British Journal of Radiology (2003) 76, 564-565
© 2003 British Institute of Radiology
doi: 10.1259/bjr/26423316
Ureteric obstruction and intravascular administration of contrast media: is there a risk?
S K Morcos, FRCS, FFRRCSI, FRCR
Department of Diagnostic Imaging, Northern General Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK
 |
Introduction
|
|---|
Experimental studies in animal models have shown that acute ureteric obstruction for 24 h or more is associated with a decrease in renal medullary blood flow and structural damage to the tubules [1, 2]. Does intravascular administration of contrast medium (CM) in the presence of acute ureteric obstruction induce further damage to the kidney? Clinical data on this subject are lacking and there is only one experimental study in the rat that has investigated this issue extensively [1]. The results of this study demonstrated that the combination of acute ureteric obstruction, inhibition of intrarenal production of the vasodilators nitric oxide (NO) and prostacycline, and intravascular administration of high osmolar CM results in extensive necrosis of the medullary thick ascending limb of loops of Henle (mTALs) [1]. The combination of insults used in the rat is not uncommon in patients suffering from acute renal colic secondary to ureteic obstruction caused by a calculus. These patients may undergo intravenous urography to determine the cause of the renal colic. Intravascular administration of CM can induce reduction of renal blood flow and a hypoxic insult to the renal medulla [3–7]. A patient with renal colic may also receive non steroidal anti-inflamatory drugs (NSAIDs) such as indomethacin for pain relief and smooth muscle relaxation. These drugs cause inhibition of intrarenal production of the vasodilator prostacycline, causing a marked decrease in medullary renal blood flow that may lead to necrosis of mTALs [1, 3]. In addition, some of these patients may be suffering from endothelial dysfunction associated with hypertension, atherosclerosis or diabetes mellitus. This causes a reduction in endogenous production of the vasodilators NO and prostacycline, which are crucial for perfusion of the renal medulla [3–7].
In this short communication, the pathophysiology of ureteric obstruction and the medullary effects of contrast media will be discussed. The harmful combination of ureteric obstruction, use of NSAIDs and intravascular injection of CM will be highlighted.
|
The pathophysiology of ureteric obstruction
|
|---|
The kidneys receive 20% of cardiac output, however intrarenal blood flow is not evenly distributed between the cortex and medulla. While the renal cortex is well perfused, the medulla is sparsely perfused, receiving only 10% of the total renal blood in spite of the high metabolic activity of this region [6]. The medullary vascular system consists of descending vasa recta, which emerge from the efferent arterioles of deep juxta medullary nephrons, penetrate the medulla down to the papillary tip and supply the intertubular capillary network (Figure 1
) [1]. The blood pressure of the medullary vessels is rather low and they can be compressed easily by an increase in the intrapelvic hydrostatic pressure. Acute ureteric obstruction can cause a marked increase in intrapelvic pressure, leading to compression of the medullary blood vessels. This results in reduction of blood flow and medullary ischaemia causing apoptosis and necrosis of mTALs. Apoptosis can be detected as early as 2 h after the onset of the acute obstruction [1]. The mechanism responsible for the development of apoptosis has not been fully elucidated, but ischaemia stimulating the production of apoptosis-related molecules is a likely explanation [2]. If the obstruction is not relieved, the structural damage will progress to tubular atrophy, interstitial fibrosis and inflammation and progressive renal tissue loss [2].
View larger version (52K):
[in this window]
[in a new window]
|
Figure 1. A simple diagram of the blood supply of the renal medulla. Thick arrows represent the increase in intrapelvic pressure secondary to acute ureteric obstruction. mTAL, medullary thick ascending limb of loop of Henle.
|
|
The presence of other conditions that also compromise renal medullary circulation is bound to exaggerate the medullary damage associated with uretreic obstruction.
|
Renal medullary effects of contrast media
|
|---|
Contrast media reduce the reabsorption of sodium and water in the renal tubules, leading to diuresis and natriuresis precipitating increases in the active uptake of sodium in the mTALs [5, 7, 8]. This effect is dependent both on osmolality and on dose of CM. The larger the dose or the higher the osmolality, the more marked the natriuretic and diuretic effects of CM [5]. Since the blood supply of the renal medulla is sparse, the increase in the metabolic activity of the medullary tubular cells in response to natriuresis induced by CM creates a state of hypoxia in the medulla leading to apoptosis and necrosis of mTALs [3–7]. In addition, the diuresis induced by CM increases the intratubular pressure leading to an increase in the intrarenal interstitial pressure that causes compression of the small renal blood vessels of the encapsulated kidney, compromising the blood flow to the renal medulla [5, 9]. CM can also stimulate production of the vasoconstrictor peptide endothelin, which decreases renal blood flow and aggravates the medullary hypoxia [5, 10–12]. In addition, CM can induce aggregation of red blood cells in the small renal blood vessels, which reduces medullary perfusion [13–15]. It has also been shown that a decrease in the production of the endogenous vasodilators NO or prostacycline owing to endothelial dysfunction or the administration of NSAIDs, respectively, exaggerates the hypoxic insult of CM in the renal medulla [3–7, 15].
|
Acute ureteric obstruction and intravascular administration of contrast media: is there a risk?
|
|---|
Although there are no clinical data available to answer the proposed question, the experimental data are compelling and indicate that the use of CM in patients with acute ureteric obstruction could be harmful. A cumulative effect has been demonstrated and the combination has produced more extensive and severe structural damage in the renal medulla than the effect of CM or ureteric obstruction alone [1].
