Contrast-induced nephropathy

　　The occurrence of contrast-induced 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 glomeruli without being absorbed by the renal tubules in the body, and their concentration in the kidney increases during dehydration, which can cause renal damage and acute renal failure. The following are the risk factors and possible risk factors that are likely to cause renal damage:

　　1. Risk factors

　　(1) Pre-existing renal insufficiency.

　　(2) Diabetes with renal insufficiency: Patients with a history of diabetes for more than 10 years, over 50 years of age, with cardiovascular complications, and renal insufficiency have a higher risk.

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

　　(4) Nephrotic syndrome.

　　(5) Liver cirrhosis with renal damage.

　　(6) Decreased blood volume or dehydration: Experimental studies in dogs have found that in a dehydrated state, contrast agents can cause significant vasoconstriction in renal vessels.

　　(7) Multiple myeloma: intravenous injection of contrast agents can cause acute renal failure. If necessary, blood volume should be carefully monitored, and the procedure can be performed after volume expansion.

　　(8) Concurrent use of other nephrotoxic drugs.

　　(9) Patients receiving multiple types of radiographic contrast agents within a short period of time.

　　(10) Dose of contrast agent: increased dose leads to increased renal damage. When the dose is greater than 30ml, the average blood pressure during contrast is less than 13.3kPa (100mmHg), and the risk increases.

　　(11) Hypercalcemia.

　　2. Possible risk factors

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

　　(2) Diabetic patients without renal damage.

　　(3) Anemia.

　　(4) Proteinuria (without nephrotic syndrome).

　　(5) Abnormal liver function.

　　(6) Hyperuricemia.

　　(7) Male patients.

　　(8) Hypertension.

　　(9) Recipients of renal transplants.

　　Second, pathogenesis

　　1. Hypertonicity leading to renal ischemia and hypoxia Since most contrast agents are hypertonic, with concentrations ranging from 1400 to 1800 mOsm/L and iodine content up to 37%, when hypertonic contrast agents reach the kidneys, on one hand, they can cause vasoconstriction of renal blood vessels, reducing renal blood flow, leading to renal ischemia; on the other hand, they can cause red blood cells to shrink, deform, and increase blood viscosity, 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.

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

　　3. Renal damage caused by allergic reactions 造影剂作为过敏原，当它被注入机体后，机体可产生相应抗体，引起全身性的过敏反应及肾脏的免疫反应。

　　What complications can contrast agent nephropathy easily lead to

　　Early in contrast agent nephropathy, oliguria may occur, but the renal function of most patients can recover naturally, and some patients may require dialysis treatment. The specific clinical manifestations are described as follows.

　　1. The serum creatinine of patients receiving contrast agents usually increases within 24 hours, reaches a peak at 96 hours, and generally returns to the baseline after 7-10 days. However, there are also reports that renal function may progressively decrease within 1-3 weeks and then return to the baseline. More than 60% of patients with contrast agent nephropathy (CAN) may present with oliguria early on, have resistance to diuretics, and some may not have oliguria. Most patients' renal function can recover naturally, 10% of patients may require dialysis treatment, and irreversible renal failure is rare, requiring long-term dialysis maintenance.

　　2. Patients with a history of contrast agent use in clinical practice may experience oliguria, anuria, rash, palpitations, cold sweat, and blood pressure drop within 24-48 hours. In severe cases, anaphylactic shock may occur, accompanied by abnormal urine tests and abrupt changes in renal function, especially obvious abnormalities in tubular function. A diagnosis of the disease can be made accordingly.

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

　　1. Strictly control the indications, dosage, and course of treatment for drugs. During the medication period, pay close attention to the monitoring of routine urine tests, urine enzymes, and renal function to detect renal toxicity early and stop the medication in time.

　　2. For the elderly, diabetics, and those with pre-existing chronic kidney disease, especially those with chronic renal insufficiency, it is best to avoid using them.

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

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

　　4. Urine examination

　　Urine examination may show 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 occasionally calcium citrate crystals may be seen; generally, there is transient proteinuria, and large amounts of proteinuria are uncommon. Most patients with acute tubular necrosis have urine sodium excretion often greater than 40mmol/L, and the sodium excretion fraction (FENa) is greater than 1%; however, 1/3 of patients with acute renal failure have urine sodium excretion below 20mmol/L, and those with oliguria have a sodium excretion fraction less than 1%.

　　2. Renal tubular function examination

　　1. The phenol red excretion test and the Moss test reflect the function of the proximal tubule: a decrease in the phenol red excretion test (PSP) indicates damage to the proximal tubule by contrast agents. Abnormal results in the Moss test suggest damage to the distal tubule.

　　2, Urine enzymes N-Acetyl-β-D-glucosaminidase (NAG) is a lysosomal enzyme. Increased NAG activity indicates kidney damage caused by contrast agents.

　　3, Urine series microprotein determination Urinary α1-microglobulin (α1-MG), β2-microglobulin (β2-MG) increase. Urinary retinol-binding protein (RBP) increases.

　　4, Urine osmolality Urine osmolality decreases to 300-400 mOsm, low urine sodium or sodium filtration fraction decreases during oliguria.

　　Third, glomerular function test

　　Blood urea nitrogen (BUN), serum creatinine, blood uric acid can all increase, and the内生肌酐清除率 (intrinsic creatinine clearance rate) decreases.

　　Fourth, radionuclide renal scan and B-ultrasound examination

　　Renal scan shows a parabolic shape; B-ultrasound renal shadow enlargement or normal.

　　Fifth, renal biopsy

　　Patients with characteristic cholesterol emboli can be distinguished from this disease. If there are changes such as destruction of the renal tubular cell skeleton structure, degeneration and necrosis of the epithelial cells, it is helpful for the diagnosis of this disease.

　　In addition to routine treatment, patients with contrast agent nephropathy should also pay attention to the following dietary matters: the diet of patients should be light and non-greasy, eat less salt, and pay attention to regular diet.

　　For patients with contrast agent nephropathy, based on the etiology and symptoms of modern clinical Guan Gai, it is often chosen to use Huanglian Wencang Decoction, Xuanfu Gaijie Decoction to clear heat and harmonize the middle and reduce reverse, or use Liangge San, Shengshang San to discharge turbid toxins, or use Qingxin Daochi Powder, Qingying Soup to clear the heart and cool the nutrient, and treat according to the syndrome differentiation. Proper and timely treatment can hope to stabilize the condition. If treatment is delayed, the disease condition will be dangerous, and the prognosis will be poor. Among them, patients with heart Qi deficiency or heart and kidney Yang deficiency are the most dangerous, and comprehensive treatment measures should be actively adopted, or combined with dialysis treatment.

　　In addition to taking internal Chinese medicine treatment, it can be combined with Chinese medicine retention enema or rectal drop therapy, which is beneficial to the excretion of turbid toxins. Common prescriptions: raw rhubarb, raw oyster, salvia miltiorrhiza, dandelion, June Snow, suitable for patients with Guan Gai due to internal accumulation of damp-heat turbid toxins; rhubarb, prepared aconite, oyster, salvia miltiorrhiza, dandelion, suitable for patients with Guan Gai due to internal accumulation of cold-damp turbid toxins and with symptoms of alternating cold and heat.