Comparative cytotoxicity of ionic and non-ionic radiocontrast agents on MDCK cell monolayers in vitro.

BACKGROUND: Intravascular radiocontrast agents may cause acute renal failure, particularly in patients with pre-existing renal insufficiency. Direct cytotoxic effects of radiocontrast agents on renal tubular cells may contribute to the pathogenesis of radiocontrast-induced nephropathy. METHODS: We analysed the cytotoxicity of the ionic radiocontrast agents diatrizoate (monomeric) and ioxaglate (dimeric), as well as of the non-ionic radiocontrast agents iohexol (monomeric) and iodixanol (dimeric) on the renal epithelial Madin Darby Canine Kidney (MDCK) cell line grown on permeable supports. The toxicity assays assessed cell viability, transmonolayer resistance and inulin permeability between the apical and basal cell culture compartment. In addition, the distribution of the tight-junction-associated membrane proteins ZO-1 and occludin was analysed using immunofluorescence microscopy. RESULTS: In all assays the high osmolal ionic compound diatrizoate had significant cytotoxic effects that included the partial redistribution of the tight-junction-associated membrane proteins into a cytoplasmic compartment. To a lesser extent this redistribution also occurred with the dimeric ionic compound ioxaglate, but not with the non-ionic radiocontrast agents. With regards to cell viability, transmonolayer resistance and inulin permeability the radiocontrast agents with reduced osmolality were significantly less toxic than diatrizoate, independent of their ionic strength. CONCLUSIONS: Physicochemical factors contribute to the cytotoxicity of radiocontrast agents in vitro. The redistribution of tight-junction-associated membrane proteins by the ionic radiocontrast agents corresponds with the loss of the barrier function of the epithelial cell monolayer, which is a major pathophysiological mechanism in acute renal failure. The radiocontrast agents with reduced osmolality are less cytotoxic than diatrizoate, independent of their ionicity. Hyperosmolality appears to be a more important determinant of the cytotoxicity of diatrizoate than ionic strength.     

The potential role of statins in contrast nephropathy

BACKGROUND: Administration of contrast agents may result in an acute reduction in renal function and occasionally end-stage renal disease. Risk factors for contrast-induced nephropathy (CN) are preexisting renal dysfunction, diabetes and reduced effective arterial volume. Hydration and use of nonionic contrast agents have been reported to ameliorate CN. Reactive oxygen species may have a role in the pathogenesis of CN. Statins decrease free oxygen radicals in animals. We retrospectively tested the hypothesis that administering statins prior to cardiac catheterization decreases the incidence of CN. METHODS: A total of 1,002 patients were studied. Patients with a stable baseline serum creatinine (SCr) > or = 1.5 mg/dl who had cardiac catheterization between July 1997 and June 2002, were included in the study. None of the patients were taking statins before admission. 250 patients were started on a statin before the procedure and 752 patients were not. The SCr was followed for 7 days after the procedure looking for an acute decrement in renal function, dialysis requirement and survival. RESULTS: The baseline characteristics, SCr, GFR, amount of intravenous fluids and contrast were similar in both groups. The post cath SCr (2.26 vs 3.1 mg/dl, p = 0.001) was significantly better in the statin group. Length of stay (2.72 vs 3.32 days, p = 0.01) and number of patients with acute renal failure (43 (17.2%) vs 168 (22.3%) patients, p = 0.028) were significantly lower in the statin group. Dialysis requirement within 7 days and 28-day survival were similar in both groups. CONCLUSION: Prophylactic administration of statins along with hydration may be associated with less CN induced by a nonionic, low-osmolality contrast.     

Nephrotoxicity of contrast media in high-risk patients with renal insufficiency: comparison of low- and high-osmolar contrast agents.

