subtle trends. However, we were more interested in determination of definite trends in the association between loss of CMD and degree of ARF as measured by sCr. A fourth limitation is that only four patients were performed with non-contrast T1FS images, because of the retrospective nature of this study. Future investigation on the relationship of renal CMD and ARF should include the following: prospective study with all patients undergoing noncontrast T1-weighted fat suppressed SGE; follow up MR studies; and correlation of the time course of ARF and CMD on MRI, to determine if MRI may play a role to help these patients, therapeutically or prognostically. In summary, the results of our study demonstrate that loss of CMD may not be present in patients with recent onset ARF with elevated sCr. Caution must therefore be exercised when interpreting MR studies in patients with recent onset ARF in that preservation of CMD does not reflect normal renal function.
References [1] Grantham JJ. Acute renal failure. In: Wyngaarden JB, Smith LH Jr, Bennett JC, editors. Cecil Textbook of Medicine. 18th edition. Philadelphia: W. B. Saunders Company, 1988:528 –33.
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[2] Mucelli RP, Bertolotto M. Imaging techniques in acute renal failure. Kidney International (Suppl) 1998:S102–5. [3] Becker JA, Carvlin M, Choyke PL, et al. Imaging of renal failure. In: Pollack HM, editor. Clinical Urology. Philadelphia: W. B. Saunders Company, 1990:2595– 614. [4] Kettritz U, Semelka RC, Brown ED, Sharp TJ, Lawing WL, Colindres RE. MR findings in diffuse renal parenchymal disease. JMRI 1996;1:136 – 44. [5] Semelka RC, Corrigan K, Ascher SM, Brown JJ, Colindres RE. Renal corticomedullary differentiation: observation in patients with differing serum creatinine levels. Radiology 1994;190:149 –52. [6] Rofsky NM, Weinreb JC, Bosniak MA, Libes RB, Birnbaum BA. Renal lesion characterization with gadolinium-enhanced MR imaging: efficacy and safety in patients with renal insufficiency. Radiology 1991;180:85–9. [7] Geisinger MA, Risius B, Jordan ML, Zelch MG, Novick AC, George CR. Magnetic resonance imaging of renal transplants. AJR 1984;143: 1229 –34. [8] Rholl KS, Lee JKT, Ling D, Sicard GA, Griffith RC, Freeman M. Acute renal rejection versus acute tubular necrosis in a canine model: MR evaluation. Radiology 1986;160:113–7. [9] Knepper MA, Rector FC. Urinary concentration and dilution. In: Brenner BM, Rector FC, editors. The kidney. 4th ed. Philadelphia: W. B. Saunders Company, 1991:445– 82. [10] Knox FG, Ritman EL, Romero JC. Intralateral distribution of blood flow: evaluation of a new approach to measurement. Kidney Int 1984;25:473–9. [11] Liou JTS, Lee JKT, Heiken JP, Totty WG, Molina PL, Flye WM. Renal transplants: can acute rejection and acute tubular necrosis be differentiated with MR imaging? Radiology 1991;179:61–5.
