Acute Kidney Injury (Aki)

Acute renal failure

From acute kidney injury is defined as the rapid loss of kidney function within days or weeks, which leads to accumulation of nitrogenous substances in the blood (azotemia). It is often the result of insufficient renal perfusion due to serious injury, illness or surgery, but is sometimes caused by a rapidly progressive internal kidney disease. Symptoms include anorexia, nausea and vomiting. Convulsions and coma can occur if no treatment is quick, disturbances develop in the water, electrolyte and acid-base balance. The diagnosis is based on laboratory tests of renal function, including serum creatinine. “Urinary indices” Harnsedimentprüfung and often imaging and other tests are needed to determine the cause. Treatment depends on the cause, but also needs to regulate the fluid and electrolyte balance and sometimes includes dialysis.

In all cases of acute kidney injury (AKI) creatinine and urea in the blood rise within a few days, and there is a fluid and electrolyte disturbance. The most dangerous faults are hyperkalemia and fluid overload (may cause pulmonary edema). A phosphate retention leads to hyperphosphatemia. Hypocalcaemia seems to occur because the impaired kidneys no longer produce calcitriol and because hyperphosphatemia causes Kalziumhosphatfällung in the tissues. Acidosis arises because hydrogen ions can not be excreted. In severe uremia coagulation can be disturbed and a pericarditis occur. Urinary excretion varies with the type and the cause of AKI.

From acute kidney injury is defined as the rapid loss of kidney function within days or weeks, which leads to accumulation of nitrogenous substances in the blood (azotemia). It is often the result of insufficient renal perfusion due to serious injury, illness or surgery, but is sometimes caused by a rapidly progressive internal kidney disease. Symptoms include anorexia, nausea and vomiting. Convulsions and coma can occur if no treatment is quick, disturbances develop in the water, electrolyte and acid-base balance. The diagnosis is based on laboratory tests of renal function, including serum creatinine. “Urinary indices” Harnsedimentprüfung and often imaging and other tests are needed to determine the cause. Treatment depends on the cause, but also needs to regulate the fluid and electrolyte balance and sometimes includes dialysis. In all cases of acute kidney injury (AKI) creatinine and urea in the blood rise within a few days, and there is a fluid and electrolyte disturbance. The most dangerous faults are hyperkalemia and fluid overload (may cause pulmonary edema). A phosphate retention leads to hyperphosphatemia. Hypocalcaemia seems to occur because the impaired kidneys no longer produce calcitriol and because hyperphosphatemia causes Kalziumhosphatfällung in the tissues. Acidosis arises because hydrogen ions can not be excreted. In severe uremia coagulation can be disturbed and a pericarditis occur. Urinary excretion varies with the type and the cause of AKI. Etiology causes of AKI (see table: major cause of acute kidney injury) can be classified prerenal Renal Renal Post A prärenaleAzotämie caused by inadequate renal blood flow as follows. The main causes are ECF volume depletion cardiovascular disease prerenal changes make 50-80% of AKI cases, but do not lead to permanent kidney damage (and thus are potentially reversible), unless the hypoperfusion is hard enough to make a tubular ischemia cause. The perfusion of an otherwise well-functioning kidney causes increased reabsorption of sodium and water, which in turn leads to oliguria with high-ranking osmolality and low urine sodium. Renal causes of AKI include diseases or damage to the kidneys with one. Renal causes are responsible for about 10-40% of cases. The disturbances, the glomeruli, the tubules and the interstitial concern. In general, the most common causes of renal ischemia Longer nephrotoxins (including the iv administration of iodinated contrast agents radioresistant). Glomerular diseases reduce the glomerular filtration rate (GFR) and increase the permeability of the glomerular capillaries of protein. They may be flammable due (glomerulonephritis) or the result of vascular damage due to ischemia or vasculitis. The tubules may also be damaged by ischemia or be obstructed by cellular debris, protein or crystal deposits or by a cellular or interstitial edema. A tubular damage interferes with the reabsorption of sodium. As a result, the sodium is increased, which is diagnostically significant. Interstitial inflammation (nephritis) is usually based on an immunological or allergic process. These mechanisms of tubular damage are complex and interdependent, so that the previously popular term acute tubular necrosis must be regarded as inaccurate description. The post-renal azotemia (obstructive nephropathy) is responsible through various forms of obstruction Harnentleerungs- and collecting area of ??the urinary system caused and for 5-10% of cases. An obstruction can also be caused within the tubules by crystals precipitate, or protein-containing material and is often associated with a post-renal kidney failure seen as an obstructive mechanism