What Are the Different Acute Renal Failure Symptoms?
Acute renal failure (ARF) refers to a clinical syndrome in which the glomerular filtration rate drops suddenly or continuously, causing nitrogenous wastes to be stored in the body, and water, electrolytes, and acid-base balance disorders. Decline in renal function can occur in patients with no previous kidney disease or in patients with stable chronic kidney disease. Sudden deterioration of renal function can occur suddenly. In 2005, the acute kidney injury (acutekidneyinjury, AKI) network (AKIN) named acute renal failure as acute kidney injury (AKI): renal function (glomerular filtration function) suddenly (within 48 hours) decreased, manifested as absolute serum creatinine The value increased by 0.3mg / dl (26.5mol / l), or increased by 50% (up to 1.5 times the baseline value), or the urine output was <0.5ml / (kg.h) for more than 6 hours (exclude obstructive nephropathy Or dehydrated). The proposal and staging of the AKI concept have positive significance for the early diagnosis and early intervention of critically ill ARF and improving the prognosis of patients.
Basic Information
- nickname
- Acute renal failure
- English name
- acuterenalfailure
- Visiting department
- Nephrology
- Contagious
- no
Causes of Acute Renal Failure
- The causes of acute renal failure are diverse and can be divided into three categories, prerenal, renal and postrenal. Common causes of prerenal ARF include decreased blood volume (such as fluid loss and bleeding for various reasons), decreased effective arterial blood volume, low cardiac output, and changes in renal hemodynamics (including renal vasoconstriction, imbalanced dilation) ) And mechanical obstruction of the renal artery. The cause of postrenal acute renal failure is mainly acute urinary tract obstruction. Acute renal failure refers to renal parenchymal damage. Renal ischemia or nephrotoxic substances damage renal tubular epithelial cells (such as acute tubular necrosis, ATN), and also include glomerular disease, renal vascular disease, and interstitial disease. The accompanying renal function decreased sharply. With the different patient groups and the surrounding environment, the etiology of ATN is various. ATN often has infections, various factors that cause effective circulation capacity or blood pressure to decline, various causes of nephrotoxic drugs, and susceptibility to ATN. The population includes patients with underlying kidney disease, hypertension, diabetes, cardiovascular disease, and older patients. The following highlights acute tubular necrosis.
Clinical manifestations of acute renal failure
- Acute tubular necrosis (ATN) is the most common type of renal ARF. Taking ATN as an example, it briefly describes the clinical manifestations of ARF. At present, it can be divided into the initial phase, the continuous phase and the recovery phase based on the clinical process.
- Initial period
- Patients in this stage have not had obvious renal parenchymal injury, and may be in the high-risk stage or injury stage of acute renal failure. The length of the initial period varies depending on the cause and degree. Usually it is several hours to several days. At this time, kidney disease is often reversible. However, with significant damage to the renal tubular epithelium, GFR suddenly decreases, and excess capacity may appear. Symptoms and signs of electrolyte and acid-base balance disorders enter the duration.
- 2. Duration
- This period is already in the stage of injury or failure, usually 1-2 weeks, but also longer. The glomerular filtration rate remained low. Many patients may have oliguria (<400ml / d), and some even have no urine (<100ml / d). However, some patients may not have oliguria, and the urine volume is above 400ml / d, which is called non-oliguria-type acute kidney injury. With the decline of renal function, a series of clinical manifestations of uremia can occur clinically. Digestive system: loss of appetite, nausea, vomiting, bloating, diarrhea, etc., severe cases can occur gastrointestinal bleeding. Respiratory system: In addition to the complications of infection, due to excessive volume load, symptoms such as dyspnea, cough, belching, and chest pain may occur. Cardiovascular system: including hypertension, arrhythmia, hypotension, myocardial disease, and congestive heart failure. Acute left heart failure is a common cause of death in patients with persistent ATN. Nervous system: symptoms of uremia encephalopathy such as disturbance of consciousness, agitation, delirium, convulsions, and coma may occur. blood system: can be manifested as mild to moderate anemia, and may have bleeding tendency. Disorders of water, electrolyte and acid-base balance: can be expressed as: metabolic acidosis: mainly due to reduced excretion of non-volatile acid metabolites, decreased renal tubular secretion of ammonia production and the ability to save sodium bicarbonate. Hyperkalemia: In addition to decreased renal excretion potassium, acidosis and excessive tissue breakdown are also major causes; in addition, iatrogenic factors such as input of old blood can aggravate hyperkalemia. Hyperkalemia can occur with nausea, vomiting, numbness in the limbs, and slowed heart rate. In severe cases, neurological manifestations can occur. For example, when the blood potassium concentration is above 6mmol / L, the electrocardiogram can display a sharp T wave. Further elevation may cause severe arrhythmias, until ventricular fibrillation. Disturbance of water and sodium balance: Patients with persistent ATN due to decreased GFR and prone to water and sodium storage in the body, such as excessive water, a large number of diuretics can cause hyponatremia. In addition, there can be hypocalcemia and hyperphosphatemia. Infection: Infection is a common complication of ARF. Common infections include the lungs, urinary tract, abdominal cavity, and surgical sites.