Acute renal failure: common occurrence of preservation of corticomedullary differentiation on MR images Jae-Joon Chunga, Richard C. Semelkaa,*, Diego R. Martina,b a
Department of Radiology, University of North Carolina, Chapel Hill, NC 27599-7510, USA Department of Radiology, Robert C. Byrd Health Sciences Center, Morgantown, WV 26506-9235, USA
b
Received 21 September 2000; accepted 8 June 2001
Abstract The purpose of this study was to evaluate the relationship between renal corticomedullary differentiation (CMD) on MR imaging and serum creatinine (sCr) level in patients with acute renal failure (ARF). Twenty-one patients with ARF were retrospectively investigated. In all 21 patients, sCr levels were obtained on the same date as the MR study, and within 8 days before and after the MR study. CMD was assessed on non-contrast T1-weighted images and immediate post-gadolinium spoiled gradient echo (Gd-SGE) images. Presence of CMD was graded into 3 groups as ‘preserved’, ‘intermediate’, or ‘loss’. On non-contrast T1-weighted images, 12/21 (57%) showed loss of CMD and 9/21 (43%) showed preserved CMD. On immediate Gd-SGE images, 5/21 (24%) showed loss of CMD, 12/21 (57%) preserved CMD, and 4/21 (19%) intermediate CMD. The sCr levels of 9 patients with preserved CMD on non-contrast T1-weighted images ranged from 1.4 to 10.5 mg/dl (mean 4.6 mg/dl), while those of 12 patients with loss of CMD ranged from 1.6 to 7.6 mg/dl (mean 4.8 mg/dl), which was not statistically significant (p ⬎ 0.2). Renal CMD can remain preserved on non-contrast T1-weighted or immediate Gd-SGE images in patients with acute presentation of ARF, independent of sCr level. © 2001 Elsevier Science Inc. All rights reserved. Keywords: Kidney, failure; Kidney, function; Kidney, MR; Magnetic resonance (MR), pulse sequences
1. Introduction Acute renal failure (ARF) is a syndrome characterized by rapid decline in glomerular filtration rate (GFR) and retention of water, crystalloid solutes, and nitrogenous metabolites in the body [1,2]. Clinically significant ARF is usually associated with progressively increasing serum creatinine (sCr) and urea nitrogen levels (azotemia) greater than 1.5 mg/dl and 10 mg/dl, respectively [1]. Acute tubular necrosis (ATN), resulting from ischemia or nephrotoxins, is the most common cause of ARF [1,2]. Approximately 20% of patients with ARF with a sCr greater than 2.5 mg/dl may require dialysis [3]. On T1-weighted MR images of the normal healthy kidney, the cortex appears hyperintense with respect to the medulla, resulting in easily visualized corticomedullary differentiation (CMD) [3,4]. Demonstration of CMD is best made on non-contrast T1-weighted fat-suppressed (T1FS) * Corresponding author. Tel.: ⫹1-919-966-6777; fax: ⫹1-919-9665934. E-mail address: [email protected] (R.C. Semelka).
spin echo or spoiled gradient echo (SGE) images [5]. Diminished CMD and globular enlargement of kidneys on T1-weighted MR imaging have been described in patients with ARF, although these findings may be nonspecific [3]. Contrast enhanced CT and fluoroscopic techniques using iodinated contrast agents are contraindicated in patients with ARF due to contrast nephrotoxicity [3]. However, no significant nephrotoxicity has been reported for paramagnetic contrast agents, either ionic or non-ionic, with concentrations used commonly in clinical practice [6]. Loss of CMD has been observed in renal insufficiency of a variety of etiologies, such as glomerulonephritis, acute tubular necrosis, end-stage chronic renal failure, obstructive hydronephrosis, and acute allograft rejection [3]. Although it is well known that CMD is lost in various causes of chronic renal failure, this has not been ascertained in ARF. Preservation of CMD may be construed as reflecting normal renal function. The purpose of this study was to determine the frequency of preservation of CMD on noncontrast T1-weighted images, in patients with ARF during the acute presentation defined as within 2 weeks from the onset of the disease process. The loss or preservation of
0730-725X/01/$ – see front matter © 2001 Elsevier Science Inc. All rights reserved. PII: S 0 7 3 0 - 7 2 5 X ( 0 1 ) 0 0 4 1 1 - 8
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J.-J. Chung et al. / Magnetic Resonance Imaging 19 (2001) 789 –793
CMD on immediate post gadolinium T1-weighted SGE images was also examined.
