Contrast Nephropathy
Introduction
Introduction to contrast nephropathy Contrastassociated nephropathy (CAN) refers to a sudden decrease in renal function caused by contrast agents. Commonly used contrast agents are generally hyperosmotic, containing up to 37% iodine, which is filtered by the glomerulus in the body without being absorbed by the renal tubules. When dehydrated, the concentration of the drug in the kidney is increased, which can cause kidney damage. Acute renal failure occurs. basic knowledge The proportion of illness: 0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: renal failure
Cause
Contrast agent nephropathy
(1) Causes of the disease
Commonly used contrast agents are hyperosmotic, which are filtered by the glomerulus in the body without being absorbed by the renal tubules. When the dehydration is increased, the concentration of the drug in the kidney is increased, which can cause renal damage and acute renal failure. The following is easy. Risk factors and possible risk factors for kidney damage:
Risk factor
(1) The original renal insufficiency.
(2) Diabetes with renal insufficiency: There is a history of diabetes for more than 10 years, and the age is over 50 years old. There is a high risk of cardiovascular complications and renal insufficiency.
(3) Congestive heart failure: Congestive heart failure with grade IV cardiac function is a significant risk factor.
(4) Nephrotic syndrome.
(5) cirrhosis with renal dysfunction.
(6) Decreased blood volume or dehydration: In the experimental study of dogs, it was found that in the dehydrated state, the contrast agent caused significant contraction of the blood vessels in the kidney.
(7) multiple myeloma: intravenous injection of contrast agent can cause acute renal failure, once thought that multiple myeloma intravenous injection of contrast agent for anti-indications, but in a group of retrospective multiple myeloma to receive contrast agents After the observation, the incidence of CAN was only 0.6% to 1.25%, so if it is needed in clinical, it can be carefully monitored and the capacity can be replenished.
(8) Apply other nephrotoxic drugs at the same time.
(9) Those who receive multiple radioactive contrast agents in a short period of time.
(10) Dose of contrast agent: The larger the dose, the greater the renal damage. When the dose is >30ml, the average blood pressure during angiography is less than 13.3 kPa (100mmHg).
(11) High blood calcium.
2. Possible risk factors
(1) Age: Due to the decrease in renal unit and renal blood flow in elderly patients, GFR decreases with age and the incidence of CAN is high.
(2) Diabetic patients without renal dysfunction.
(3) Anemia.
(4) proteinuria (without nephrotic syndrome).
(5) Abnormal liver function.
(6) hyperuricemia.
(7) Male patients.
(8) High blood pressure.
(9) Those who receive kidney transplantation.
(two) pathogenesis
1. Hyperosmotic causes renal ischemia, hypoxia: Because the general contrast agent is hyperosmotic, the concentration is 1400 ~ 1800mOsm / L, its iodine content is as high as 37%, when the hypertonic contrast agent reaches the kidney, On the one hand, it can cause renal vasoconstriction, renal blood flow is reduced, leading to renal ischemia; on the other hand, red blood cells can be shrunk, deformed, and blood viscosity increased in renal blood flow, causing slowing of renal blood flow, stasis, and renal hypoxia Sexual injury, due to renal ischemia and hypoxia, renal hypoperfusion, glomerular filtration rate decreased, oliguria occurred.
2. Direct toxic effects on renal tubules: Contrast agents increase the influx of calcium ions in renal tubular epithelial cells (especially proximal tubules), increase intracellular calcium concentration, and destroy the skeleton structure of cells, leading to degeneration and necrosis of tubular epithelial cells. death.
3. Allergic reaction causes kidney damage: The contrast agent acts as an allergen. When it is injected into the body, the body can produce corresponding antibodies, causing systemic allergic reactions and kidney immune response.
Prevention
Contrast kidney disease prevention
1. Strictly grasp the indications for medication, drug dosage and course of treatment. During the medication, we should pay close attention to the strict monitoring of urine routine, urine enzymes and renal function, so as to detect the nephrotoxicity and stop the drug in time.
2. For the elderly, diabetics and patients with chronic kidney disease, especially those with chronic renal insufficiency, avoid using them as much as possible.
3. Avoid repeated use of contrast agents in the short term.
Complication
Contrast nephropathy complications Complications, renal failure
Renal Failure.
Symptom
Contrast agent nephropathy symptoms common symptoms tubular proteinuria cold sweat heart uric acid crystal no urine oliguria blood pressure drop shock
1. Serum creatinine in contrast recipients usually rises within 24h, peaks at 96h, and generally returns to the baseline value after 7-10 days, but it has also been reported that renal function declines progressively within weeks and then returns to the baseline value. More than 60% of patients with CAN can develop oliguria in the early stage, resistant to loop diuretics, and non-oliguric. Most patients can recover naturally, 10% require dialysis treatment, and irreversible renal failure is rare. Long-term dialysis.