- 3. Recovery period
- Regeneration and repair of renal tubular cells and restoration of renal tubular integrity. GFR gradually returned to normal or close to normal. During this period, the urine output increased gradually. The urine output of patients with oliguria or anuria entered 500ml / d and entered the recovery period. Some patients have polyuria, the daily urine output exceeds 2500ml / d, usually lasts 1 to 3 weeks, and then returns to normal. In the polyuria period, hypokalemia is sometimes caused by excessive potassium excretion or the use of potassium excretion diuretics and reduced intake. For example, patients with serum potassium <3mmol / L may experience fatigue, nausea and vomiting, abdominal distension, weakened or disappeared bowel movements, and severe People may have respiratory muscle paralysis, disorientation, drowsiness, and coma. ECG shows that T wave is wide and low, QT interval is prolonged, U wave appears, and even ventricular fibrillation and cardiac arrest occur. The renal tubular reabsorption function is slower and delayed than the glomerular filtration function. Over 3 months, a small number of patients may have varying degrees of renal structural and functional impairment.
Acute renal failure examination
- Blood test
- Mild to moderate anemia. Serum creatinine and urea nitrogen increase gradually. If combined with hypercatabolism and rhabdomyolysis, the rate of rise is high, and hyperkalemia (greater than 5.5mmol / l) may occur. Blood pH is often lower than 7.35, and HCO 3 - levels are usually slightly reduced. Blood sodium concentration is normal or low, there may be decreased blood calcium, increased blood phosphorus.
- 2. Urine test
- Changes in urine output: oliguria or anuria often prompts ATN. Routine urine examination: cloudy appearance and dark urine. Urine protein is mostly ~~ +, which is mainly composed of small and medium molecular proteins. Urinary sediment can be seen in renal tubular epithelial cells, epithelial cell casts, and granular casts, and a few red and white cells can be seen. The urine specific gravity is usually below 1.015. Urine osmotic pressure is lower than 350mOsm / kg, and the ratio of urine to blood osmotic concentration is lower than 1.1. Due to the decrease of sodium reabsorption by the renal tubules, the increase of urinary sodium is mostly between 20 and 60 mmol / l; the ratio of urinary creatinine to blood creatinine decreases, often below 20; the ratio of urea urea nitrogen to blood urea nitrogen decreases, often below 3 Renal failure index is often greater than 1; sodium excretion fraction is often greater than 1.
- 3. Imaging examination
- B-mode ultrasound is most commonly used. Kidney volume often increases and the renal cortex thickens during acute renal failure, while kidney volume often decreases and the renal cortex becomes thinner during chronic renal failure. In addition, ultrasound examination can also help to identify the presence of retrorenal obstruction. Bilateral ureteral dilatation or bilateral hydronephrosis can be seen in upper urethral obstruction, and bladder urinary retention can be seen in lower urinary obstruction. Plain radiographs, veins or retrograde pyelography, CT or magnetic resonance imaging are often helpful in finding the exact cause of a suspected urinary tract obstruction.
- 4. Kidney biopsy
- It is an important diagnostic method, and renal biopsy is generally not required for ATN patients with typical clinical manifestations. For those with clinical manifestations that meet the ATN, but whose oliguria is more than 2 weeks or whose etiology is unknown, and whose renal function cannot be recovered within 3-6 weeks, clinical considerations exist for other severe renal parenchymal diseases that cause acute kidney injury. Renal biopsy should be performed as soon as possible In order to make the early diagnosis of the cause.
Acute renal failure diagnosis
- The diagnosis of ARF is based on: GFR can be diagnosed in a short period of time (hours to days) by more than 50% or blood creatinine rises by more than 50%. If the urine volume is <400ml / d, it is an oliguria type ARF; if there is no oliguria, it is a non-oliguria type ARF. According to the primary etiology, the progressive decline of GFR, combined with the corresponding clinical manifestations and laboratory tests, the diagnosis of ARF is generally not difficult to make.
- In terms of differential diagnosis, acute renal failure based on chronic renal insufficiency should be ruled out first, and prerenal and postrenal properties should be ruled out. Once the renal parenchyma is determined, the renal tubules, glomeruli, and renal blood vessels should be identified. Or acute renal failure caused by renal interstitial disease.
Differential diagnosis of acute renal failure
- 1. Differentiation from prerenal azotemia
- (1) Before the onset of the fluid replacement test , there is a history of insufficient capacity and fluid loss. If physical examination reveals dry skin and mucous membranes, hypotension, and jugular vein filling are not obvious, prerenal oliguria should be considered first. Infusion (5% glucose solution) can be tried. 200 ~ 250ml) and injection of diuretic diuretics (furosemide 40 ~ 100mg) to observe the load of the circulatory system after infusion. If blood pressure returns to normal after supplementing blood volume and urine output increases, it supports the diagnosis of prerenal oliguria. A long period of hypotension, especially when the elderly with poor heart function, those who have increased urine output after fluid replacement should suspect that prerenal azotemia has transitioned to ATN.
