Localized renal necrosis

Introduction 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.

Cause

According to the different causes of acute renal failure 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 Renal tubular necrosis, large area crush injury, etc.; post-renal 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. Localized renal necrosis can also be seen in nasal malignant granuloma and kidney.

an examination

Related inspection

Urine routine renal function test renal plasma flow effusion lactate dehydrogenase

Diagnosis of acute renal failure:

First, medical history and symptoms

Most of the patients have no history of kidney disease, but the cause is clear, such as severe trauma, surgery, severe infection, sepsis, obstetric complications, severe vomiting or diarrhea, circulatory dysfunction or nephrotoxic drugs, causing insufficient renal blood flow or nephrotoxicity. And other reasons. Most of the patients except the clinical manifestations of the primary disease, the majority of oliguric ATN, often 1-2 days after the primary disease, oliguria or anuria, urine volume after rehydration does not increase, early loss of appetite, nausea and vomiting, diarrhea If the urinary tract symptoms persist, if there is persistent oliguria, high blood pressure, acute pulmonary edema, some arrhythmia and pericardial effusion, aggravation of nausea and vomiting with hyperkalemia, arrhythmia, and apathy and lethargy may occur in the late stage. I am restless and even coma. Easy to combine with gastrointestinal bleeding and various infections, often respiratory and urinary tract infections. After 1 to 2 weeks, the amount of urine increased. When it was >400ml/d, it entered the period of polyuria. After about 1 week, serum creatinine and urea nitrogen began to decrease, and various symptoms gradually improved. If the continuous lack of urine and electrolytes, there may be symptoms such as nausea, fatigue, muscle relaxation, numbness of the limbs, and bloating. If not corrected, it may die of dehydration and electrolyte imbalance.

Second, physical examination found

Acute disease, in addition to the primary disease signs, may have mild anemia, oliguria often have high blood pressure, edema, severe patients with consciousness disorders, rapid breathing, heart expansion or arrhythmia.

Third, auxiliary inspection

(1) urinary specific gravity between 1.010 and 1.020, urine protein + ~ ++, may have red, white blood cells and renal tubular epithelial cells, cell tube type and granular tube type, and the large epithelial cell cast type is most meaningful.

(2) There is no large amount of blood loss or hemolysis, and there is no serious anemia. The hemoglobin is not less than 80g/L.

(3) Renal function test: Ccr decreased by more than 50% compared with normal value, and can be reduced to 1~2ml/min, and serum creatinine and urea nitrogen increased rapidly. Urine N-oxygen-D-aminoglucose, lysozyme, and 2-microglobulin are often increased.

(4) Biochemical tests often have electrolyte disorders such as hyperkalemia and decreased carbon dioxide binding. Blood gas analysis shows metabolic acidosis.

Differential diagnosis

Acute renal failure should first be differentiated from those with a rapid deterioration of chronic renal failure. ATN should be differentiated from acute renal failure caused by pre-renal azotemia, post-renal acute renal failure, and severe glomerulonephritis.

Nasal malignant granuloma should be distinguished from nasal tuberculosis, atrophic rhinitis, malignant tumors, etc. The only way is to repeat multiple biopsies.

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