2. Materials and methods 2.1. Patients A total of 21 consecutive patients (9 men, 12 women), ranging from 13 to 64 years in age (mean, 40 years), with a clinical diagnosis of ARF were assessed retrospectively, based upon a review of our MR records. Inclusion criteria for all 21 patients were that the sCr level was obtained on the MR examination date and within 8 days before and 8 days after the MR examination. No follow-up MR study was available in any of the patients. At our institution, a sCr level less than 1.2 mg/dl is within normal limits. No patient was on an established hemodialysis regimen prior to the MR study. Five patients underwent initial hemodialysis between 2 to 3 days before the MR examination. Five patients underwent percutaneous or open renal biopsy within 5 days after the MR scan. The underlying causes of ARF included exogenous agent induced ATN (n ⫽ 7), rhabdomyolysis (n ⫽ 4), Grampositive cocci bacteremia (n ⫽ 2), sepsis (n ⫽ 2), postinfectious glomerulonephritis (n ⫽ 1), bacterial endocarditis (n ⫽ 1), malakoplakia (n ⫽ 1), pancreatitis (n ⫽ 1), cocaine overdose (n ⫽ 1), and Klippel-Trenaunay-Weber syndrome (n ⫽ 1). The histopathological assessment of renal biopsies in 5 patients were ATN (n ⫽ 2), post-infectious glomerulonephritis (n ⫽ 1), malakoplakia (n ⫽ 1), and chronic glomerulonephritis with advanced glomerular sclerosis in a patient with Klippel-Trenaunay-Weber syndrome (n ⫽ 1). Indications for the MR studies in 21 patients were determined from the requisition data submitted in each patient’s electronic medical file, including: suspected abdominal abscess (n ⫽ 8), questionable hepatic or pancreatic lesion (n ⫽ 6), suspected renal lesion (n ⫽ 3), retroperitoneal hemorrhage (n ⫽ 2), bowel ischemia (n ⫽ 1), and malignant lymphoma (n ⫽ 1). 2.2. MR technique MR studies were performed on a 1.5 Tesla superconducting magnet (SP 4000 or VISION, Siemens Medical Systems, Iselin, NJ) using the following sequences: non-contrast T1-weighted spoiled gradient echo (SGE) (17 patients) (TR ⫽ 150 msec/TE ⫽ 4 msec/Flip angle ⫽ 80°/section thickness ⫽ 8 –10 mm/intersection gap ⫽ 20%/FOV ⫽ 350 ⫻ 400 mm/effective matrix ⫽ 128 ⫻ 256/number of signal averages ⫽ 1/22 section in a 20-s breath hold) and T1-weighted fat-suppressed SGE (T1FS-SGE) (4 patients) images. Images were acquired in the transverse and coronal planes, and images encompassing the entire kidneys were obtained in one acquisition. SGE was performed before
contrast administration and immediately post-gadolinium administration (Gd-SGE) in all patients. Gadolinium (Magnevist, Berlex, Wayne, NJ or Omniscan, Nycomed, NY, NY) was administrated in a dosage of 0.1 mmol/kg at 2 cc/sec followed by an injection of 10 cc normal saline at 2 cc/sec. Immediate Gd-SGE scanning was initiated 18-s after initiation of the gadolinium administration. All patients fasted for 6 h prior to MR scanning. 2.3. Image interpretation Visual assessments for presence of CMD on non-contrast T1-weighted SGE or T1FS-SGE images, and on immediate Gd-SGE images, were performed independently by two radiologists. Readers were blinded to the underlying cause of renal disease or the sCr level of the patients. Presence of CMD was graded into three categories according to the following criteria: ‘preserved’ (clearly visualized throughout all segments of both kidneys), ‘intermediate’ (present but less conspicuous or with absence of CMD in portions of the kidneys), and ‘loss’ (not visualized anywhere throughout both kidneys). Agreement on the presence or absence of CMD was found in all cases. In 3 cases, there was disagreement of classification between preserved and intermediate CMD, but all cases were resolved by consensus reassessment. The sCr levels were correlated with MR imaging findings, and the trend (increasing, decreasing, or stable) in sCr was also determined.
3. Results On non-contrast T1-weighted images, 12 (57%) of 21 patients demonstrated loss of CMD and 9 (43%) demonstrated preserved CMD. The sCr levels of 9 patients with preserved CMD on non-contrast T1-weighted images ranged from 1.4 to 10.5 mg/dl (mean 4.6 mg/dl), while those of 12 patients with loss of CMD ranged from 1.6 to 7.6 mg/dl (mean 4.8 mg/dl), which was statistically not significant (p ⬎ 0.2). On immediate Gd-SGE images, 5 (24%) of 21 patients showed loss of CMD, 12 (57%) showed preserved CMD, and 4 (19%) showed intermediate CMD. The sCr levels of 16 patients with preserved CMD on immediate Gd-SGE images ranged from 1.4 to 10.5 mg/dl (mean 4.6 mg/dl), while those of 5 patients with loss of CMD ranged from 2.9 to 7.5 mg/dl (mean 5.2 mg/dl), which was statistically not significant (p ⬎ 0.2). Of 12 patients with loss of CMD on non-contrast T1weighted images, 5 patients (42%) had loss of CMD on immediate Gd-SGE images. Of the remaining 7 patients, 3 patients (25%) showed intermediate CMD and 4 (33%) showed preserved CMD (Fig. 1) on immediate Gd-SGE images. Of 9 patients with preserved CMD on non-contrast T1-weighted images, 8 patients (89%) showed preserved CMD (Fig. 2) and 1 (11%) showed intermediate CMD on
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Fig. 1. Acute renal failure with acute tubular necrosis (sCr level ⫽ 7.6 mg/dl). Non-contrast SGE image (TR/TE ⫽ 150/4 msec) (a) shows intermediate loss of CMD in both kidneys with globular enlargement. On Gd-SGE image (TR/TE ⫽ 150/4 msec) (b), CMD is intermediately demonstrated in both kidneys. This patient had worsening renal function at the time of MR imaging.
