Sameh K. Morcos

Risk of contrast-medium-induced nephropathy in high-risk patients undergoing MDCT – A pooled analysis of two randomized trials

The incidence of contrast-medium-induced nephropathy (CIN) following intravenous (IV) CM administration of contrast media to renally impaired patients undergoing multidetector computed tomography (MDCT) is not well characterized. Our objective was to investigate the incidence of CIN in patients with glomerular filtration rate (GFR) <60xa0ml/min undergoing contrast-enhanced MDCT examinations and to compare the rates of CIN following the IV administration of low-osmolar contrast media (LOCM, iopamidol and iomeprol) and an iso-osmolar contrast medium (IOCM, iodixanol). A total of 301 adult patients with moderate-to-severe renal failure received a similar IV contrast dose (40 gI). Serum creatinine (SCr) was measured at screening, baseline and 48–72u2009±u20096 h after the MDCT examination. Primary CIN outcome was an increase in SCr ≥0.5 mg/dl (≥44.2xa0μmol/l) from baseline. The CIN rates were 2.3% in the total population, 0.6% when GFR >40xa0ml/min, 4.6% when GFR <40xa0ml/min and 7.8% in patients with GFR <30xa0ml/min. The incidence of CIN was significantly higher after iodixanol than after LOCM (seven patients, 4.7% following IOCM, no CIN cases following the LOCM; pu2009=u20090.007). Significant differences in favor of the LOCM were also observed in patients with GFR <40xa0ml/min and GFR <30xa0ml/min. Following the IV administration of nonionic contrast agents in patients with moderate-to-severe renal insufficiency, the risk of significant CIN seems to be low. The IOCM iodixanol caused a higher rate of CIN than the LOCM iopamidol and iomeprol, especially in high-risk patients. Differences in osmolality between these LOCM and iodixanol do not play a role in the genesis of CIN.

Haemodynamic effects of water-soluble contrast media on the isolated perfused rat kidney

The precise mechanism underlying the nephrotoxicity of radiocontrast media remains ill defined. In this study we have examined the direct effect of a wide range of low- and high-osmolar water-soluble contrast media (WSCM) on the vascular resistance of the isolated perfused rat kidney (IPRK). Water-soluble contrast media led to a significant fall in the renal perfusate flow and an increase in the renal vascular resistance (RVR). The magnitude of these haemodynamic changes was independent of the osmolality of the tested agents. This study shows a direct effect of WSCM on the vascular resistance of the isolated perfused rat kidney.

Relationship between the diuretic effect of radiocontrast media and their ability to increase renal vascular resistance

The relationship between diuresis and natriuresis induced by radiocontrast media (RCM) and their renal haemodynamic effects were investigated. The effects of the iso-osmolar iotrolan and the hyperosmolar diatrizoate on the renal vascular resistance (RVR) were studied in the filtering and non-filtering variants of the isolated perfused rat kidney (IPRK) preparation. In the non-filtering model, no tubular regulatory process can be activated. The effect of diatrizoate on the RVR of the filtering IPRK in the presence of fursemide (0.3 mmol l-1) an inhibitor of the tubuloglomerular feedback (TGF) was also investigated. There was no significant difference (p > 0.05) in the response of the filtering (n = 6) and non-filtering (n = 6) IPRK to iotrolan. The induced reduction in the renal perfusate flow (RPF) by iotrolan was 20.5 +/- 3.05% and 22.9 +/- 3.03%, respectively. The reduction in the RPF which was observed with diatrizoate in the non-filtering IPRK (n = 5, 17.5 +/- 3.04%) was significantly less (p < 0.05) in comparison to that of the filtering IPRK (n = 6, 26.9 +/- 4.28%). In the frusemide experiments, a reduction in the RPF comparable to that of the non-filtering kidney was observed (n = 5, 13.7 +/- 4.34%). This study demonstrates that the renal vascular effect of diatrizoate is partially dependent on the TGF response. No tubular regulatory mechanism was accountable for the haemodynamic effect of iotrolan. The activation of the tubular response is osmolarity dependent.

