Contrast agent nephropathy

　　The occurrence of contrast agent nephropathy is closely related to pre-existing renal insufficiency, diabetes with renal insufficiency, congestive heart failure, and nephrotic syndrome, etc. The specific etiology and pathogenesis are described as follows.

　　First, etiology

　　Commonly used contrast agents are hypertonic, filtered by the glomerulus in their original form without being absorbed by the renal tubules. In the case of dehydration, the concentration of this drug in the kidney increases, which can cause renal damage and acute renal failure. The following are the risk factors that are likely to cause renal damage and possible risk factors:

　　1、Risk factors

　　（1）Pre-existing renal insufficiency.

　　（2）Diabetes with renal insufficiency: with a history of diabetes10years, age over50 years old, with cardiovascular complications and renal insufficiency, the risk is even greater.

　　（3）Congestive heart failure: Congestive heart failure with heart function IV is a significant risk factor.

　　（4）Nephrotic syndrome.

　　（5）Liver cirrhosis with renal dysfunction.

　　（6）Decreased blood volume or dehydration: In dog experiments, it was found that in a dehydrated state, contrast agent can cause significant vasoconstriction in renal vessels.

　　（7）Multiple myeloma: Intravenous injection of contrast agent can cause acute renal failure. If necessary, blood volume should be carefully monitored and supplemented before proceeding.

　　（8）Patients who are concurrently using other nephrotoxic drugs.

　　（9）Patients who have received multiple radiographic contrast agents in a short period of time.

　　（10）The dose of contrast agent: as the dose increases, renal damage increases. When the dose is greater than30ml, the average blood pressure during contrast imaging is less than13.3kPa（100mmHg), the risk increases.

　　（11）Hypercalcemia.

　　2、Possible risk factors

　　（1）Age: Due to the reduction in renal units and the decrease in renal blood flow in the elderly, glomerular filtration rate (GFR) decreases with age, and the incidence of contrast agent nephropathy (CAN) is high.

　　（2）Diabetic patients without renal dysfunction.

　　（3）Anemia.

　　（4）Proteinuria (not accompanied by nephrotic syndrome).

　　（5）Abnormal liver function.

　　（6）Hyperuricemia.

　　（7）Male patients.

　　（8）Hypertension.

　　（9）Patients who have received renal transplantation.

　　Second, pathogenesis

　　1Hypertonicity leads to renal ischemia and hypoxia Since most contrast agents are hypertonic, their concentration is1400～1800mOsm/L, its iodine content reaches37％, when hypertonic contrast agent reaches the kidneys, on one hand, it can cause renal vasoconstriction, reduce renal blood flow, leading to renal ischemia; on the other hand, it can cause red blood cells in renal blood to shrink, deform, and increase blood viscosity, thereby slowing down and stagnating renal blood flow, resulting in renal hypoxic injury. Due to renal ischemia, hypoxia, and insufficient renal perfusion, glomerular filtration rate decreases, leading to oliguria.

　　2Direct toxic effect on renal tubules The contrast agent increases the influx of calcium ions into renal tubular epithelial cells (especially the proximal tubules), leading to an increase in intracellular calcium concentration, destruction of the cell's skeletal structure, and ultimately causing tubular epithelial cell变性, necrosis, and death.

　　3、Allergic reactions lead to renal damage As an allergen, when contrast agents are injected into the body, the body can produce corresponding antibodies, causing systemic allergic reactions and renal immune reactions.

　　Most patients with contrast agent nephropathy can recover their renal function naturally,10％of patients require dialysis treatment, irreversible renal failure is rare, requiring long-term dialysis maintenance. Severe cases may develop anaphylactic shock, abnormal urinalysis, and abrupt changes in renal function, especially significant tubular function abnormalities.

　　Early in contrast agent nephropathy patients can present with oliguria, but most patients' renal function can recover naturally, some patients need dialysis treatment, and the specific clinical manifestations are described as follows.

　　1、Serum creatinine in patients receiving contrast agents is usually24h increased,96h reached the peak, generally7～10Days after returning to the baseline. But there are also reports that renal function in1～3Weeks decreased progressively, then returned to the baseline.6％above contrast agent nephropathy (CAN) patients may present with oliguria early, resistant to diuretics, and there are also non-oliguric patients. Most patients' renal function can recover naturally,10％of patients require dialysis treatment, and irreversible renal failure is rare, requiring long-term dialysis maintenance.

