What are the symptoms of acute renal failure?

Acute renal failure is a kidney disease, it will have nausea, anorexia, fatigue, anemia and other symptoms appear, the disease is not a lot of people know, because many patients are not aware of this disease and what kind of symptoms produced, so The early detection of missed opportunity. Then I'll tell you this, what kind of symptoms of kidney disease, so that we do self-examination, early detection and early treatment to achieve a goal.
Symptoms of acute renal failure are:
Acute renal failure, renal tubular necrosis on pathology and repair in two stages, ATN is the biggest characteristic of renal function can be restored to normal, the process including the restoration of damaged cells, necrotic cell lumen tube removal, cell regeneration, and finally to the integrity of the renal tubular epithelial cells fully restored, acute renal failure, according to the common law of the clinical manifestations and course of the disease, generally divided into oliguria, polyuria and recovery of three phases:
1 Clinical manifestations of little or no urine oliguria mainly nausea, vomiting, headache, dizziness, irritability, fatigue, drowsiness and coma, as oliguria body of water, sodium accumulation, patients may present with hypertension, pulmonary edema and heart failure, when the product of protein metabolism can not be excreted by the kidneys, resulting in nitrogenous substances accumulate in the body appears azotemia, as accompanied by infection, injury, fever, then accelerate protein catabolism, blood urea nitrogen, creatinine increased rapidly, that the formation of uremia, the current main features are:
(1) decreased urine output:
        Or decreased urine output plummeted, continuing daily urine output of less than 400ml are known as oliguria, who called no less than 50ml of urine, ATN patients rarely completely free urine, no urine continued poor prognosis and should, except renal obstruction and bilateral renal cortical necrosis due to causes and varying severity, duration oliguria inconsistent, generally 1 to 3 weeks, but a few cases oliguria Sustainable three months or more, who is generally believed that the duration of renal toxicity short, while those of longer duration ischemic If oliguria lasting more than 12 weeks should reconsider the diagnosis of ATN, there may exist renal cortical necrosis or renal papillary necrosis, oliguria prolongation should be noted fluid retention, congestive heart failure, hyperkalemia, hypertension and various complications.
Non-oliguric ATN, refers to patients during the period azotemia continued in 500ml of urine a day or more, or even 1000 ~ 2000ml, the incidence of non-oliguric there is an increasing trend in recent years, up to 30% to 60%, The reason for the people to raise awareness of this type of renal toxicity and antibiotic widely used diuretics such as furosemide, mannitol and other early applications, etc., and does not reduce the amount of urine There are three reasons to explain:
① impaired renal units each with varying degrees of renal blood flow and glomerular filtration rate in the presence of a small part of the nephron, while the corresponding tubular reabsorption of significant barriers to function.
The degree of impairment of renal units ② all had the same, but much lower than tubular reabsorption dysfunction glomerular filtration rate in proportion to the extent of reducing weight.
③ renal medulla ability to form deep hyperosmolar state is reduced, resulting in medullary loop filtrate water reabsorption reduce non-oliguric common cause of long-term use of nephrotoxic drugs, major abdominal surgery, and after open-heart surgery, general believes that non-oliguric although fewer urinary-type light condition, shorter hospital stay, need to lower the percentage of dialysis treatment, fewer upper gastrointestinal bleeding and other complications, but the incidence of oliguric hyperkalemia caused by similar non-small Urine-based mortality is still as high as 26%, the treatment can not be ignored in any aspect.
(2) progressive azotemia:
        Because of reduced glomerular filtration rate caused little or no urine, resulting in the discharge of nitrogen and other metabolic wastes qualitative reduction in plasma creatinine and urea nitrogen increased, which increases the speed and state of body protein breakdown, in the absence of complications and treatment right cases, increased blood urea nitrogen slower day, about 3.6mmol / L (10mg/dl), increased plasma creatinine concentration of only 44.2 ~ 88.4μmol / L (0.5 ~ 1.0mg/dl), but in the high resolution state, such as with extensive tissue trauma, sepsis, etc., every day can be increased urea nitrogen 7.1mmol / L (20mg/dl) or more, plasma creatinine increase 176.8μmol / L (2mg/dl) or more a day to promote proteolytic hyperthyroidism factors still insufficient supply of heat, muscle necrosis, hematoma, gastrointestinal bleeding, infection, fever, glucocorticoid and so on.
(3) water, electrolyte imbalance and acid-base balance disorders:
① too much water: seen moisture control is not strict, excessive intake or fluid volume, the amount of water such as vomiting, sweating, wound infiltration capacity, etc. as well as the estimated amount of liquid supplement inaccurate ignored when calculating raw, with oliguria prolonged prone to excessive water, expressed as the dilution hyponatremia, soft tissue edema, weight gain, high blood pressure, heart failure and acute cerebral edema.