We have compared the renal effects of ioxitalamate, ioxaglate, and iopamidol in patients with chronic renal failure. Sixty consecutive patients with an estimated creatinine clearance (ECRCl) less than 60 ml/min were randomly assigned to receive either ioxitalamate, iopamidol, or ioxaglate. All patients received 500 cm3 isotonic saline before the procedure. Serum creatinine and ECRCl were estimated before, 1 and 2 or 3 days after the procedure. There was no statistical difference between the three groups with respect to age, sex, weight, renal function, amount of iodine, and type of procedure. Mean serum creatinine and ECRCl remained unchanged after administration of contrast media. No patient had nephrotoxicity or acute oliguria requiring dialysis as a result of the administration of contrast material. The number of patients with an increase in the serum creatinine level greater than 10% from the basal value did not differ in the treatment groups. The maximal increases in serum creatinine were 52 mumol/l (29%) in the ioxitalamate group, 56 mumol/l (18%) in the ioxaglate group, and 57 mumol/l (23%) in the iopamidol group (p = NS). Using a population carefully randomized and matched for renal insufficiency, we could not show any differences in nephrotoxicity between these three contrast agents. Clinically serious renal impairment was uncommon in our study, regardless of the contrast agent used. However, the interpretation of these favorable findings requires a cautionary note. All patients in this study were well hydrated before and after uro-/angiography, and none had a recent renal injury or a treatment with a nephrotoxic agent that would predispose to injury from contrast material.(ABSTRACT TRUNCATED AT 250 WORDS)     

Renal failure in 57 925 patients undergoing coronary procedures using iso-osmolar or low-osmolar contrast media

We compared the Swedish Coronary Angiography and Angioplasty Registry with the Swedish 'Hospital Discharge Register' to assess contrast media (CM)-induced renal failure. Hospitals used only one type CM. From 2000 to 2003, iodixanol (iso-osmolar) was used in 45 485 patients, ioxaglate (low osmolar) in 12 440 subjects. To include the earlier used CM iohexol (low osmolar), analysis extended back to 1990 (86 334 patients). Incidence of clinically significant renal failure was greatest for patients receiving the iso-osmolar CM iodixanol (1.7%). Ioxaglate-treated patients had a significantly lower renal failure incidence (0.8%, P<0.001). The odds ratio for iodixanol-treated patients was significantly higher than for ioxaglate (1 vs 0.48, P<0.001). In subsets of either diabetic patients or patients with previous renal failure, odds ratios for renal failure remained greater in the iodixanol groups (P<0.01). Hospitals switching CM to iodixanol experienced a doubling in clinically significant renal failure after cardiac procedures. Dialysis was required in 0.2% of patients receiving iodixanol, which was significantly higher (P<0.01) than for ioxaglate-treated patients (0.1%). Iohexol-treated patients had a similar low risk for developing clinically significant renal failure (0.9%) as ioxaglate. In conclusion, risk of developing renal failure and required dialysis after coronary procedures is higher when patients received iodixanol than ioxaglate or iohexol.     

Safety of gadolinium contrast angiography in patients with chronic renal insufficiency

OBJECTIVE: To prevent iodinated contrast medium-induced nephrotoxicity, gadolinium has been used increasingly for magnetic resonance angiography (MRA) or conventional digital subtraction angiography (DSA) to visualize arterial anatomy in patients undergoing vascular surgery who are considered at high risk because of chronic renal insufficiency. We assessed the safety of gadolinium-based contrast medium as a substitute for iodinated contrast medium-enhanced examinations. We determined the incidence of gadolinium-induced nephrotoxicity in a clinical setting and searched for contributing risk factors.Patients and methods In a single-center retrospective study from December 1999 to January 2001, 218 inpatients underwent MRA and 42 inpatients underwent DSA, with gadolinium as the sole contrast agent. Patient comorbid conditions, indications for vascular imaging, contrast dose, urine output, baseline and post-procedure serum creatinine concentration (SCr), and outcome were recorded for all patients in whom gadolinium-induced renal failure developed. RESULTS: Of 260 patients who received gadolinium-based contrast agents, at a dose of 0.25 mmol/kg or more, 195 patients (75%) had pre-test baseline chronic renal insufficiency. In 7 of 195 patients (3.5%) acute renal failure developed after gadolinium-based contrast medium administration, for MRA (n = 153) in 3 patients (1.9%) and DSA (n = 42) in 4 patients (9.5%). Average baseline SCr in the 195 patients with chronic renal insufficiency was 38.2 +/- 1.6 mL/min/1.73 m(2), and in the 7 patients in whom acute renal failure developed, baseline SCr was 32.5 +/- 7.8 mL/min/1.73 m(2) (P =.33). Respective intravenous and intra-arterial gadolinium doses in these 7 patients ranged from 0.31 to 0.41 mmol/kg for MRA and 0.27 to 0.42 mmol/kg for DSA. Acute renal failure did not develop in any of 65 patients with normal baseline SCr. CONCLUSION: Despite reports of negligible nephrotoxicity, rarely gadolinium-based contrast agents can cause acute renal failure in patients with underlying chronic renal insufficiency. Estimation of creatinine clearance alone does not enable prediction of which patients are likely to have acute renal failure. Patients at high-risk should be identified, and prophylactic measures should be taken to reduce the risk for nephrotoxicity.     

