2 English reference contrast nephropathy
3 disease code ICD:N 14. 1
4 disease classification kidney disease
5 disease overview With the extensive development of modern contrast technology, contrast-associated nephropathy (CAN) has attracted more and more attention from nephrologists. CAN refers to the sharp decline of renal function caused by contrast agent.
6 Disease Description With the extensive development of modern imaging technology, contrast-associated nephropathy (CAN) has attracted more and more attention from nephrologists. CAN refers to the sharp decline of renal function caused by contrast agent. Commonly used contrast agents are generally hypertonic, with iodine content as high as 37%. In vivo, they are filtered by glomeruli in their original form and are not absorbed by renal tubules. During dehydration, the concentration of drugs in the kidney will increase, which will lead to kidney damage and acute renal failure. There are more and more reports of acute renal failure caused by contrast media, and its incidence even exceeds that of aminoglycoside antibiotics. A large number of studies have reported that CAN with renal insufficiency is 6% ~ 92%, and can without renal insufficiency is 0 ~ 22%. A large number of prospective controlled studies have pointed out that the serum creatinine value after injection of contrast media is higher than 25% or 50% of the basic value, which is of diagnostic significance.
Symptoms and Signs Serum creatinine generally rises within 24 hours, reaches the peak at 96 hours, and generally returns to the basic value after 7 ~ 10 days. However, it has also been reported that the renal function gradually decreased within 1 ~ 3 weeks, and then returned to the basic value. More than 60% patients with CAN can have oliguria in the early stage, and they are resistant to loop diuretics, and some of them are non-oliguria. Most patients can recover renal function naturally, 10% need dialysis treatment, irreversible renal failure is rare, and long-term maintenance dialysis is needed. Urine test showed that renal tubular epithelial cells, casts and various fragments appeared in urine, which was nonspecific and had nothing to do with renal function changes. Uric acid salt crystals are common, occasionally calcium citrate crystals can be seen, and a lot of proteinuria is not common. In most patients with acute tubular necrosis, urinary sodium excretion is usually greater than 40mmol/L, and sodium excretion fraction (FENa) is greater than 65438 0%. However, the urinary sodium excretion in patients with acute renal failure with13 is less than 20mmol/L, and the urinary sodium excretion fraction in patients with oliguria is less than 1%.
The X-ray film of renal development lasting for 24 ~ 48 hours after the application of contrast agent is the characteristic manifestation of CAN. Older found that the sensitivity and specificity of X-ray films reached 83% and 93%, but there were also false positive and false negative results. Therefore, it is necessary to combine the serum creatinine measured in 24 ~ 48 hours to define CAN. CAN should be differentiated from renal failure caused by cholesterol microemboli. Cholesterol embolus is caused by vascular injury caused by catheter insertion during angiography. Acute patients may have symptoms and signs of vascular embolism (such as leg pain or foot pain, abdominal pain, back pain, numbness or even paralysis of limbs, pale skin of lower limbs) after receiving contrast media, and the diagnosis is difficult. Due to multiple organ infarction, patients may have hypotension, oliguria and even death. Chronic patients usually show progressive renal insufficiency for more than several weeks and develop into irreversible renal failure. The diagnosis of microembolization syndrome is based on the appearance of reticular green spots on the skin, the increase of amylase and eosinophils in peripheral blood. Urine sediment test was negative, and renal biopsy showed characteristic cholesterol embolus.
The contrast agents commonly used in the etiology of this disease are hypertonic, and they are filtered by glomerulus in vivo without being absorbed by renal tubules. During dehydration, the concentration of drugs in the kidney will increase, which will lead to kidney damage and acute renal failure. The following risk factors and possible risk factors are easy to cause renal damage:
1. Risk factors
(1) Primary renal insufficiency.
(2) Diabetes complicated with renal insufficiency: People with diabetes history over 65,438+00 years and over 50 years old are at great risk.
(3) Congestive heart failure: Congestive heart failure with cardiac function grade IV is an obvious risk factor. Because contrast agent can constrict renal blood vessels and reduce renal blood flow, it increases the risk of ischemic renal failure in patients with congestive heart failure.
(4) Nephrotic syndrome.
(5) Liver cirrhosis with renal insufficiency.
(6) Decreased blood volume or dehydration: In the experimental study of dogs, it was found that in the dehydrated state, the contrast agent can cause significant contraction of renal blood vessels.
(7) Multiple myeloma: Intravenous injection of contrast media can cause acute renal failure. It was once thought that intravenous contrast media was a bad indication for patients with multiple myeloma. However, it was found that the incidence of CAN was only 0.6% ~ 1.25% in a group of patients with retrospective multiple myeloma who received contrast media. Therefore, if necessary in clinic, it can still be carried out after careful monitoring and replenishment of capacity.
(8) Use other nephrotoxic drugs at the same time.