② hyperkalemia: 90% of the normal intake of potassium excretion from the kidneys, ATN oliguria due to the decrease in urinary excretion of potassium, if the state of the body while the presence of high resolution, such as crush injuries when muscle necrosis, hematoma and other infections, inadequate caloric intake due to proteolysis in vivo, releasing potassium ions, intracellular acidosis transferred to the extracellular potassium, and sometimes severe hyperkalemia can occur within a few hours, if the patient could not be diagnosed in time, intake of Potassium more food or drink, intravenous infusion of large doses of penicillin potassium (potassium per 1 million U penicillin potassium 1.6mmol); enter a large inventory of blood when bleeding (stock 10 days up to 22mmol potassium per liter of blood ); may cause or aggravate hyperkalemia, generally without medical complications cause ATN daily rise in serum potassium less than 0.5mmol / L, hyperkalemia can no characteristic clinical manifestations, or nausea, vomiting, numbness of limbs and other sensory abnormalities, heart rate, severe neurological symptoms, such as fear, irritability, apathy consciousness until late sinus room or atrioventricular block, sinus still, intraventricular conduction delay or ventricular fibrillation, blood potassium ECG changes disorder may precede the clinical manifestations of potassium, so the ECG effects of hyperkalemia on cardiac care is important, generally potassium concentration in 6mmol / L, the electrocardiogram showed tall and narrow base of the T wave, with blood potassium increased P wave disappeared, QRS widening, ST segment can not be identified, the final integration and T wave, followed by severe arrhythmia, until ventricular fibrillation, cardiac toxic effects of potassium sodium is still affected by the body, calcium and acid-base balance impact, while at the same existence sodium, hypocalcemia or acidosis, hyperkalemia more significant ECG and easy to induce arrhythmia, is worth mentioning that between serum potassium concentration and ECG sometimes the existence of inconsistencies, hyperkalemia is one common cause of death in patients with oliguria, early dialysis can prevent its occurrence, but severe muscle tissue necrosis often persistent hyperkalemia should completely remove necrotic tissue in order to control the high treatment potassium blood.
③ metabolic acidosis: normal daily fixed acid metabolite is 50 ~ 100mmol, 20% and bicarbonate ions, 80% excreted by the kidneys, acute renal failure when, due to the discharge of acidic metabolites decreased renal tubular secretion of acid ability and decreased ability to save, such as sodium bicarbonate, resulting in daily plasma bicarbonate concentration decreased to varying degrees; decreased at high resolution state more quickly, mostly from endogenous proteolytic fixed acid, a small part from the sugar and fat oxide, phosphate and other organic anions are released and accumulate in body fluids, resulting in increased anion gap of the patients, oliguria ongoing metabolic acidosis cases if not fully correct, rapid muscle breakdown in vivo, in addition, still acidosis reduce the ventricular fibrillation threshold, ectopic rhythm, hyperkalemia, severe acidosis and hypocalcemia, hyponatremia is a serious condition acute renal failure in patients already receiving dialysis Although less common, but in some cases drugs during dialysis still correct metabolic acidosis.
④ hypocalcemia, hyperphosphatemia: ATN when hypocalcemia and hyperphosphatemia is better when chronic renal failure outstanding performance, but there are reports oliguria 2 days hypocalcemia can occur, due to the often accompanied by acid poisoning, so that an increase in extracellular free calcium ions, the common clinical manifestations of hypocalcemia does not occur, hypocalcemia and more as hyperphosphatemia caused by normal intake of 60% to 80% of phosphate excreted in urine, ATN oliguria often mildly elevated serum phosphorus, but if there are significant metabolic acidosis, hyperphosphatemia compared prominent, but rarely significantly increased after correction of acidosis, phosphorus may have declined to a certain extent, this If the continued acceptance of total parenteral nutrition therapy patients should pay attention to hypophosphatemia occurred.
⑤ hyponatremia and hypochloremia: both multi-exist, the reason may be due to hyponatremia caused by too much water dilution hyponatremia due to burns or vomiting, diarrhea or gastrointestinal lost from the skin caused by, or on non-oliguric patients large doses of furosemide reactions still occur loss of sodium hyponatremia, severe hyponatremia can cause blood osmotic concentration decreased, resulting in moisture penetration into cells, cell edema occurs, manifestations of acute cerebral edema symptoms, clinical manifestations of fatigue, weakness, lethargy or unconsciousness, disorientation disappeared, even hypotonic coma, low chlorine levels common in vomiting, diarrhea or non-oliguric with plenty of loop diuretics, bloating or shallow breathing, convulsions and other metabolic alkalosis performance.
⑥ Hypermagnesemia: 60% of the normal intake of magnesium excreted in the feces and 40% excreted in the urine, as magnesium and potassium are the major intracellular cation, potassium and therefore often parallel rise in serum magnesium concentration when ATN when muscle damage Hypermagnesemia more prominent, and magnesium ions inhibit the central nervous system, severe hypermagnesemia can cause respiratory depression and cardiac depression, should be vigilant, Hypermagnesemia ECG changes also showed PR prolongation and widened QRS complex, when corrected hyperkalemia, ECG PR interval prolongation still occurs and (or) QRS widening should be suspected, hypermagnesemia hyponatremia, hyperkalemia and acidosis were increased myocardial toxicity of magnesium ions.