2. Urine examination shows renal tubular epithelial cells, casts and various fragments in the urine, non-specific, not related to changes in renal function, urate crystals are common, even calcium citrate crystals are visible, and large amounts of proteinuria are not common. In most patients with acute tubular necrosis, urinary sodium excretion is often greater than 40mmol/L, and sodium excretion fraction (FENa) is greater than 1%; but 1/3 of patients with acute renal failure have lower urinary sodium excretion below 20mmol/L. The sodium excretion fraction is less than 1%.
3. After the application of contrast agent, X-ray film double kidney development lasted for 24 ~ 48h for the characteristic performance of CAN. Older found in the observation that X-ray film sensitivity is 83%, specificity is as high as 93%, but there are also fake Positive and false negative results, so CAN still needs to be combined with serum creatinine measurements within 24 to 48 hours to be clear.
Examine
Contrast kidney disease examination
1. Urine examination : Urine examination shows renal tubular epithelial cells, red blood cells, white blood cells and epithelial cell casts, which are non-specific, not related to renal function changes, urate crystals are common, and even calcium citrate can be seen. Crystallization; generally a transient proteinuria, a large number of proteinuria is not common, most patients with acute tubular necrosis, urinary sodium excretion is often greater than 40mmol / L, sodium excretion fraction (FENa) is greater than 1%; but there are 1/3 acute kidney The urinary sodium excretion is less than 20mmol/L, and the sodium excretion fraction of oliguria is less than 1%.
2. Renal tubular function test
(1) Phenol red excretion test and Mohs test: Phenol red excretion test (PSP) reflects the function of proximal convoluted tubules: PSP reduction suggests contrast agent damage to proximal convoluted tubules, and Mohs test abnormalities suggest distal convoluted tubule damage.
(2) Urine enzyme: N-acetyl--D-glucosaminidase (NAG) is a lysosomal enzyme. The increase in NAG activity indicates that the contrast agent causes kidney damage.
(3) Determination of urine microprotein: urine 1-MG, 2-MG increased, and urinary retinol binding protein (RBP) increased.
(4) Urine osmotic pressure: the urine osmotic pressure is reduced at 300-400 mOsm, and the low urinary sodium or sodium filtration fraction is decreased during oliguria.
3. Glomerular function test : blood BUN, serum creatinine, blood uric acid can be increased, endogenous creatinine clearance rate is reduced.
4. Radionuclide kidney diagram and B-ultrasound examination : The kidney diagram is parabolic; B-ultrasound is enlarged or normal.
5. Renal biopsy : Patients with characteristic cholesterol emboli can be identified with the disease, such as the destruction of tubular cytoskeleton structure, degeneration and necrosis of epithelial cells, which is helpful for the diagnosis of this disease.
Diagnosis
Diagnostic and differential diagnosis of contrast nephropathy
Clinically, there is a history of contrast agent application. In 24 to 48 hours, oliguria, no urine, rash, palpitations, cold sweat, blood pressure drop, severe anaphylactic shock, abnormal urine test, sudden changes in renal function, especially abnormal tubule function , you can make a diagnosis of this disease.
Differential diagnosis
1. Analgesic nephropathy: This disease is caused by long-term abuse of painkillers, mainly chronic interstitial nephritis, aseptic pyuria, accompanied by gross hematuria and renal colic.
2. Kidney damage caused by aminoglycoside antibiotics: The disease mainly manifests as mild proteinuria after 5-7 days of administration, which may be associated with hematuria and tubular urine, which may cause acute tubular necrosis and acute renal failure. The oliguria is more common.
3.CAN must be differentiated from renal failure caused by cholesterol microembolism: cholesterol emboli is caused by catheter insertion of damaged blood vessels during angiography, and acute type may have symptoms of vascular embolism after receiving contrast agent. Signs (such as leg or foot pain, abdominal pain, back pain, limb numbness and even paralysis, pale skin of the lower limbs), difficult diagnosis, patients may have hypotension, oliguria and even death due to multiple organ infarction, chronic type usually appears as Progressive renal insufficiency for more than a few weeks and development of irreversible renal failure, microembolic syndrome diagnosis based on skin reticular bluish, amylase increased and peripheral blood eosinophilia, urine sediment test negative, Renal biopsy showed characteristic cholesterol emboli.