　　2、There is a history of contrast agent use in clinical practice, and patients in24～48Within h, oliguria, anuria, rash, palpitations, cold sweat, blood pressure drop, and severe allergic shock may occur, with abnormal urinalysis and abrupt changes in renal function, especially significant tubular function abnormalities, and the diagnosis of the disease can be made.

　　The prevention of contrast agent nephropathy includes strict control of the indications, drug dosage, and course of treatment, and the specific preventive measures are described as follows.

　　1、Strictly control the indications, drug dosage, and course of treatment. During the period of medication, attention should be paid to the strict monitoring of urine routine, urine enzymes, and renal function, so as to discover the nephrotoxic effects early and stop the medication in time.

　　2、Especially for the elderly, diabetics, and those with chronic kidney disease, and those with chronic renal insufficiency, it is best to avoid using them.

　　3、Avoid repeated use of contrast agents in a short period of time.

　　The examination of contrast agent nephropathy includes urine, renal tubular function, glomerular function, ultrasound, and renal biopsy, etc., and the specific examination methods are described as follows.

　　一、Urine Examination

　　Urine examination shows renal tubular epithelial cells, red blood cells, white blood cells, and epithelial cell casts in the urine, which are non-specific and not related to changes in renal function. Urate crystals are common, and calcium citrate crystals are occasionally seen; generally, transient proteinuria is present, and massive proteinuria is uncommon. Most patients with acute tubular necrosis have a urine sodium excretion greater than40mmol/L, sodium excretion fraction (FENa) is greater than1％; but there is1/3Acute renal failure patients have lower urine sodium excretion than20mmol/L, sodium excretion fraction in oliguria is less than1％

　　二、Renal Tubular Function Examination

　　1、Phenol Red Excretion Test and Moss Test Phenol Red Excretion Test (PSP) reflects the function of the proximal tubule: Decreased PSP indicates damage to the proximal tubule from contrast agents. Abnormality in the Moss test suggests damage to the distal tubule.

　　2、尿酶 N-乙酰-β-氨基葡萄糖苷酶（N-acetyl-β-D-glucosaminidase，NAG）是一种溶酶体酶。NAG活性增高说明造影剂造成肾损害。

　　3、尿系列微量蛋白测定 尿α1-微球蛋白（α1-MG）、β2-微球蛋白（β2-MG）升高。尿视黄醇结合蛋白（RBP）升高。

　　4、尿渗透压 尿渗透压降低在300～400mOsm，少尿期低尿钠或钠滤过分数降低。

　　三、肾小球功能检查

　　血尿素氮（BUN）、血清肌酐、血尿酸均可升高，内生肌酐清除率降低。

　　四、核素肾图及B超检查

　　肾图呈抛物线型；B超肾影增大或正常。

　　五、肾活检

　　显示有特征性的胆固醇栓子者可与本病鉴别。如有肾小管细胞骨架结构破坏、上皮细胞变性坏死等改变，有助于本病诊断。

　　造影剂肾病患者除了常规的治疗外，饮食上还要注意以下事项：患者的饮食多以清淡为主，少吃含盐量高的饮食，同时注意饮食要规律。

　　造影剂肾病患者根据现代临床关格的病机、症状，常选用黄连温胆汤、旋复代赭汤清热和中降逆，或用凉隔散、升降散泄浊解毒，或以清心导赤散、清营汤清心凉营辨证施治。治疗恰当及时，可望使病情趋于稳定。若治疗延误，则病势险恶，预后不良。其中以心气虚衰或心肾阳衰者最为凶险，应积极给予中西医措施综合救治，或结合透析治疗。

　　Εκτός από τη λήψη της ενδοφλέβιας θεραπείας με χημειοθεραπεία, μπορεί να συνδυαστεί με τη θεραπεία του ενδοσκοπικού πλυσίματος ή της θεραπείας της δροσιάς, που είναι ευεργετική για την εκκένωση του βρώμικου τοξίνης. Οι συχνές συνταγές περιλαμβάνουν: Ζωντανή σκόρδο, Ζωντανή οστρακοειδής, Σανσενσέ, Σανσενσέ, Ιουνιέτα, Αξιοποιούνται για τους ασθενείς με ενδοσκόπηση και σύνθετη ασθένεια. Χαρακτηριστικά του χρυσού, Χαρακτηριστικά του φαρμάκου, Οστρακοειδής, Σανσενσέ, Σανσενσέ, Αξιοποιούνται για τους ασθενείς με κρύο και υγρασία και ασθένεια με μυωπάτη.