The effect of sodium iothalamate on the vascular resistance of the isolated perfused rat kidney

The direct effects of sodium iothalamate on renal vascular resistance (RVR) were examined using the isolated perfused rat kidney experimental model. A concentration-dependent biphasic change in RVR was produced with the hyperosmolar solution of sodium iothalamate [(Conray 420), 420 mgI/ml, 2500 mOsmol/kg/H2O]. The response characterized by an initial fall followed by a prolonged increase in RVR on discontinuation of the iothalamate infusion. No significant change in RVR was observed when iothalamate was infused as an iso-osmotic solution (60 mgI/ml, 280 mOsmol/kg/H2O) at a rate of 0.525 ml/min. to produce a concentration of 4.2 mgI/ml in the renal perfusate. We conclude that sodium iothalamate can exert direct biphasic effects on RVR which are mediated by its hyperosmolality rather than its chemical content.

Effect of diatrizoate on the function of the isolated perfused rat kidney

The mechanism of the nephrotoxicity of water-soluble contrast media (WSCM) remains ill defined. We have studied the effect of diatrizoate on the isolated perfused rat kidney (IPRK). Emphasis was on the effect of low- and high-dose diatrizoate on glomerular filtration rate (GFR), renal perfusate flow (RPF), fractional excretion of albumin (FE Alb) and fractional reabsorption of sodium (FR Na). The addition of diatrizoate to the IPRK led to a dose-dependent biphasic change in RPF and GFR characterized by an initial transient increase followed by a marked and sustained decrease. Diatrizoate induced a diuresis and a parallel increase in urinary sodium excretion (fall of FR Na). Fe Alb was also increased in kidneys exposed to diatrizoate. Electron microscopy of a control kidney showed preservation of cellular architecture, which contrasted with the observed cytoplasmic vacuolation of proximal tubular cells after perfusion with diatrizoate. This study confirms a direct effect of WSCM on the function of the IPRK. In this experimental model, diatrizoate reproduces the effects observed in vivo on GFR and renal perfusion.

The functional effects of gadolinium-DTPA on the isolated perfused rat kidney

Clinical experience suggests that Gd-DTPA has no deleterious effect on renal function. We have evaluated the effects of a large dose (0.6 ml/kg body weight) of this contrast agent on the function of the isolated perfused rat kidney. Gd-DTPA led to a mild, transient increase in glomerular filtration rate with no subsequent fall during the 30 minute observation period. However, Gd-DTPA induced an increase in renal vascular resistance (+ 10%, P < 0.05) as a mild decrease in renal perfusate flow was observed during the experimental phase when compared to that of control kidneys. No significant effect was demonstrated on the fractional excretion of albumin or the fractional reabsorption of sodium. These data support, in an ex vivo experimental model, the clinical experience of the safety of this paramagnetic contrast agent in relation to renal function.

Erratum — letter to the Editor

The Publisher apologizes to both the authors and the readers for an error which appeared in this letter which was published in the May 1992 issue of the British Journal of Radiology. The error occurred in the paragraph which covered the creatinine clearance values preand post-administration of contrast media. In the interests of clarity the letter has been reprinted. The use of theophylline, an adenosine antagonist in the prevention of contrast media induced nephrotoxicity Impaired renal perfusion has been implicated in the pathogenesis of contrast media (CM) induced nephrotoxicity (El-Sayed et al, 1991). Animal and, more recently, clinical studies have suggested that endogenous adenosine may mediate the renal haemodynamic response to intra vascular CM (Arend et al, 1987;Katholietal, 1991). We have recently attempted to evaluate the protective effect of an adenosine antagonist, theophylline against CM-induced nephrotoxicity.