is present. Hampering the ultrafiltrate in the tubules or more distally increases the pressure in the urine portion of the glomerulus and reduces GFR. The obstruction also affects the renal blood flow by initially increasing the flow and pressure in the glomerular capillaries by reducing the afferent arteriolar-resistance. Within 3-4 hours of the renal blood flow is reduced, however, and has fallen by 24 hours because of the increased resistance in the renal vasculature to <50% of normal. It can take up to 1 week until the renovascular resistance after unloading for 24 hours obstruction returns to normal values. To lead to severe azotemia, obstruction must apply to both ureters, unless the patient has only a single functioning kidney. The most common cause of sudden and often complete drying up of urine in men is probably a bladder outlet obstruction. Major cause of acute kidney injury due examples prerenal ECF volume depletion Excessive diuresis, bleeding, gastrointestinal losses, loss of intravascular fluid into the extravascular space (due to ascites, peritonitis, pancreatitis or burns), loss of skin and mucous membranes, "renal SALT and water -wasting states "Low cardiac output, myocardial infarction, pericardial tamponade, pulmonary embolism, pulmonary hypertension, positive pressure ventilation Low systemic vascular resistance septic shock, liver failure, antihypertensive drugs Increased renal vascular resistance NSAIDs, cyclosporine, tacrolimus, hypercalcemia, anaphylaxis, some anesthetics, renal artery obstruction, renal vein thrombosis, sepsis, hepatorenal syndrome Decreased efferent arteriolar tone (leading to decreased GFR of reduced glomerular transcapillary pressure , especially in patients with bilateral renal) ACE inhibitors or angiotensin II receptor blockers Kidney Acute tubular injury ischemia (prolonged or heavy prerenal stage): surgery, hemorrhage, arterial or venous obstruction, NSAIDs, cyclosporine, tacrolimus, amphotericin B toxins: aminoglycosides, amphotericin B, foscarnet, ethylene glycol, hemoglobin (such as hemoglobinuria), myoglobin ( as in myoglobinuria), ifosfamide, heavy metals, methotrexate, radiation-resistant contrast agent, streptozotocin Acute glomerulonephritis ANCA-associated: crescent glomerulonephritis, m ikroskopische polyangiitis, granulomatosis with polyangiitis (anti-GBM glomerulonephritis: Goodpasture's syndrome immune complex: lupus glomerulonephritis, postinfectious glomerulonephritis, "cryoglobulinemic glomerulonephritis " Acute tubulointerstitial nephritis drug reaction (eg. B. Beta-lactams, NSAIDs, sulphonamides, ciprofloxacin, thiazide diuretics, furosemide, cimetidine, phenytoin, allopurinol), pyelonephritis, papillary acute vascular nephropathy vasculitis, malignant hypertension, thrombotic microangiopathy, systemic sclerosis, Atheroembolie Infiltrative diseases lymphoma, sarcoidosis, leukemia post renal tubular precipitation of uric acid (tumor lysis), sulfonamides, triamterene acyclovir, indinavir, methotrexate, calcium oxalate (ethylene glycol recording) myeloma protein, myoglobin Ureteral obstruction Intrinsic: stone formation, blood clots, abgestoßenes kidney tissue, fungus ball, edema, cancer, congenital defects Extrinsically: cancer, retroperitoneal fibrosis, Uretertrauma during surgery or "high impact injury" bladder obstruction Mechanical: Benign prostatic hyperplasia, prostate cancer, bladder cancer, urethral stricture, phimosis, paraphimosis, urethral valves , non-through underlying bladder catheter Neurogen: anticholinergics, lesion of the upper or lower motor neurons ANCA = antineutrophil cytoplasmic antibody; GBM = glomerular basement membrane. Symptoms and complaints beginning to weight gain and peripheral edema be the only findings. Often the predominant symptoms are those of the underlying disease or those caused by surgical complications and cause a deterioration of renal function. The symptoms of uremia may develop later as a nitrogen accumulated products. Such symptoms include nausea, vomiting, anorexia weakness myoclonus seizures confusion coma asterixis and hyperreflexia may be present during the inspection. Chest pain (usually worse on inspiration or lying), pericardial friction sounds and findings of cardiac tamponade may be detectable in uremic pericarditis. Fluid accumulation in the lungs causing dyspnea, and crackles on auscultation. Other findings depend on the cause. The urine may be colored cola in glomerulonephritis or myoglobinuria. When the bladder outlet obstruction is probably palpable. The kostovertebrale angle can be sensitive if the kidney is enlarged acute. Changes in urine prerenal causes manifest themselves typically in the form of oliguria, but not as anuria. Anuria usually develops only when obstructive uropathy or, less frequently in bilateral renal artery occlusion, acute Nierenrindennekrose or rapidly progressive glomerulonephritis. A relatively good urinary excretion of 1 to 2.4 l / day is initially still present in most nephrogenic causes. In acute tubular injury elimination may proceed in three phases: the prodrome phase, usually with normal urine output varies in duration depending on the causative