(9) Those who receive multiple radioactive contrast agents in a short period of time.
(10) contrast agent dose: The greater the dose, the greater the renal damage. When the dose is greater than 30ml and the average blood pressure is less than 13.3 kPa( 100mmHg), the risk increases.
(1 1) hypercalcemia.
2. Possible risk factors
(1) Age: Due to the decrease of nephron and renal blood flow in the elderly, GFR decreases with age, and the incidence of CAN is high.
(2) Diabetic patients without renal impairment.
(3) anemia.
(4) Proteinuria (no nephrotic syndrome).
(5) Abnormal liver function.
(6) Hyperuricemia.
(7) Male patients.
(8) Hypertension.
(9) renal transplant recipients.
1. Hypertonic causes renal ischemia and hypoxia. Because contrast agents are generally hypertonic, the concentration is 1400 ~ 1800 mo * */L, and its iodine content is as high as 37%. When hypertonic contrast agent reaches the kidney, on the one hand, it can cause renal vasoconstriction, reduce renal blood flow and lead to renal ischemia; On the other hand, it can make red blood cells in renal blood flow contract, deform, increase blood viscosity, slow down and stagnate renal blood flow, resulting in renal hypoxia injury. Due to renal ischemia and hypoxia and insufficient renal perfusion, glomerular filtration rate decreased and oliguria appeared.
2. Direct toxic effect on renal tubules Contrast agents increase the influx of calcium ions in renal tubular epithelial cells (especially proximal tubules), increase the intracellular calcium concentration, destroy the cytoskeleton structure of cells, and lead to degeneration, necrosis and even death of renal tubular epithelial cells.
3. As an allergen, the contrast agent caused by allergic reaction can produce corresponding antibodies when injected into the body, causing systemic allergic reaction and renal immune response.
9 pathophysiology 1. Hypertonic causes renal ischemia and hypoxia. Because contrast agents are generally hypertonic, the concentration is 1400 ~ 1800 mo * */L, and its iodine content is as high as 37%. When hypertonic contrast agent reaches the kidney, on the one hand, it can cause renal vasoconstriction, reduce renal blood flow and lead to renal ischemia; On the other hand, it can make red blood cells in renal blood flow contract, deform, increase blood viscosity, slow down and stagnate renal blood flow, resulting in renal hypoxia injury. Due to renal ischemia and hypoxia and insufficient renal perfusion, glomerular filtration rate decreased and oliguria appeared.
2. Direct toxic effect on renal tubules Contrast agents increase the influx of calcium ions in renal tubular epithelial cells (especially proximal tubules), increase the intracellular calcium concentration, destroy the cytoskeleton structure of cells, and lead to degeneration, necrosis and even death of renal tubular epithelial cells.
3. As an allergen, the contrast agent caused by allergic reaction can produce corresponding antibodies when injected into the body, causing systemic allergic reaction and renal immune response.
10 Diagnosis: There is a history of using contrast media in clinic, and the diagnosis of this disease can be made if oliguria, anuria, rash, palpitation, cold sweat and blood pressure drop occur within 24 ~ 48h, anaphylactic shock, abnormal urine test and sudden change of renal function occur in severe cases, especially obvious abnormality of renal tubular function.
Laboratory examination:
1. Urine test showed that renal tubular epithelial cells, red blood cells, white blood cells and epithelial cell casts appeared in urine, which were nonspecific and had nothing to do with renal function changes. Uric acid salt crystals are common, and occasionally calcium citrate crystals can be seen; Generally, there is transient proteinuria, and massive proteinuria is not common. In most patients with acute tubular necrosis, urinary sodium excretion is usually greater than 40mmol/L, and sodium excretion fraction (FENa) is greater than 65438 0%. However, the urinary sodium excretion in patients with acute renal failure with13 is less than 20mmol/L, and the urinary sodium excretion fraction in patients with oliguria is less than 1%.
2. Renal tubular function examination
(1) Phenol red excretion test and Mohs test: Phenol red excretion test (PSP) reflects the function of proximal convoluted tubule; The decrease of PSP indicates that the proximal convoluted tubule is damaged by contrast agent. Abnormal Mohs test indicates distal convoluted tubule injury.
(2) Uricase: n- acetyl-β-glucosaminidase (NAG) is a lysosomal enzyme. The increase of NAG activity indicates that the contrast agent causes renal damage.
(3) Determination of urinary microprotein series: urinary α 1MG, β2MG increased. Urinary retinol binding protein (RBP) increased.
(4) urine osmotic pressure: Urine osmotic pressure decreased at 300 ~ 400 mo * *, and sodium or sodium filtration fraction decreased at oliguria.
3. Blood BUN, serum creatinine and serum uric acid can be increased, while endogenous creatinine clearance rate is decreased.