Urogenital imaging : a problem-oriented approach

Foreword . Preface. Contributors. 1 Adrenal Imaging (Khaled M. Elsayes, Isaac R. Francis, Melvyn Korobkin and Gerard M. Doherty). 1.1 Introduction. 1.2 Cushings syndrome. 1.3 Primary hyperaldosteronism. 1.4 Pheochromocytoma. 1.5 Adrenal cortical carcinoma. 1.6 Adrenal incidentaloma. 2 Retroperitoneal Masses (Pietro Pavlica, Massimo Valentino and Libero Barozzi). 2.1 Introduction. 2.2 Retroperitoneal anatomy. 2.3 Pathological conditions. 2.4 Primary solid retroperitoneal tumors. 2.5 Retroperitoneal lymphoma. 2.6 Cystic retroperitoneal masses. 2.7 Retroperitoneal metastases. 2.8 Retroperitoneal fibrosis (Ormonds disease). 2.9 Retroperitoneal fluid collections (traumatic and non-traumatic). References. 3 Imaging of Renal Artery Stenosis (Robert Hartman). 3.1 Introduction. 3.2 Clinical features. 3.3 Pathology. 3.4 Imaging of suspected renal artery stenosis. References. 4 Renal Masses (Philip J. Kenney). 4.1 Introduction. 4.2 Symptomatic renal carcinoma. 4.3 Incidental renal masses. 4.4 Patients with a known cancer (other than RCC). 4.5 Renal mass in patients with symptoms. 4.6 Vascular lesions presenting as a renal mass. 4.7 Renal mass in patients with cystic disease. 4.8 Treatment. References. 5 Non-neoplastic Renal Cystic Lesions (Sameh K. Morcos). 5.1 Introduction. 5.2 Classification. 5.3 Cystic lesions affecting renal cortex. 5.4 Cystic lesions of renal medulla. 5.5 Cystic diseases affecting both the cortex and medulla. References. 6 Urological and Vascular Complications Post-renal Transplantation (Tarek El-Diasty and Yasser Osman). 6.1 Introduction. 6.2 Vascular complications. 6.3 Urological complications. 6.4 Ureteric strictures. 6.5 Post-transplant lymphocele. 6.6 Delayed graft function (DGF). 6.7 Post-transplant bladder malignancy. References. 7 Urinary Tract Injuries (Elliott R. Friedman, Stanford M. Goldman and Tung Shu). 7.1 Introduction. 7.2 Renal trauma. 7.3 Adrenal trauma. 7.4 Ureteral trauma. 7.5 Bladder trauma. 7.6 Urethral trauma. 7.7 Penile and scrotal trauma. References. 8 Urinary Tract Infections (Mikael Hellstr..om, Ulf Jodal, Rune Sixt and Eira Stokland). 8.1 Symptomatic urinary tract infection in children. 8.2 Symptomatic upper urinary tract infection in adults. 8.3 Emphysematous pyelonephritis. 8.4 Xanthogranulomatous pyelonephritis. 8.5 Urinary tract infection in the immunocompromised patient. 8.6 Tuberculosis. 8.7 Schistosomiasis. 8.8 Hydatid disease (echinococcosis). 8.9 Urethritis. References. 9 Imaging of the Genitourinary System - Urolithiasis (Sami A Moussa and Paramananthan Mariappan). 9.1 Introduction. 9.2 Pathology. 9.3 Clinical features. 9.4 Evaluation of patients with suspected urinary stones. 9.5 Treatment. 9.6 Imaging. References. 10 Hematuria (Thomas Bretlau, Kirstine L. Hermann, Jorgen Nordling and Henrik S. Thomsen). 10.1 Definition. 10.2 Clinical considerations. 10.3 Diagnosis of hematuria. 10.4 Epidemiology. 10.5 Distribution of malignancy in patients with hematuria. 10.6 Imaging. 10.7 Summary. References. 11 Bladder Cancer (G. Heinz-Peer and C. Kratzik). 11.1 Introduction . 11.2 Clinical features. 11.3 Pathology. 11.4 Imaging findings. 11.5 Treatment planning. 11.6 Post-treatment Imaging. 11.7 Summary. References. 12 Imaging of Urinary Diversion (Sameh Hanna and Hesham Badawy). 12.1 Introduction. 12.2 Indications for urinary diversion. 12.3 Types of urinary diversion. 12.4 Non-continent cutaneous form of diversion. 12.5 Continent cutaneous urinary diversion ( Continent Catheterizing Pouches ). 12.6 Non-orthotopic continent diversion, relying on the anal sphincter for continence. 12.7 Orthotopic form of diversion to the native, intact urethra (neobladder). 12.8 Contraindications to urinary diversion. 12.9 Complications of urinary diversions. 12.10 The role of radiologist in urinary diversion includes. 12.11 Imaging studies. 12.12 Imaging of complications. 12.13 Summary. References. 13 Imaging of the Prostate Gland (FrancCois Cornud). 13.1 Introduction. 13.2 Zonal anatomy and benign prostatic hypertrophy. 13.3 Diagnosis of prostate cancer: TRUS features. 13.4 Diagnostic of prostate cancer: MRI. 13.5 Contrast-enhanced (dynamic) MRI. 13.6 Magnetic Resonance Spectroscopic Imaging (MRSI). 13.7 Diffusion-weighted imaging. 13.8 Indications of functional MRI. 13.9 Extension of prostate cancer. 13.10 Local extension by TRUS and TRUS-guided biopsy. 13.11 MRI and staging of prostate cancer. 13.12 Local staging. 13.13 Lymph node metastases: lympho-MRI. 13.14 Bone metastases: whole marrow MRI. 13.15 Benign disorders of the prostate (BPH excluded). References. 14 Haemospermia (Drew A. Torigian, Keith N. Van Arsdalen and Parvati Ramchandani). 14.1 Introduction. 14.2 Clinical features. 14.3 Pathology. 14.4 Imaging findings. 14.5 Summary. References. 15 Scrotal Masses (Lorenzo E. Derchi and Alchiede Simonato). 15.1 Introduction. 15.2 Clinical features. 15.3 Pathology. 15.4 Imaging. 15.5 Important principles in assessment of scrotal masses. 15.6 Important problems in differentiating benign from malignant lesions. References. 16 Gynaecological Adnexal Masses (John A. Spencer and Michael J. Weston). 16.1 Introduction. 16.2 Clinical features. 16.3 Pathology. 16.4 Imaging. 16.5 Standard radiographic techniques. 16.6 Ultrasound (US). 16.7 MR Imaging (MRI). 16.8 Computed Tomography. References. 17 Imaging of Abnormal Uterine Bleeding (Patricia No..el, Evis Sala and Caroline Reinhold). 17.1 Abnormal uterine bleeding. 17.2 Adenomyosis. 17.3 Leiomyomas. 17.4 Endometrial polyp. 17.5 Endometrial hyperplasia. 17.6 Endometrial carcinoma. 17.7 Summary. References. 18 Female Pelvic Floor Dysfunction (Rania Farouk El Sayed). 18.1 Introduction. 18.2 Anatomical considerations. 18.3 Pathophysiology of pelvic floor dysfunction. 18.4 Clinical features. 18.5 Imaging of pelvic floor dysfunction. 18.6 Magnetic resonance imaging (MRI). References. 19 Imaging of female infertility (Ahmed-Emad Mahfouz and Hanan Sherif). 19.1 Introduction. 19.2 Polycystic ovary syndrome. 19.3 Abnormalities of the fallopian tubes (Hydrosalpinx/Hematosalpinx, tubal block). 19.4 Fibroids. 19.5 Adenomyosis. 19.6 Developmental anomalies of the uterus. 19.7 Endometriosis. 19.8 Imaging. Index.