Effects of gentamicin,lipopolysaccharide, and contrast media on immortalized proximal tubular cells

Aminoglycosides are widely used in the treatment of gram-negative bacterial infections. Gentamicin (GE) acts mainly in proximal tubular cells, where it is uptake via organic anion transport system and it induces a high incidence of nephrotoxicity, which is characterized by tubular necrosis [5] leading to acute renal failure in 10 to 50% of patients. Gram-negative bacteria has lipopolysaccharide (LPS) which is an endotoxin that cause renal damage. [1] Moreover, many patients are undergone exams using radiologic contrast, which is a risk factor to induce a hemodynamic change in the kidney and to develop acute renal failure. [6] Intracellular calcium [Ca2+]i is involved in renal cellular injury [7,3] and maybe mediate the effects provoked by these drugs. This study was performed to evaluate necrosis, apoptosis, and intracellular calcium levels ([Ca2+]i) in LLC-PK1 (epithelial cell line from pig kidney) induced by GE associated with LPS and a low-osmolality media, Hexabrix (HE).     

Vacuolization of tubules in gadolinium-associated acute renal failure

While gadolinium was initially thought to be a safe alternative to iodinated contrast agents for patients with chronic renal insufficiency, many reports of gadolinium-associated acute renal failure have now been recorded, particularly in patients with underlying renal insufficiency. In addition, animal models have demonstrated tubule vacuolization with experimental gadolinium administration that is similar to vacuolization seen with other contrast agents. We present a case of a patient with nephrotic-range proteinuria and chronic renal insufficiency, who developed acute renal failure following gadolinium administration undergoing furosemide stimulated diuresis. This case is the first report of pathologic tubule vacuolization in gadolinium-associated nephropathy in a human kidney biopsy. This case suggests a relationship between the pathogenesis of CIN with standard contrast media and CIN with gadolinium. Research is needed to better understand the pathologic findings and pathogenesis of gadolinium-associated nephrotoxicity.     

Nephrotoxicity of low-osmolality versus iso-osmolality contrast agents: impact of N-acetylcysteine

BACKGROUND: Recent data support that iodixanol, an iso-osmolality contrast agent, is less nephrotoxic than low-osmolality contrast agents when hydration is the only prophylactic strategy used. We evaluated the nephrotoxicity of iso- and low-osmolality contrast agents with prophylactic administration of N-acetylcysteine (NAC) along with hydration. METHODS: Two hundred and twenty-five patients with chronic renal insufficiency (serum creatinine >1.5 mg/dL or an estimated glomerular filtration rate <60 mL/min/1.73 m(2)), referred to our institution for coronary and/or peripheral procedures, were assigned to receive low-osmolality (iobitridol group; N = 115) or iso-osmolality (iodixanol group; N = 110) contrast dye. In all cases prophylactic administration of 0.45% saline intravenously and NAC (1200 mg orally twice daily) was used. RESULTS: Baseline creatinine levels were similar in the 2 groups [iobitridol group = 1.70 (IQR: 1.54-1.98) mg/dL; iodixanol group = 1.73 (IQR: 1.56-2.00) mg/dL, P = 0.33]. The risk score for contrast nephrotoxicity was 5.0 +/- 1.6 in the iobitridol group versus 5.0 +/- 1.8 in the iodixanol group (P = 0.44). Increase of at least 0.5 mg/dL of the creatinine concentration 48 hours after the procedure occurred in 4/115 patients (3.5%) in the iobitridol group and 3/110 patients (2.7%) in the iodixanol group (P = 1.00; OR 0.78; 95% CI 0.17-3.56). Amount of contrast media administration was similar in the 2 groups (iobitridol group = 167 +/- 90 mL; iodixanol group = 164 +/- 82 mL; P = 0.61). CONCLUSION: Nephrotoxicity of iso-osmolality and low-osmolality contrast agents was similar when a prophylactic strategy of hydration plus NAC was utilized.     