- (2) Examination of urine diagnostic indicators
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- * Renal failure index = urine sodium / (urine creatinine / blood creatinine)
- ** Sodium excretion fraction (%) = (urine sodium / blood creatinine) / (blood sodium / urine creatinine) * 100
- 2. Differentiation from retrorenal urinary tract obstruction
- Have a history of primary causes of urinary tract obstruction such as stones, tumors, and enlarged prostate; Sudden reduction in urine output or alternating with anuria; Patients have conscious renal colic, pain in the flank or lower abdomen; Pain in the kidney area Obstruction at the exit of the bladder, the bladder area swells due to urination, and the percussion is dull; there is no significant change in urine routine. Ultrasound imaging and X-ray examination can help confirm the diagnosis.
- 3. Identification of glomerular or renal microvascular disease
- Severe acute glomerulonephritis, aggressive nephritis, secondary nephropathy such as lupus nephritis, purpuric nephritis, and a large number of proteinuria periods of nephrotic syndrome can also cause idiopathic acute kidney injury. Others are caused by small vasculitis, hemolytic uremic syndrome, and malignant hypertension. Medical history, laboratory tests, and kidney biopsy can help identify.
- 4. Differentiation from acute interstitial nephritis
- According to the recent history of medication, clinical manifestations such as fever, rash, lymphadenopathy, joint pain, and eosinophilia in blood appear. Urine tests are abnormal and renal tubule and glomerular function are damaged for identification. A kidney biopsy can help confirm the diagnosis.
- 5. Differentiation from renal vascular obstruction
- Acute renal injury can be caused by bilateral renal or solitary renal renal arterial embolism or venous thrombosis, which is rare clinically and can be manifested as severe back pain, hematuria, and anuria. Angiography can confirm the diagnosis.
Acute Renal Failure Treatment
- 1. Actively control the primary cause and remove reversible factors that aggravate acute kidney injury
- Acute kidney injury must first correct the reversible cause. All kinds of severe trauma, heart failure, acute blood loss, etc. should be treated accordingly, including expansion, correction of insufficient blood volume, shock, and control of infection. Discontinue drugs that affect renal perfusion or nephrotoxicity. Pay attention to adjusting the dose of the drug, and if possible check the serum drug concentration.
- 2. Maintain the body's water, electrolyte and acid-base balance
- (1) Maintaining body fluid balance During oliguria, patients are prone to excessive water load, which can easily lead to pulmonary edema. In severe cases, cerebral edema can also occur. The patient's weight, blood pressure, and cardiopulmonary symptoms and signs should be closely observed, and the 24-hour fluid intake and output of patients should be strictly calculated. Follow the principle of "pay as you go" during rehydration. Daily fluid replacement volume = dominant fluid loss + non-dominant fluid loss-endogenous water. If acute heart failure occurs, the most effective treatment is dialysis.
- (2) Correction of hyperkalemia When the blood potassium exceeds 6.0mmol / L, the heart rate and electrocardiogram should be closely monitored and urgently treated: 10% calcium gluconate is given intravenously slowly; 11.2% sodium lactate is injected intravenously, and those with metabolic acidosis may Intravenous infusion of 5% sodium bicarbonate; 200ml of 25% glucose plus intravenous insulin; oral potassium-lowering resin drugs or furosemide and other potassium-releasing diuretics to promote urine excretion. If the above measures are not effective, dialysis treatment should be carried out as soon as possible.
- (3) To correct metabolic acidosis such as HCO 3 - below 15mmol / L, intravenous drip of 5% sodium bicarbonate can be used according to the situation. For patients with severe acidosis, dialysis treatment should be started immediately.
- (4) Other electrolyte disorders If weight gain, sodium should be restricted, if sodium is normal, water should not be restricted. If symptoms of water poisoning such as disorientation, pumping, coma occur, hypertonic saline drip or dialysis can be given. No treatment is required for asymptomatic hypocalcemia. After correcting acidosis, the free calcium concentration in the blood often causes convulsions in the hands and feet. 10% calcium gluconate can be given intravenously after dilution.
- 3. Control infection
- Once there are signs of infection, effective antibiotic treatment should be actively used. Drugs that are non-toxic or low-toxic to the kidney can be selected according to bacterial culture and drug sensitivity tests, and the dose can be adjusted according to eGFR.
- 4. Blood purification treatment
- Blood purification plays a key role in the treatment of acute renal failure. Commonly used modes include hemodialysis, hemofiltration and peritoneal dialysis. It has a good effect on correcting symptoms of azotemia, heart failure, severe acidosis and encephalopathy. In recent years, the application of continuous renal replacement therapy (CRRT) has greatly reduced its mortality rate.
- 5. Recovery period treatment
- At the beginning of polyuria, because the glomerular filtration rate has not yet fully recovered, attention should still be paid to maintaining water, electrolyte and acid-base balance, controlling azotemia, treating the primary disease and preventing various complications. After a lot of diuresis, dehydration and electrolyte loss should be prevented and supplemented in time. According to the recovery of renal function, the number of dialysis is gradually reduced until the dialysis is stopped.