Contrast-induced nephropathy is an acute renal dysfunction that occurs within 1-3 days after administration of the radiopaque drug, leading to an increase in serum creatinine by at least 26.5 mmol / l (25%) or more in comparison with the baseline level. It usually proceeds asymptomatically. In severe cases, it is manifested by oliguria, renal edema, weakness, drowsiness, loss of appetite, nausea. It is diagnosed on the basis of data on the dynamics of creatinine and potassium concentrations in blood serum, the results of a general urinalysis, blood biochemistry, kidney samples. For treatment, infusion alkalizing drugs are administered, renal replacement therapy is performed.
ICD 10
N14.1 Nephropathy caused by other drugs, medications or biologically active substances
Meaning
Contrast-induced variant of nephropathy in patients with normal renal function occurs in no more than 0.5-5% of cases of studies using iodine-containing radiopaque agents. The likelihood of developing a disorder increases significantly in the presence of risk factors. Thus, according to the results of clinical observations in the field of modern urology, after CT of various organs, peripheral and cardiac angiography, renal dysfunction was manifested to one degree or another in 50-90% of patients with diabetic renal parenchyma lesion.
Taking into account the growing popularity of computed tomography and other modern methods of X-ray studies, the urgency of timely identification of risk factors and prevention of acute renal dysfunction, which is possible with the use of iodine-based contrast agents, increases.
Causes
Acute iatrogenic kidney damage is associated with the administration of an iodine-containing radiopaque substance. The highest nephrotoxicity is shown by highly osmolar drugs with a high density and concentration of iodine. Specialists in the field of nephrology identify five key factors that cause toxic damage to various elements of renal tissue when contrast is introduced:
- Increased osmolarity in the renal tubules. Iodine-containing contrast compounds are well filtered by nephrons and are not reabsorbed, which makes urine more concentrated. The increase in viscosity has a direct damaging effect on the epithelial cells of the tubules.
- Violation of renal hemodynamics. Contrast-induced dilation and subsequent spasm of the renal arteries affects the intensity of blood flow in the microvascular bed. After a temporary rush of blood, the intensity of the renal blood supply drops sharply, ischemia occurs in the tissues.
- Release of reactive oxygen species. After the restoration of adequate blood flow in ischemic tissues, a reperfusion “oxygen paradox” develops. Due to the abrupt activation of lipid peroxidation, oxygen free radicals are formed, which have a toxic effect on cell membranes.
- Inflammatory reaction. In response to the administration of an iodine-containing drug in various organs, including the kidneys, contrast-mediated activation of complement and release of cytokines occurs. As a result, toxic damage to the parenchyma can be aggravated by the action of inflammatory mediators.
- Tubular obstruction. Precipitation of intracranial proteins induced by radiopaque substance disrupts the intrarenal passage of urine. Due to the obstruction of the tubules, the reabsorption of urine is disrupted, and the indirect effect on the nephrons worsens the filtration processes.
The probability of contrast-induced nephropathy increases in patients suffering from pyelonephritis, glomerulonephritis, amyloidosis, gouty nephropathy, polycystic and other chronic kidney diseases, CRF, who have undergone kidney transplantation. The risk group includes patients with severe concomitant pathology — arterial hypertension, type 2 diabetes mellitus, liver cirrhosis, cardiac diseases with congestive heart failure, a decrease in the left ventricular ejection fraction to 35% or less, multiple myeloma.
Predisposing factors are also considered to be age over 75 years, proteinuria, serum creatinine content above 1.5 mg / dl, taking diuretics, ACE inhibitors, nephrotoxic drugs (NSAIDs, aminoglycosides, sulfonamides, immunosuppressants, lithium salts, antitumor drugs). The disorder develops more often in the presence of pathological conditions that aggravate tissue hypoxia — persistent hypotension, anemia, blood loss, dehydration, acute myocardial infarction, cardiogenic shock. A direct relationship has been established between the probability of induced nephropathy and the volume of contrast injected.
Pathogenesis
The mechanism of contrast-induced renal dysfunction is based on the combined manifestation of ischemic and toxic effects. The starting point in the development of the pathological process is a local violation of hemodynamics. Under the influence of radiopaque compounds, angiotensin II, vasopressin, dopamine 1, adenosine, endothelin are activated, causing renal vasoconstriction. At the same time, the activity of prostaglandins and nitric oxide, which have a vasodilating effect, decreases. As a result of prolonged spasm of the arteries and arterioles, ischemia occurs in the brain layer most susceptible to hypoxia.
The high viscosity of the X-ray contrast potentiates the aggregation of red blood cells and the slowing of renal blood flow, aggravating ischemia and reducing the glomerular filtration rate. The growth of medullary hypoxia is also facilitated by compensatory blood bypass into the cortical layer. Due to the direct toxic effect of the contrast agent on renal epithelial cells, vacuolization of cells occurs, cell membranes are damaged, mitochondrial dysfunction occurs, which ultimately leads to interstitial inflammation, tissue necrosis, apoptosis with impaired renal function.