The safety of gadolinium in patients with stage 3 and 4 renal failure.

BACKGROUND: Although there is a well-documented risk of acute renal failure (ARF) with the iodinated contrast agents, intravenous gadolinium-based contrast agents are considered non-nephrotoxic and have been widely used for magnetic resonance imaging (MRI). However, debate continues regarding the safety issue of gadolinium, especially in patients with kidney failure. Therefore, we aimed to evaluate the safety of gadolinium in patients with stage 3 and 4 renal failure as well as risk factors for nephrotoxicity. METHOD: We retrospectively analysed 473 patients with chronic renal failure who underwent angiographic MRI procedures in our centre from February 1999 to March 2005 in whom gadolinium was used as the sole contrast agent at a dose of 0.2 ml/kg. Among them, 91 patients with stage 3 or 4 renal failure according to K/DOQI definition, who had available data in their files, were enrolled in the study. The ARF was defined as an increase of at least 0.5 mg/dl in serum creatinine level over baseline after using gadolinium. RESULTS: Eleven of 91 (52 males, 39 females; median age 59 years; median estimated glomerular filtration rate (eGFR) 33 ml/min/1.73 m2) patients developed ARF (12.1%). The median eGFR was lower in patients with ARF than in those who did not develop ARF. The risk factors for ARF were baseline eGFR, older age, diabetic nephropathy and low baseline haemoglobin and albumin levels. Baseline eGFR and diabetic nephropathy were determined as the independent risk factors in regression analysis. CONCLUSIONS: An ARF can occur after gadolinium-based contrast agents in patients with moderate to severe chronic renal failure. Risk factors for ARF after gadolinium toxicity include diabetic nephropathy and low GFR.     

N-Acetylcysteine in nephrology; contrast nephropathy and beyond

PURPOSE OF REVIEW: Since the first publication appeared in 2000 showing that prophylactic oral administration of the antioxidant acetylcysteine, along with adequate hydration, can prevent the reduction in renal function induced by non-ionic, low-osmolality contrast agents, acetylcysteine has rapidly become widely used in clinical practice. Meanwhile, other applications of acetylcysteine in nephrology have been reported. This review analyses recent literature on the effects of acetylcysteine on radiocontrast-induced nephropathy, on plasma homocysteine concentrations, and on cardiovascular events in patients with end-stage renal failure. RECENT FINDINGS: At least 19 randomized trials evaluating acetylcysteine for the prevention of radiocontrast-induced nephropathy, at least five meta-analyses, and several reviews on that topic have been published within the past 4 years. The studies on radiocontrast-induced nephropathy showed remarkably mixed results, probably as a result of study heterogeneity. One study recently indicated that the administration of acetylcysteine during a haemodialysis session significantly lowered plasma homocysteine concentrations. Another study indicated that long-term antioxidative treatment with acetylcysteine significantly reduced cardiovascular events in patients with end-stage renal failure. SUMMARY: Although there are controversies on dosing and timing, the use of acetylcysteine together with hydration should be considered to protect patients from radiographic contrast media-induced nephropathy. Long-term antioxidative treatment with acetylcysteine in patients with end-stage renal failure may also be useful to prevent adverse cardiovascular events.     

Postoperative chronic renal failure: a new syndrome?

Of 125 patients with postsurgical acute tubular necrosis, 87 died, 34 regained clinical normal renal function, and 4 survivors (9.5%) were left with severe permanent renal failure, two of whom required chronic dialysis and transplantation. Preoperatively these 4 patients had normal renal function. The 4 patients were above age 60, two had undergone methoxyflurane anesthesia, and nephrotoxic antibiotics were used in all. The incidence of permanent renal failure is much higher than ever reported and may reflect the survival of patients who previously died because of less ideal dialysis. We believe that the cause of this permanent lesion is multifactorial, including age (over 60 years), nephrotoxic antibiotics (particularly cephalothin and gentamicin sulfate), and nephrotoxic anesthetic (methoxyflurane) agents. This combination of factors should be avoided whenever possible.     

