Renal ischemia

Introduction Renal ischemia is one of the causes of acute renal failure. Hyperosmoticity leads to renal ischemia and hypoxia. Because the general contrast agent is hyperosmotic, the concentration is 1400-1800 mOsm/L, and its iodine content is as high as 37%. When the hypertonic contrast agent reaches the kidney, it can be Causes renal vasoconstriction, reduced renal blood flow, leading to renal ischemia. The kidney is an important organ for the body to maintain its internal environment. Severe renal ischemia such as severe trauma, extensive burns, major surgery, massive blood loss, obstetric hemorrhage, severe infection, sepsis, dehydration and electrolyte imbalance, especially in patients with shock, can easily lead to acute tubular necrosis.

Cause

Acute renal failure is a clinical syndrome in which the kidney itself or extra-renal causes a sharp decrease in renal urinary function, resulting in a serious disorder in the body's environment. Mainly manifested as oliguria or anuria, azotemia, hyperkalemia and metabolic acidosis. According to the different causes of the disease and their respective pathophysiological characteristics, the etiology can be divided into pre-renal such as blood loss, shock, severe water loss, electrolyte imbalance, acute circulatory failure, etc., renal such as acute glomerulonephritis, acute tubular necrosis, Large area crush injury, etc.; post-renal sex such as complete urinary tract obstruction. Among them, acute tubular necrosis is the most common and most characteristic, and the sustained development of prerenal failure will also be converted into acute tubular necrosis.

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 may cause renal damage and acute renal failure. The following are 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. Because contrast agents can cause renal vasoconstriction, renal blood flow is reduced, increasing the risk of ischemic renal failure in patients with congestive heart failure.

(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 considered that multiple myeloma intravenous injection of contrast agent is a counter-indication. However, in a group of retrospective multiple myeloma after receiving contrast agents, the incidence of CAN was found to be only 0.6% to 1.25%. Therefore, if necessary, clinical monitoring, careful monitoring, and capacity can still be carried out.

(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 13.3kPa (100mmHg), the risk increases.

(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.

an examination

Related inspection

Rehydration test retroperitoneal angiography

Laboratory inspection:

1. Urine examination Urine examination showed that tubular epithelial cells, red blood cells, white blood cells and epithelial cell casts were found to be non-specific and not related to renal function changes. Urinary acid crystals are common, even calcium citrate crystals can be seen; generally have a proteinuria, a large number of proteinuria is not common, most patients with acute tubular necrosis, urinary sodium excretion often greater than 40mmol / L, sodium excretion fraction (FENa ) is greater than 1%; but 1/3 of patients with acute renal failure have a urinary sodium excretion of less than 20 mmol/L, and those with oliguria have a sodium excretion score of 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. An abnormal Mohs test suggests a distal convoluted tubule lesion.

(2) Urine enzyme: N-acetyl--D-glucosaminidase (NAG) is a lysosomal enzyme. An increase in NAG activity indicates that the contrast agent causes kidney damage.

(3) Determination of urine microprotein: urine 1-MG, 2-MG increased. Urinary retinol binding protein (RBP) is elevated.

(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 decreased.

Other auxiliary inspections:

1. The radionuclide kidney map and B-ultrasound kidney pattern are parabolic; B-ultrasound kidney enlargement or normal.

2. Renal biopsy shows that a characteristic cholesterol embolus can be identified with the disease. If there is a change in the structure of the tubular cytoskeleton, degeneration and necrosis of the epithelial cells, it is helpful for the diagnosis of this disease.

Differential diagnosis

1. Hyperosmolarity leads to renal ischemia and hypoxia. Because the general contrast agent is hyperosmotic, the concentration is 1400-1800 mOsm/L, and its iodine content is as high as 37%. When the hypertonic contrast agent reaches the kidney, one It can cause renal vasoconstriction, renal blood flow is reduced, leading to renal ischemia; on the other hand, red blood cell shrinkage, deformation, and blood viscosity can be increased in renal blood flow, causing renal blood flow to slow down, stasis, and renal hypoxia damage. Due to renal ischemia and hypoxia, renal perfusion is insufficient, resulting in decreased glomerular filtration rate and oliguria.

2. Direct toxic effect on renal tubules Contrast agent increases the calcium influx of renal tubular epithelial cells (especially proximal tubules), increases intracellular calcium concentration, destroys the skeleton structure of cells, and causes degeneration, necrosis and death of tubular epithelial cells. .

3. Allergic reaction-induced kidney damage as an allergen, when it is injected into the body, the body can produce antibodies, causing systemic allergic reactions and kidney immune response.

Clinically, there is a history of contrast agent application. Within 24 to 48 hours, oliguria, anuria, 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.

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