Symptoms
Pathology develops during the first day after intravascular administration of radiopaque substances. In most patients, nephropathy proceeds without clinical manifestations, with changes in laboratory parameters of biochemical blood and urine tests. A severe variant of the course of the disorder is manifested by symptoms characteristic of acute renal failure (acute renal failure): a decrease in the daily amount of urine up to the complete cessation of its excretion, swelling on the face. With contrast-induced kidney damage, disorders of the general condition may also occur — drowsiness, weakness, nausea, loss of appetite.
Complications
With the progression of the condition, tubular necrosis is observed, which leads to a decrease in the filtration capacity of the organ. Due to the functional failure of the kidneys in patients suffering from a contrast-induced variant of nephropathy, clinical signs of violations of the water-electrolyte composition of the blood may occur. Most often, hyperkalemia develops, which is manifested by muscle weakness, bradycardia, in adverse cases — pulmonary edema, cardiac arrhythmia up to cardiac arrest. Against the background of urinary disorders and a prolonged increase in the volume of circulating blood, arterial hypertension and congestive heart failure may develop.
Diagnostics
The probable contrast-induced origin of nephropathy is indicated by the temporary connection of renal pathology with contrast X-ray examination. The diagnostic search is aimed at identifying characteristic markers of the disorder and assessing the functional viability of the kidneys. The most informative diagnostic methods are:
- Determination of serum creatinine content. In contrast-induced renal dysfunction, its concentration increases by 25% or 26.5 mmol/l or more in comparison with the initial data within 24-48 hours after the procedure. The peak level of creatinine in serum is reached on 2-5 days, after which the indicator gradually decreases for 7-10 days. In some patients, SC remains elevated for 3 weeks.
- Analysis of the concentration of potassium in the blood. A characteristic laboratory symptom of contrast-induced nephropathy is hyperkalemia. An increase in the index of more than 5.1 mmol / l serves as a marker of toxic damage to the tubules. Hyperkalemia is often combined with a decrease in blood pH of less than 7.2 (in the study of acid-base state), signs of hemolysis, a drop in platelet count, an increase in bilirubin concentration.
In the general analysis of urine with contrast-induced renal dysfunction, proteinuria, cylindruria, erythrocyturia, leukocyturia are often detected. In severe nephropathy, laboratory signs of uremia are noted. The disorder of the filtration function of the glomeruli is indicated by an increase in the levels of urea nitrogen, uric acid, a change in the serum concentration of calcium, sodium, inorganic phosphorus in the biochemical analysis of blood with a violation of the corresponding indicators in the nephrological complex. A decrease in the glomerular filtration rate of creatinine in the Rehberg sample is determined.
Instrumental examination methods involving the introduction of X-ray contrast are prohibited. The results of ultrasound of the kidneys are often nonspecific. Changes in the ECG are characteristic, indicating a violation of conductivity due to hyperkalemia. According to the indications, in addition to a nephrologist or urologist, the patient is advised by a therapist, cardiologist, pulmonologist, rheumatologist, anesthesiologist, resuscitator, toxicologist, oncologist, oncogematologist.
The contrast-induced form of nephropathy is differentiated with renal atheroembolism, rapidly progressing glomerulonephritis, chronic pyelonephritis, gouty interstitial nephritis, acute renal failure of prerenal, renal, postrenal origin, nephrological pathology in systemic connective tissue diseases, amyloidosis, berylliosis, sarcoidosis.
Treatment
The tactics of management of patients with damage to the renal parenchyma by radiopaque substances is similar to the therapeutic scheme for acute renal failure. Patients with contrast-induced nephropathy are hospitalized in a urological hospital or intensive care unit of the intensive care unit. The first day shows bed rest with subsequent transfer to the general ward.
In the diet, with sufficient caloric intake, the intake of table salt and liquid is limited, taking into account the volume of diuresis. With the appearance and increase of renal edema, the amount of protein products is reduced. The main goal of treatment is the correction of metabolic disorders. Taking into account the data on the filtering function of nephrons, it can be recommended:
- Infusion alkalizing therapy. To correct the tissue and systemic effects of metabolic acidosis, hyperkalemia, calcium preparations, glucose with insulin, sodium bicarbonate are administered intravenously. Infusion therapy is supplemented with oral administration or rectal administration of chelated forms of calcium under the control of potassium levels every 2-4 hours.
- Renal replacement therapy. With a significant decrease in diuresis, an increase in laboratory and clinical signs of renal insufficiency, the transfer of the patient to a RRT is considered. Taking into account the patient’s condition and the technical capabilities of the medical institution, hemodialysis, hemofiltration, hemodiafiltration, peritoneal dialysis are prescribed.
Prognosis and prevention
In patients who do not have a history of kidney disease, there is usually a normalization of the work of the organ for several days without any treatment. In other cases, the prognosis is also usually favorable. To prevent contrast-induced nephropathy, it is necessary to limit the conduct of studies with the introduction of X-ray contrast, if other methods can be used for diagnosis. When assessing the probability of renal dysfunction, verified scales and stratification tables are used.
Patients from the risk group are recommended to administer isoosmolar nonionic contrast agents in minimal doses. In order to improve the elimination of drugs, preliminary hydration therapy is performed with an infusion of saline solution before and after the procedure. To prevent the development of nephropathy, acetylcysteine may be additionally prescribed the day before the study.