immediate Gd-SGE images. Table 1 summarizes the correlation of CMD on non-contrast T1-weighted or Gd-SGE images relative to sCr level. Of 5 patients with biopsy-proven histopathology, 2 patients with ATN (see Fig. 1) and 1 patient with KlippelTrenaunay-Weber syndrome showed preserved CMD on either non-contrast T1-weighted images or immediate GdSGE images. One patient with malakoplakia showed loss of CMD on both non-contrast T1-weighted images and immediate Gd-SGE images. One patient with post-infectious glomerulonephritis showed loss of CMD on non-contrast T1weighted images and preserved CMD on immediate GdSGE images. Fourteen patients (67%) had worsening renal function and 7 patients (33%) had abnormal but progressively improving renal function at the time of MR imaging. Table 2 summarizes the CMD relative to worsening or improving phase on MR study date. Within 8 days after MR study, 16 patients (76%) showed decrease of sCr value and 5 patients (24%) showed persistent or increased elevation of sCr value.
Comparing the trend in sCr, either increasing or decreasing during the time of MR imaging, revealed that a greater fraction of patients with improving sCr level had preserved CMD (Fig. 2). Conversely, a greater fraction of patients with worsening sCr demonstrated loss of CMD. However, these differences were not statistically different. Similar observation of CMD preservation based upon Gd-SGE images was also observed, despite the fact that the physiology for CMD is based upon a different mechanism. Our study showed that CMD was preserved in a large fraction (43%) of patients with ARF on both non-contrast T1-weighted and Gd-SGE images. There was no statistically significant difference between the sCr levels of the ARF group showing preserved CMD versus the group with loss of CMD.
4. Discussion It is presumed that renal CMD on non-contrast T1FS images correlates with differences in water content between
Fig. 2. Acute renal failure with acute tubular necrosis (sCr level ⫽ 6.0 mg/dl). Non-contrast SGE image (TR/TE ⫽ 150/4 msec) (a) shows intermediate loss of CMD in both kidneys with mild globular enlargement. Diffuse low signal intensity of both kidneys on this image results from iron deposition. On Gd-SGE image (TR/TE ⫽ 150/4 msec) (b), CMD is well demonstrated in both kidneys. This patient had improving renal function at the time of MR imaging.
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Table 1 Presence of CMD on T1-weighted and Gd-SGE images relative to sCr level sCr level (mg/dl) (n ⫽ 21)
CMD on T1WI & Gd-SGE No CMD on T1WI, CMD on Gd-SGE No CMD on T1WI or Gd-SGE
⬍1.2
1.2⬃1.9
3.0⬃8.5
⬎8.5
1 1
2 1
5 5
1
1
4
Note—Numbers are numbers of patients. CMD: corticomedullary differentiation. T1WI: noncontrast T1-weighted image. Gd-SGE: immediate post-gadolinium spoiled gradient echo image. sCr: serum creatinine.