Histopathologic evaluation of lupus patients with transient renal failure

Patients with lupus nephritis and severe renal failure progress to end-stage renal disease despite aggressive therapy to suppress immunologic function. Within this group is a small subset presenting with rapid progression of renal failure and requiring dialytic support. We reviewed the clinicopathologic data of four such patients who were able to terminate dialysis after acute renal failure due to lupus nephritis. Three of these patients have remained independent of dialysis up to 4 years, and one patient returned to dialysis 1 month following discontinuation. Although glomerular pathology was variable in the four patients, a lesion common to all at presentation was acute tubular necrosis. It is suggested that tubular necrosis may cause reversible renal failure when part of the nephropathy of disseminated lupus treated with corticosteroids.     

Acute renal failure associated with hematuria in IgA nephropathy

Severe acute deterioration of renal function, which occurred during the episode of massive gross hematuria, is described in two patients with IgA nephropathy (IgAN). The renal failure abated gradually after dialytic support. Renal pathology in each case revealed focal proliferative glomerulonephritis with less than 14% of the glomeruli affected by crescents or sclerosis. In contrast to the mild glomerular lesions, acute tubular cell injury in relation to phagocytosis of erythrocytes or pigments and/or tubular obstruction was prominent. We think our observations support the previous reports that tubular lesions in relation to heavy glomerular bleeding may be a cause of severe acute renal failure in patients with IgAN.     

Contrast-induced nephrotoxicity in renal allograft recipients

BACKGROUND: Intravenous administration of radiographic contrast agents is an important cause of acute renal failure, accounting for one third of the cases of hospital-acquired acute renal failure in patients with native kidneys. The safety of intravenous contrast has not been studied in renal allograft recipients since the availability of cyclosporine as a maintenance immunosuppressive therapy. As patients with renal transplantation may be at a higher risk of contrast-induced nephrotoxicity (CIN) due to concomitant use of cyclosporine and higher prevalence of diabetes and renal insufficiency, we retrospectively studied development of CIN in these patients. PATIENTS AND METHODS: We identified 44 patients (1988 1997) with functioning renal allograft who underwent different intravenous or intraarterial contrast studies (ICS). Pre- and post-ICS renal function tests were done in 35 of these patients. The following were the various ICS done in these patients: coronary angiogram (6), CT scan with intravenous contrast ( 11), angiogram for evaluation of peripheral vascular disease (11), allograft angiogram with angioplasty (5), pulmonary angiogram (1) and intravenous pyelogram (1). The mean age of the patients was 42 +/- 2.1 years and the mean serum creatinine was 2.3 +/- 0.25 mg/dl (mean +/- SEM). Fourty percent of patients (14 of 35) had diabetes, and 25.7% (9 of 35) had chronic rejection. Ninety four percent (33 of 35) of the patients were taking cyclosporine at the time of ICS. RESULTS: Nine patients had > or = 25% increase in serum creatinine from baseline after ICS. Two of these patients were excluded from the analysis as renal functions in these patients had deteriorated prior to ICS and renal failure was attributed to sepsis. Of the remaining 7 patients, 5 had diabetes and 2 had chronic rejection. Only 4 of these 7 patients with CIN received prophylaxis (I/V hydration) prior to ICS. The baseline serum creatinines were not different in patients who had no change in renal function to those who developed CIN (1.97 +/- 0.20 vs 1.54 +/- 0.17 mg/dl, p = 1.5, mean +/- SEM). More than 50% increase in baseline serum creatinine was seen in only 3 of these 7 patients, 2 of these patients had diabetes and third had chronic rejection and congestive heart failure. None of these patients received prophylaxis for CIN. Dialysis was not required in any patient. Three patients also had a > 25% decrease in baseline serum creatinine after ICS, and all of them had allograft angiography with angioplasty for renal artery stenosis. CONCLUSION: In our retrospective study, the incidence of CIN in renal allograft recipients applying a broader classification of > or = 25% increase in baseline serum creatinine was 21.2% (7 of 33 patients). The incidence of CIN was lower 15.3% (4 of 26) in patients who received intravenous hydration compared to 42.8% (3 of 7) in patients who received no prophylaxis prior to ICS.     