Gadolinium Chelates and Stability

The gadolinium ions which enhance the signals in MR images are very toxic, so in the contrast medium molecule they have to be strongly attached to a chelate to avoid adverse effects. The linear chelate molecules are open chains which can fold and unfold off the gadolinium ion with ease. In contrast, the macrocyclic chelate molecules are rigid rings of almost optimal size to cage the gadolinium ion. Experimental data, both in vitro and in vivo, and clinical observations, have confirmed the lower stability of the linear gadolinium-based molecules compared to the more stable macrocyclic agents.

A European View-Point on NSF

About three and a half years ago, a causal relation between nephrogenic systemic fibrosis (NSF) and exposure to gadolinium based contrast agents (Gd-CAs) was suggested. All evidence now suggests that low stability Gd-CAs can trigger the development of NSF. All studies indicate with no exception that macrocyclic Gd-CAs release significantly less free gadolinium than the linear agents, particularly the non-ionic ones which have the highest potential of gadolinium release. The longer the Gd-CA stays in the body the larger the amount of gadolinium that is retained in the body. The magnitude of the NSF problem remains uncertain; the condition seems to be underreported. The demonstration of a link between NSF and low stability Gd-CAs has had major consequences for patients with reduced renal function. Currently, if contrast administration is clinically deemed; necessary the preferred approach is contrast enhanced MRI using a macrocyclic Gd-CA. Contrast enhanced CT is at least as risky if not more as an enhanced MRI with low stability Gd-CAs.