Acute renal failure (ARF) is a clinical syndrome that occurs within hours to days due to a rapid decline in glomerular filtration rate. ARF can be defined as a sudden increase of blood creatinine over 177umol/L in patients with normal renal function or a sudden increase of blood creatinine over 50% in patients with abnormal renal function accompanied by nitrogen metabolites such as urea nitrogen, etc. ARF can be divided into oliguric (400 ml/d) and non-oliguric types, and the treatment of ARF caused by various kinds of primary pathologies is very different, and the prognosis is closely related to the early diagnosis and good treatment. Its prognosis is closely related to early diagnosis and good treatment. Improper diagnosis and treatment may lead to irreversible stage of renal function damage and even require maintenance dialysis treatment. The diagnosis of ARF can be divided into two parts, firstly, the etiology of ARF should be clarified, and then the complications of ARF should be determined.If patients with ARF can get the etiology diagnosis at an early stage, remove the triggers in time, and take effective treatment measures, most of the patients can recover their function basically or purely; and active treatment of the complications of ARF can shorten the time of recovering renal function, and reduce the mortality rate of ARF. Mortality. I. Diagnosis of primary disease: There are many causes of ARF, which can be categorized into pre-renal ARF, renal ARF and post-renal ARF, and the above categorization only represents the cause of the disease at the time of diagnosis, some ARF patients can be caused by a variety of reasons, and it is difficult to categorize some patients into a certain category, and in the development of the disease, pre-renal can also be converted into renal ARF, and post-renal ARF can be converted into chronic renal failure if it is left untreated for a long period of time. Post-renal ARF, if left untreated for a long time, can also turn into chronic renal failure. In the process of diagnosis, we should first identify whether it is acute exacerbation of chronic renal insufficiency or not, and then identify whether it is postrenal ARF or prerenal ARF, and then make differential diagnosis of renal diseases one by one. Acute exacerbation of chronic renal insufficiency is the result of acute renal failure due to the rapid deterioration of renal function in pre-existing chronic renal disease. The cause may be a rapid progression of the original chronic kidney (e.g., persistent progressive immune injury) or a sudden increase in the number of injurious factors of renal damage (e.g., infections, urinary tract obstruction, use of nephrotoxic drugs, high-protein diets, hypercalcemia, hyperuricemia, and a sharp increase in blood pressure). Differential diagnosis should be noted whether there is previous hypertension, abnormal urine pickup, swelling, nocturia, repeated urinary tract infections and family history of kidney. Auxiliary investigation found that kidney shrinkage, anemia also suggests that there is chronic renal insufficiency, identification difficulties can be done when the renal biopsy to clarify the presence of chronic renal lesions. Post-renal urinary tract obstruction post-renal factors are easier to identify, but of course, often overlooked. Causes of obstruction include urinary tract tuberculosis, tumor, prostatic hypertrophy and so on. ARF is usually manifested by bilateral ureteral obstruction or loss of function of one kidney with ureteral obstruction on the opposite side, which is often manifested clinically as anuria in addition to the primary manifestations. Patients may have previous symptoms such as dysuria and dyspareunia, and may have a history of urologic surgery. On examination, sometimes a distended bladder can be palpated, positive percussion pain in the renal region, and positive findings on rectal and pelvic examination. Urine routine often shows a small amount of proteinuria, with no abnormalities or a few leukocytes on microscopic examination of the urine sediment. Suspicious patients need indwelling urinary catheter, B-mode ultrasonography is very helpful in the diagnosis of retrorenal obstruction, and sometimes X-ray abdominal plain film, intravenous pyelogram, radionuclide imaging and other imaging tests are needed to clarify the cause of the disease and the location of the lesion. Prerenal ARF, also known as prerenal azotemia, is the most common cause of ARF. Pre-renal ARF is due to decreased glomerular perfusion, there is no obvious damage to the glomerular structure, and glomerular filtration function can return to normal when renal blood flow and perfusion are restored. To diagnose prerenal ARF, there must be factors that lead to insufficient glomerular perfusion, such as a decrease in the volume of effective extracellular fluid or the application of drugs that affect the kidney’s self-regulatory function. The former include hemorrhage, decreased blood volume due to loss of fluid through the gastrointestinal tract, skin, and third lumen in the kidney, decreased cardiac output due to heart failure, pericardial tamponade, etc. and systemic vasodilatation due to medications, sepsis, and hepatic failure. The latter are primarily drugs that cause constriction of the small glomerular entry arteries or dilation of the small exit arteries, including nonsteroidal steroidal anti-inflammatory drugs, cyclosporine A, amphotericin B, epinephrine, norepinephrine, and type I receptor antagonists of ACEI and angiotensin II. When diagnosing prerenal ARF, it is important to take a medical and medication history regarding its etiology. Physical examination of the patient may reveal hypotension, increased heart rate, tachypnea, dry skin, loss of elasticity (first seen in the forearms and upper chest, and in the elderly, the forehead and sternal stalk may be examined), a dry tongue, and sunken orbits, and in some patients, manifestations of heart failure may be present. For prerenal factors, urinalysis may provide diagnostic clues. The specific gravity of the patient’s urine is more than 1.020, urine osmolality is often greater than 500mOsm/(kg,H2O), and urine sediment microscopy is often without obvious abnormality. If urinary sodium 20mmol/L, urinary creatinine/blood creatinine 40, filtered sodium excretion fraction 1%, renal failure index is less than 1 also suggests prerenal ARF.For patients with prerenal azotemia caused by blood volume insufficiency, vigilant rehydration until the blood volume is corrected, prerenal renal failure can often be restored. If urine output does not increase and renal function does not improve. Then the diagnosis of acute tubular necrosis should be considered. Renal diseases causing ARF can be categorized into renal vascular disease, glomerular disease and tubulointerstitial disease. Clinically, renal vascular disease (including renal large and small vessel disease), glomerular and renal interstitial disease should be excluded in the order of renal vascular disease, and the diagnosis of acute tubular necrosis should be considered in the end if the above causes can be excluded. Renal macrovascular disease includes bilateral renal vein thrombosis, bilateral renal artery thrombosis or embolism and unilateral renal incompetence with contralateral renal macrovascular lesions. Care should be taken to look for underlying conditions that produce arterial embolism, such as bacterial endocarditis, atrial fibrillation and any recent cardiac interventional procedures. Patients often have a sudden onset of disease, severe hematuria (most often with hematochezia), moderate to severe proteinuria, severe low back pain or epigastric pain, and renal tenderness. Those with renal infarction may have fever and elevated white blood cells. Radionuclide renal imaging, renal arteriovenous Doppler ultrasound is helpful for diagnosis, and renal angiography is feasible when necessary. Glomerular diseases and renal small vessel lesions that can cause ARF include acute glomerulonephritis, acute glomerulonephritis, IgA nephropathy, other primary glomerular diseases accompanied by severe nephrotic syndrome, and secondary glomerular diseases such as lupus nephritis, etc.; renal small vessel diseases include systemic vasculitis, hemolytic uremic syndrome, thrombotic platelet thrombocytopenic purpura, and malignant hypertension. The first is systemic vasculitis, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, and malignant hypertension. This kind of disease edema, hypertension, large amount of proteinuria, oliguria is more prominent, urine sediment microscopy can be seen more glomerular red blood cells, sometimes visible red blood cell tubular pattern. The discovery of capillaropathic hemolytic anemia, thrombocytopenia and immunological examination abnormalities help in the differential diagnosis. Second, acute glomerulonephritis Acute glomerulonephritis often refers to acute post-streptococcal infection glomerulonephritis, children and adolescents are common, antecedent infection 1~4 weeks after the emergence of acute nephritis syndrome such as obvious hematuria, edema, hypertension, accompanied by proteinuria, the deterioration of renal function than the degree of acute glomerulonephritis is mild. Serum complement is often decreased and anti-chain O is often positive. And acute progressive glomerulonephritis often starts sharply, with obvious oliguria or anuria as the main, there are obvious aberrant red blood cells in the urine, glomerular proteinuria, there can be rapid development of anemia, hypoproteinemia, accompanied by hypertension, rapid deterioration of renal function. Third, acute tubulointerstitial diseases Acute tubulointerstitial diseases include acute interstitial nephritis and acute tubular necrosis. Acute interstitial nephritis can be caused by allergy, infection and idiopathic factors. The allergic acute interstitial nephritis caused by drug allergy should have a recent history of drug use, and there may be systemic allergic manifestations (fever, rash, arthralgia, etc.), and leukocytes and eosinophils can be seen in the urine sediment, and blood eosinophils and blood IgE are increased. Acute tubular necrosis often has renal ischemia or nephrotoxicity (e.g. antibiotics, contrast agents, heavy metals) and other pathogenic factors, and often has a characteristic course, such as the emergence of oliguria, and enter the polyuria period after 1~3 weeks. Urinary indicators of acute tubular necrosis are helpful in determining prerenal ARF and acute tubular necrosis: urine specific gravity in acute tubular necrosis is mostly below 1.018, urine osmolality is less than 350mOsm/(kg,H2O), urine sodium is 40mmol/L, urinary creatinine/blood creatinine is 20, FENa is 1%, and renal failure index is greater than 1. Proteinuria in acute tubular necrosis is mild, and urine sediment microscopy without obvious abnormalities. Special types of ARF In the differential diagnosis of ARF, some special types of ARF should also be noted, such as acute renal cortical necrosis (mostly seen as a complication of pregnancy), epidemic hemorrhagic fever, hepatorenal syndrome, sepsis, etc. Important complications of ARF include disorders of electrolyte and acid-base balance (the first and foremost is hyperkalemia, metabolic acidosis), acute left heart failure, infections, gastrointestinal hemorrhage, neurological Abnormalities of the nervous system, etc. These complications should be diagnosed in time and appropriate treatment measures should be taken.