the renal cortex and medulla [7,8] with the medulla having more water content per unit tissue mass than the cortex [9] resulting in relatively diminished signal. Pathologic processes causing cortical edema leads to prolongation of T1 relaxation with diminution of CMD. Decreased tubular flow, or deposition of proteinaceous or bloody material in the medulla may result in increased SI in the medulla [4], which could also diminish CMD on non-contrast T1weighted images. CMD on Gd-SGE images results from differential blood flow to the renal cortex and medulla, with approximately tenfold greater flow to the cortex [10]. Pathologic processes that alter the differential blood flow or impair delivery and filtration of intravascular gadolinium should diminish CMD on post-gadolinium images. Even though we assessed the visibility of CMD after gadolinium injection, we are not certain that this is also representative of the same process as loss of CMD on non-contrast T1-weighted images, because the appearance after gadolinium injection probably relates to not only water content but also perfusion in renal cortex or medulla. Kettritz et al. [4] and Semelka et al. [5] reported that there was a good correlation between loss of CMD and increasing level of sCr concentration in the majority of patients with renal diseases. It was also shown that the degree of renal dysfunction, rather than the etiology of underlying renal disease, was the more important factor determining loss of CMD [4]. This consistent observation of Table 2 CMD relative to worsening or improving phase on MR study date Worsening
Good CMD Moderate CMD No CMD
Improving
T1WI
Gd-SGE
T1WI
Gd-SGE
5 (36%)
7 (50%) 3 (21%) 4 (29%)
4 (57%)
5 (71%) 1 (14%) 1 (14%)
9 (64%)
3 (43%)
Note—Numbers are numbers of patients. CMD: corticomedullary differentiation. T1WI: noncontrast T1-weighted image. Gd-SGE: immediate post-gadolinium spoiled gradient echo image. sCr: serum creatinine.
loss of CMD was observed in patients with various forms of chronic renal failure [4,5]. These prior studies also found that CMD on non-contrast T1FS images was consistently lost with sCr value ⬎ 3 mg/dl, whereas CMD on Gd-SGE images was not lost until sCr reached a level of 8 mg/dl. This showed that loss of CMD on Gd-SGE images was relatively insensitive to decreased renal function, although the authors postulated that it might reflect irreversible renal damage [4]. We think the state of hydration can affect the CMD on MR images, even though it is difficult to document the state of hydration of patients readily. The prognosis for recovery of renal function after presentation with ARF depends on the etiology of the disorder [1]. ARF due to prerenal causes, as well as certain renal pathologies such as glomerulonephritis, vasculitis, and renal tubular injury, are potentially reversible [1]. Liou et al. [11] found that loss of CMD, identified on non-contrast T1weighted MR scans of patients with ARF due to ATN, was reversible in patients who had successful treatment of ARF with improvement of renal function measured by decreased sCr. Therefore, loss of CMD on non-contrast T1-weighted images does not necessarily indicate a poor prognosis for recovery of renal function [5]. A key difference between these previous studies and the current study is that, here, we selected patients based upon a clinical history of recent onset ARF, while previously, the patients were imaged at least 2 weeks or longer beyond initial clinical presentation of renal insufficiency. It is likely that there is a delay between the initial clinical presentation of ARF, and the MR imaging findings of loss of CMD. The findings in this current study illustrates that CMD on noncontrast images is in fact commonly preserved in the early period (within 2 weeks) of developing ARF. Our belief is that there is a time lag between the renal parenchymal insult and the development of fluid changes in the cortex and medullary compartments. The clinical importance of this observation is that preservation of CMD in ARF should not be misconstrued as reflecting normal renal function, because of the known finding that CMD is invariably lost in chronic renal failure. Patients with ARF and preserved CMD may have severe renal dysfunction, as our results have shown. This study has a few limitations. First, no follow-up MR renal scans were available in any of the patients. This limits the ability to determine a time course relationship between initial presentation and loss of CMD. Based upon previously published reports, it is presumed that there is a delay between onset of ARF and loss of CMD on MR imaging, and that this delay is in the order of at least 2 weeks. A second limitation is that only sCr was available for quantitative assessment of renal function in all patients, and was used to reflect GFR. A more accurate measure such as creatinine clearance was not available. Nevertheless, many studies have previously depended upon sCr as a reasonable estimate of GFR. A third limitation is that the number of patients in this study would not yield robust statistical data
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for detection of more subtle trends. However, we were more interested in determination of definite trends in the association between loss of CMD and degree of ARF as measured by sCr. A fourth limitation is that only four patients were performed with non-contrast T1FS images, because of the retrospective nature of this study. Future investigation on the relationship of renal CMD and ARF should include the following: prospective study with all patients undergoing noncontrast T1-weighted fat suppressed SGE; follow up MR studies; and correlation of the time course of ARF and CMD on MRI, to determine if MRI may play a role to help these patients, therapeutically or prognostically. In summary, the results of our study demonstrate that loss of CMD may not be present in patients with recent onset ARF with elevated sCr. Caution must therefore be exercised when interpreting MR studies in patients with recent onset ARF in that preservation of CMD does not reflect normal renal function.
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