I. Etiology and pathogenesis
(A) Pre-renal azotemia
1. Causes of decreased intravascular volume Hemorrhage, gastrointestinal loss, dehydration, excessive diuresis, etc.
2. Conditions of systemic vascular resistance Sepsis, allergic reactions, anesthesia, use of drugs to reduce cardiac afterload Angiotensin-converting enzyme inhibitors, nonsteroidal anti-inflammatory drugs, epinephrine, norepinephrine, anesthetics, and cyclosporine can cause a decrease in glomerular filtration function.
3. Insufficient cardiac output leads to insufficient effective circulating volume Cardiogenic shock, congestive heart failure, pulmonary embolism, pericardial tamponade, etc. cause a decrease in renal blood perfusion.
(B) post-renal azotemia
This includes urethral obstruction, abnormal bladder function or obstruction, ureteral or renal pelvis obstruction. Prostatic hypertrophy, bladder, prostate or cervical cancer, retroperitoneal fibrosis or neurogenic bladder can all lead to urinary tract obstruction.
Less common causes include bilateral ureteral stones, urethral stones, and renal papillary necrosis. In patients with isolated kidney, unilateral urinary tract obstruction can cause postrenal azotemia.
(C) Renal parenchymal ARF
1, glomerular disease Acute progressive nephritis, post-severe infectious glomerulonephritis and nephrotic syndrome with ARF.
2, acute interstitial nephritis Pathological manifestations are interstitial inflammatory reaction with edema and renal tubular injury.
It is mainly caused by drugs, other causes include infectious diseases, immune diseases or idiopathic.
3, acute tubular necrosis The etiology is ischemia and toxicity.
4, renal vascular disease Less common
(D) ARF occurring on the basis of chronic renal insufficiency
Chronic glomerular disease combined with acute interstitial nephritis, diabetic nephropathy combined with contrast nephropathy, various glomerular diseases after the application of ACE resulting in prerenal ARF
II. Clinical manifestations
Performance is divided into oliguric and non-oliguric types.
Hypercatabolic ARF: Tissue catabolism metabolism is fast, blood urea nitrogen and blood creatinine increase at a rate of >14.3mmol/L (40mg/dl) and >170umol/L (2mg/dl) per day, respectively.
1.Pre-renal azotemia Oliguria, elevated blood urea nitrogen
2.Post-renal azotemia Sudden absence of urine or intermittent absence of urine
3.Renal parenchymal may vary depending on the site of involvement.
(1) RPCN has the syndrome of acute progressive nephritis.
(2) Oliguric ATN typical of oliguric phase, polyuric phase and recovery phase.
(3) Drug-induced AIN Mostly with a history of drug use, and a few with a history of allergy. Has manifestations of interstitial tubular impairment, such as anemia, hypokalemia, normal glucose with positive urine glucose and acidosis that do not parallel the decline in renal function.
(4) Renal vascular ARF with malignant hypertension, one or bilateral macrovascular lesions.
Third, diagnosis and differential diagnosis of acute and chronic renal failure
1, ARF is caused by a variety of reasons to make the excretory function of the two kidneys in a short period of time rapidly decreases, the average daily increase in blood creatinine ≥ 44.2umol / L.
2, further determined as oliguric, non-oliguric, or hypercatabolic?
3, pay attention to the following two points: the application of diuretics can increase urinary sodium excretion, so at this time can not rely on urinary sodium excretion and sodium excretion fraction as a basis for diagnosis; with proteinuria or diabetes and the application of mannitol, dextrose or contrast agents, can make the urinary specific gravity and urinary osmolality increase, so should not be used as a basis for diagnosis.
4. Chronic renal failure should also be excluded. The application of ultrasound to measure the size of the kidney and nail creatinine measurement can help identify acute and chronic renal failure. ultrasound kidney is not small, the thickness of the kidney parenchyma is not thin to support acute renal failure. Nail creatinine represents the level of blood creatinine in the patient’s serum 3 months ago, so if the nail creatinine is normal also supports the diagnosis of acute renal failure.
5. The gold standard is the pathological diagnosis of kidney biopsy. Emergency kidney biopsy should be performed as soon as possible to clarify the diagnosis.
IV. Treatment and prognosis
1. The treatment of pre-renal azotemia should be based on finding the cause of the disease.
If ARF is suspected to be caused by post-renal obstruction, a urinary catheter should be placed in the bladder. The residual urine volume of the bladder may be increased or a large amount of urine retained due to obstruction may be exported.
3. Renal parenchymal ARF
RPCN should be treated with immunosuppressive therapy; glomerulonephritis after severe acute streptococcal infection should be supported and symptomatic, and dialysis can be applied if necessary; nephrotic syndrome combined with ARF should be treated with active application of hormones for nephrotic syndrome, supplemented with dialysis therapy if necessary.
The key to the treatment of ATN is to discontinue the allergy-causing drugs, and corticosteroid treatment is required if necessary.
The treatment of mild ATN is based on conservative treatment such as support and symptomatic treatment.
Malignant hypertension should be treated by gradual and aggressive lowering of blood pressure. Early renal macrovascular disease such as renal artery or renal vein thrombosis or embolism can be treated with thrombolytic and anticoagulant therapy accordingly.