Anuric renal failure precipitated by indomethacin and triamterene

We report a patient with compensated congestive heart failure who developed acute anuric renal failure immediately after indomethacin and triamterene had been added to the treatment regimen. Renal function failed to improve promptly with discontinuation of these medications, anuria persisting for 11 days. While it is well known that patients suffering from edematous states are prone to develop renal insufficiency when given nonsteroidal anti-inflammatory agents, it is not generally appreciated that the specific combination of prostaglandin inhibitors with triamterene may carry a particularly high risk of acute renal failure, even in euvolemic subjects.     

Nephrotoxicity of high- and low-osmolality contrast media

Nephrotoxicity of radio-opaque contrast media (CM) is generally believed to involve toxic injury of proximal tubular cells. Measurement of urinary tubular enzyme excretion has been advocated as a sensitive marker of such toxic injury. It has been claimed that the new low-osmolality or nonionic CM reduce the incidence of nephrotoxicity but this remains uncertain. We studied 23 patients with normal renal function undergoing coronary angiography; patients were randomized into three groups receiving either diatrizoate (1,800 mmol/kg H2O), ioxaglate (600 mmol/kg H2O) or iohexol (850 mmol/kg H2O). Urinary excretion of a panel of enzymes increased significantly in all groups by 20 h (p less than 0.05 to less than 0.005). Alanine aminopeptidase excretion at 20 h was greater after the administration of high osmolality ionic CM than with the others but all three CM produced a similar pattern of enzyme excretion. No significant change in glomerular filtration rate was found in any group so the significance of the enzymuria remains uncertain.     

Acute renal failure in children with idiopathic nephrotic syndrome

Acute renal failure (ARF) is an uncommon but alarming complication of idiopathic nephrotic syndrome. The renal failure could be secondary to causes evident from the history and evaluation, such as severe intravascular volume depletion, acute tubular necrosis, allergic interstitial nephritis, bilateral renal vein thrombosis, acute pyelonephritis, or rapid progression of the original glomerular disease. It may be termed idiopathic if the underlying cause is undetermined. We present three children with idiopathic nephrotic syndrome who were admitted with acute renal failure. One case was due to drug-induced allergic interstitial nephritis. The other two were idiopathic in nature. Improvement in renal function occurred in the three patients over a variable period of 10 days to 4 weeks. After careful exclusion of well-known causes of acute renal failure, idiopathic acute renal failure (IARF) should be considered as a diagnostic possibility in these patients. The exact pathophysiology of IARF is not understood. Possible proposed explanations include interstitial edema, tubular obstruction, altered glomerular permeability, and unrecognized hypovolemia.     

Acute deterioration of renal function associated with enteric hyperoxaluria

Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.     

Viscosity of contrast media perturbs renal hemodynamics

Contrast-induced nephropathy is a common cause of acute renal failure, and the mechanisms underlying this injury are not completely understood. We sought to determine how physicochemical properties of contrast media may contribute to kidney damage in rats. We administered contrast media of equivalent iodine concentrations but differing physiocochemical properties: the high-osmolality iopromide was compared to the high-viscosity iodixanol. In addition, the non-iodinated substances mannitol (equivalent osmolality to iopromide) and dextran (equivalent viscosity to iodixanol) were also studied. Both types of contrast media transiently increased renal and hindquarter blood flow. The high-osmolality agents iopromide and mannitol markedly increased urine production whereas iodixanol, which caused less diuresis, significantly enhanced urine viscosity. Only the high-viscosity agents iodixanol and dextran decreased renal medullary blood flux, erythrocyte concentration, and pO2. Moreover, iodixanol prolonged the tubuloglomerular feedback response and increased plasma creatinine levels to a greater extent than iopromide or dextran. Therefore, the viscosity of contrast media may play a significant role in contrast-induced nephropathy.     

Excretory urography in acute and chronic renal failure: Current concepts and technique

Excretory urography may be usefully and safely performed on patients with severe renal failure, both acute and chronic. Dehydration is to be avoided. Large doses of radiographic contrast medium combined with meticulous x-ray exposures are required. Important information as to the cause of renal insufficiency will be gained in most patients with chronic renal disease, regardless of the level of laboratory values. The diagnosis of various entities producing acute renal failure will depend on a careful study of the nephrogram phase of the urogram with respect to time. More invasive procedures such as renal biopsy or arteriography may be avoided.