(4) the performance of the cardiovascular system:
① Hypertension: In addition to renal ischemia neurohormonal factors induce the secretion of active substances increased vasoconstrictor factors, too much water can cause excessive load capacity increased blood pressure, hypertension early ATN rare occurrence, but if sustained less urine, about 1/3 of patients with mild to moderate hypertension, usually in 18.62 ~ 23.94/11.97 ~ 14.63kPa (140 ~ 180/90 ~ 110mmHg), and sometimes higher, even hypertensive encephalopathy, accompanied by pregnancy in particular, should be closely observed.
② acute pulmonary edema and heart failure: oliguria is a common cause of death, which is mainly caused by fluid retention, but high blood pressure, severe infections, arrhythmias and acidosis are factors, the higher the incidence of early and take corrective missing oxygen, water and the control measures early dialysis incidence has decreased significantly, but still is a common cause of death in severe type of ATN.
③ arrhythmias: In addition to hyperkalemia caused by sinus pause, sinus still, sinus room block, varying degrees of atrioventricular block and bundle branch block, ventricular tachycardia, ventricular fibrillation, can still due to virus infection and digitalis applications caused ventricular contraction and paroxysmal atrial fibrillation occurred ectopic rhythm.
④ pericarditis: an annual rate of 18%, taking early dialysis reduced to 1%, more performance for pericardial friction sound and chest pain, unusual large pericardial effusion.
⑤ digestive performance: most early manifestation of ATN, common symptoms are significantly reduced appetite, nausea, vomiting, abdominal distension, hiccups or diarrhea, upper gastrointestinal bleeding is a common late complication, gastrointestinal symptoms and diseases are still the primary water , electrolyte imbalance, or other relevant acidosis, persistent, severe gastrointestinal symptoms often prone to electrolyte imbalance significantly increase the complexity of the treatment of early gastrointestinal symptoms suggestive of significant early implementation of dialysis treatment.
⑥ nervous system Lightweight patients without neurological symptoms: Some patients with early signs of fatigue, poor spirit, if early consciousness apathy, irritability, lethargy or even coma, severe illness prompted Benedict, should not delay dialysis, nervous system and severe infection, epidemic hemorrhagic fever, some heavy heavy metal poisoning, severe trauma, multiple organ failure and other causes related.
⑦ blood system performance: ATN early rare anemia, due to the extent of the primary disease, duration of disease, and so closely related to the presence or absence of bleeding complications, severe trauma, major surgery, blood loss, hemolytic anemia factor, ATN and other serious infections and emergency situations, Anemia can be more severe if there is clinical bleeding tendency, thrombocytopenia, low consumption of coagulation and fibrinolysis signs of disease, has not a early DIC.
2 Multi urine of urine of daily 2.5L said polyuria, ATN diuretic early common urine gradually increased after as little or no urine in the urine within 24h increased and appeared more than 400ml, can be considered a period of polyuria start, polyuria period lasts about two weeks time, urine output may increase exponentially every day, diuresis of 3 to 5 days up to 1000ml, then daily urine output of up to 3 ~ 5L; progressive increase in urine output began to recover renal function a sign, but the symptoms of polyuria beginning of uremia is not improved, even more serious, and the GFR is still 10ml/min or less; When urea nitrogen began to decline, the condition gradually improved, polyuria Early still hyperkalemia, sustained more urine can occur hypokalemia, hyponatremia, dehydration and, in addition, this period is still prone to infection, cardiovascular complications and upper gastrointestinal bleeding, it should be closely observed water, electrolyte and acid-base balance.
Polyuria clinical manifestations are mainly physical weakness, malaise, palpitations, shortness of breath, weight loss, anemia, during this period due to renal function is not fully restored, the patient is still in azotemia state, the lower the resistance is prone to infection, upper gastrointestinal bleeding and cardiovascular complications, so there is still some risk.
(3) recovery according to etiology, disease severity, polyuria duration, complications and age and other factors, ATN patients in early recovery varied greatly, may have no symptoms, feel good about themselves, or physical weakness, fatigue, weight loss; When the blood urea nitrogen and creatinine decreased urine output gradually returned to normal, except for a few, the glomerular filtration rate returned to normal more than 3 to 6 months, but in some cases of renal tubular dysfunction concentrated than 1 year of sustainable If renal function does not recover lasting, permanent legacy may suggest kidney damage.
Read my introduction, surely we should be aware of the symptoms of this disease, and if it appears the above-mentioned symptoms, you should be vigilant, because this could be a precursor to the disease appeared, then you should do is go to the hospital for examination and treatment, if diagnosed, should adopt a positive attitude to face. Finally, I wish a speedy recovery to early majority of patients through treatment.