Other auxiliary inspections:
1. Radionuclide renogram and B-ultrasound renogram are parabolic; B-ultrasound showed swelling or normal.
2. Renal biopsy shows that patients with characteristic cholesterol embolus can be distinguished from this disease. It is helpful for the diagnosis of this disease if there are changes such as destruction of renal tubular cytoskeleton structure and degeneration and necrosis of epithelial cells.
1 1 differential diagnosis 1. Painkiller nephropathy is caused by long-term abuse of painkillers, which is mainly manifested as chronic interstitial nephritis with aseptic pyuria, gross hematuria and renal colic.
2. Renal damage caused by aminoglycoside antibiotics This disease is mainly characterized by mild proteinuria, which may be accompanied by hematuria and tubular urine, acute tubular necrosis and acute renal failure, especially oliguria.
3.CAN should be distinguished from renal failure caused by cholesterol microemboli, which is vascular injury caused by catheter insertion during angiography. Acute patients may have symptoms and signs of vascular embolism (such as leg pain or foot pain, abdominal pain, back pain, numbness or even paralysis of limbs, pale skin of lower limbs) after receiving contrast media, and it is difficult to diagnose. Due to multiple organ infarction, patients may have hypotension, oliguria and even death. Chronic patients usually show progressive renal insufficiency for more than several weeks and develop into irreversible renal failure. The diagnosis of microembolization syndrome is based on the appearance of reticular green spots on the skin, the increase of amylase and eosinophils in peripheral blood. Urine sediment test was negative, and renal biopsy showed characteristic cholesterol embolus.
12 treatment plan 1. Mastering the indications of medication For patients with high-risk factors, angiography should be avoided as far as possible, such as patients with original renal insufficiency, the elderly, dehydration, diabetes, multiple myeloma, hyperuricemia and so on. When the diagnosis cannot be confirmed after B-ultrasound examination, and angiography is necessary, the indications should be strictly controlled, normal saline should be supplemented before angiography, and angiography should be carried out after dehydration, hypotension and electrolyte disorder are corrected.
2. Avoid repeated radiography in a short time. It is not advisable to have another contrast within 3 months after the first contrast, so as to avoid renal damage caused by contrast agent.
3. In order to avoid or reduce the nephrotoxicity of alkalized urine after hydration treatment and contrast, 20% mannitol (250~500ml) and furosemide (40 ~ 100mg) can be used intravenously, starting at 1h before contrast, which can increase renal perfusion, reduce blood viscosity, increase renal blood flow and strengthen diuresis. After angiography, patients were encouraged to drink more water, and 5% sodium bicarbonate (250 ml) was injected intravenously to alkalize urine to increase uric acid excretion.
4. Change the type of contrast agent. For patients with high risk factors or iodine allergy, iodine-free contrast media (such as iopromide) or nonionic and hypotonic contrast media should be selected to reduce their nephrotoxicity.
5. Active treatment of acute renal failure Once oliguric acute renal failure occurs, those who are still ineffective after volume expansion and diuresis should be treated with emergency dialysis and treated as acute renal failure.
6. Others
(1) Calcium channel blockers: It has been proved that calcium channel blockers can inhibit contrast-induced renal vasoconstriction in dogs. Calcium antagonists can prevent renal ischemia by inhibiting intracellular calcium influx, block renal vasoconstriction and prevent renal tubular cell death.
(2) vasodilator:
① Atrial natriuretic peptide (ANP): It CAN prevent CAN and block the decrease of renal blood flow and glomerular filtration rate caused by contrast agent. Aortic atrial natriuretic peptide can reduce creatinine clearance and contrast-induced renal blood flow reduction.
② Adenosine antagonist: After 40 patients with serum creatinine ≤ 160μmol/L received contrast agent, the Ccr of adenosine antagonist group decreased by 21%4%, while that of placebo group decreased by 39% 5% (P < 0.05), suggesting that it has a certain protective effect on renal vasoconstriction caused by contrast agent.
13 complications have no relevant data.
14 prognosis and preventive prognosis: the lesions of most patients are reversible after stopping using contrast media. If symptomatic treatment can be given in time, the prognosis is good, and some clinical syndromes can be relieved by themselves. However, if the drug is not stopped in time, the renal function will continue to deteriorate and acute tubular necrosis will occur.
Prevention:
1. Strictly control indications, dosage and course of treatment. During medication, we should pay close attention to monitoring urine routine, urinary enzymes and renal function, so as to find nephrotoxicity early and stop taking drugs in time.
2. For the elderly, diabetic patients, patients with chronic kidney disease, especially those with chronic renal insufficiency, try to avoid using it.
3. Avoid repeated use of contrast agent in a short time.
The incidence of CAN in 15 epidemiological literature is widely reported. There are more and more reports of acute renal failure, and its incidence even exceeds that caused by aminoglycoside antibiotics, accounting for about 6% ~ 92%.
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