In my view, the answer to the proposed question must be "yes", and CM can augment the deleterious effects of ureteric obstruction. Extra care is therefore advisable in dealing with patients suffering from acute renal colic. The use of high osmolar and a large volume of CM should be avoided in these patients as well as the administration of NSAIDs. Unenhanced helical CT of the abdomen could be helpful in this situation [16]. The examination does not require the injection of CM and has an excellent diagnostic yield. However, this modality may not be easily accessible and the radiation dose of the examination can be a source of concern, particularly in dealing with young patients.
Received for publication August 27, 2002.
Revision received March 21, 2003.
Accepted for publication June 10, 2003.
|
References
|
|---|
- Heyman SN, Fuchs S, Jaffe R, Shina A, Ellezian L, Brezis M, et al. Renal microcirculation and tissue damage during acute ureteral obstruction in the rat: effect of saline infusion, indomethacin and radiocontrast. Kidney Int 1997;51:653–63.[Medline]
- Choi YJ, Baranowska-Daca E, Nguyen V, Koji T, Ballantyne CM, Sheikh-Hamad D, et al. Mechanism of chronic obstructive uropathy: increased expression of apoptosis-promoting molecules. Kidney Int 2000;56:1481–91.
- Agmon Y, Peleg H, Greenfield Z, Rosen S, Brezis M. Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat. J Clin Invest 1994;94:1069–75.
- Morcos SK, Oldroyd S, Haylor J. Effect of radiographic contrast media on endothelium derived nitric oxide-dependent renal vasodilatation. Br J Radiol 1997;70:154–9.[Abstract]
- Morcos SK. Contrast media-induced nephrotoxicity; questions and answers. Br J Radiol 1998;71:357–65.[Abstract]
- Morcos SK, Epstein FH, Haylor J, Dobrota M. Aspects of contrast media nephrotoxicity. Eur J Radiol 1996;23:178–84.[CrossRef][Medline]
- Heyman SN, Rosen S, Brezis M. Radiocontrast nephropathy: a paradigm for synergism between toxic and hypoxic insults in the kidney. Exp Nephrol 1994;2:153–7.[Medline]
- Morcos SK, Brown PWG, Oldroyd S, El Nahas AM, Haylor J. Relationship between the diuretic effect of radiocontrast media and their ability to increase renal vascular resistance. Br J Radiol 1995;68:850–3.[Abstract/Free Full Text]
- Katzberg RW, Schulman G, Meggs L, et al. Mechanism of the renal response to contrast medium in dogs. Decrease in renal function due to hypertonicity. Invest Radiol 1983;18:74–80.[CrossRef][Medline]
- Heyman SN, Clark BA, Kaiser N, et al. Radiocontrast agents induce endothelin release in vivo and in vitro. J Am Soc Nephrol 1992;3:58–65.[Abstract]
- Oldroyd S, Slee SJ, Haylor J, Morcos SK, Wilson C. Role for endothelin in the renal responses to radiocontrast media in the rat. Clin Sci 1994;87:427–34.[Medline]
- Oldroyd SD, Haylor JL, Morcos SK. Bosentan, an orally active endothelin antagonist: effect on renal response to contrast media. Radiology 1995;196:661–5.[Abstract/Free Full Text]
- Liss P, Nygren A, Olsson U, Ulfendahl HR, Erikson U. Effects of contrast media and mannitol on renal medullary blood flow and red cell aggregation in the rat kidney. Kidney Int 1996;49:1268–75.[Medline]
- Nygren A, Ulfendahl HR, Hansell P, Erikson U. Effects of intravenous contrast media on cortical and medullary blood flow in the rat kidney. Invest Radiol 1988;23:753–61.[CrossRef][Medline]
- Morcos SK, Dawson P, Pearson JD, et al. The haemodynamic effects of iodinated water soluble radiographic contrast media: a review. Eur J Radiol 1998;29:31–46.[CrossRef][Medline]
- Sudah M, Vanninen RL, Partanen K, Kainulainen S, Malinen A, Heino A, et al. Patients with acute flank pain: comparison of MR urography with unenhanced helical CT. Radiology 2002;223:98–105.[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
|
|
 
I Kayani, A M Groves, R Syed, N Nagabushan, F Pakzad, E M Prvulovich, and J B Bomanji
The absent kidney in 99Tcm-MAG3 renogram: a dramatic reversible consequence of contrast nephrotoxicity superimposed on renal obstruction
Br. J. Radiol.,
April 1, 2005;
78(928):
349 - 352.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Introduction
The pathophysiology of ureteric...