factors,. As the recorded amount of toxin, the duration and severity of hypotension. The oliguric phase precipitates between 50 and 400 ml / day takes 10-14 days on average, but varies from one day to 8 weeks. Many patients will never oliguric. Nichtoligurische patients have a low mortality and morbidity and require less frequent dialysis. In the postoligurischen phase, urine output gradually rises again to normal, but the serum creatinine and -harnstoffspiegel remain for several days increased. A tubular dysfunction may persist for a few days or weeks and with a sodium loss, polyuria (possibly very severe), which does not respond to vasopressin or manifest hyperchloraemic metabolic acidosis. Clinical Calculator: index for renal diagnostic serum creatinine Harnsediment Harndiagnostische indices residual urine volume, when a post-renal cause is suspected An LCI is assumed if the urine output decreases or serum urea or creatinine rise. The investigation should elicit the existence and nature of AKI and investigate the cause. Among the blood tests generally include complete blood count, urea, creatinine and electrolytes (including calcium and phosphate). Among the urine tests include the determination of sodium and creatinine and microscopic examination of the sediment. increase early diagnosis and treatment, the chance of regression of kidney failure and prevent this in some cases before. A daily progressive increase in serum creatinine is indicative of an LCI. The serum creatinine may - depending on the extent of Kreatininproduktion (which depends on the muscle mass) and the total body water - up to 2 mg / dl / day rise (180 .mu.mol / l / day). An increase of> 2 mg / dl / day suggests an overproduction due to rhabdomyolysis. The urea increases to 10-20 mg / dl / day (3.6 to 7.1 mmol / L / day), but this value may be misleading because it is often in response to a by surgery, trauma, corticosteroids, combustion, transfusion reaction, parenteral nutrition, gastrointestinal or internal bleeding-related increase in protein metabolism is increased. With rising creatinine levels of 24-h urine collection for the determination of creatinine clearance and the various formulas for the calculation of creatinine clearance from serum creatinine are too inaccurate and should not be used to estimate GFR, as the increase in serum creatinine delayed action GFR loss is. Other laboratory findings are progressive acidosis, hyperkalemia, hyponatremia and anemia. With plasma bicarbonate of 15-20 mmol / l acidosis is usually moderate. The potassium concentration in the serum rises slowly but can at greatly accelerated catabolism up to 1-2 mmol / l / day rise. The hyponatremia is usually only moderately pronounced (serum sodium 125-135 mmol / l) and correlated with an excess of water. Normochromic-normocytic anemia with a hematocrit of 25-30% is typical. Hyperphosphatemia undHypokalzämie are widely used in AKI and can be pronounced in patients with rhabdomyolysis or tumor lysis syndrome. E ine profound hypocalcemia in rhabdomyolysis apparently results from the combined effects of calcium deposition in necrotic muscle, reduced Calcitriolproduktion and a resistance of the bone compared to parathyroid hormone (PTH) and hyperphosphatemia caused. During the recovery phase of AKI following a Rhabdomyolose-induced acute tubular necrosis, hypercalcemia may develop if renal Calcitriolbildung increases, the bone again responding to the PTH and the calcium deposit from the damaged tissue is released again. Hypercalcemia during recovery from AKI is otherwise rare. Determining the cause Immediately reversible prerenal or post-renal causes must be ruled out first. ECF volume depletion and obstruction be considered in all patients. The drug history must be exactly collected and all potentially nephrotoxic drugs should be discontinued. Partly urological diagnostic indices (see table: Urological diagnostic indices in pre-renal azotemia and acute tubular damage) useful for the classification prerenal azotemia from acute tubular damage, which are the most common causes of AKI in the hospital. Prerenal causes are often clinically obvious. In this case, the correction of the underlying hemodynamic disorder should be tried. For example, in hypovolemia, a volume infusion can be tried in heart failure diuretics and drugs that reduce afterload and liver failure octreotide. The decay of AKI then confirms the prerenal cause. Urological diagnostic indices Tubular at prerenal azotemia and acute tubular injury index prerenal damage U / P-osmolality> 1.5 1-1.5 urinary sodium (mmol / l) <10> 40 portion of the excretion of Na (FENa) * <1% > 1% Kidney Failure Index † <1> 2 ??BUN / creatinine ratio> 20 <10 * U / P Na ÷ U / P creatinine. † urine sodium ÷ U / P-creatinine ratio. AGN = acute glomerulonephritis; Na = sodium; U / P = urine-to-plasma ratio. Adapted from Miller TR, Anderson RJ, Lina SL, et al: Urological diagnostic indices for acute renal failure. Annals of Internal Medicine89 (1): 47-50, 1978; used by permission of the American College of Physicians and the author. Clinical Calculator: proportion of excreted sodium Post renal causes should be sought in most cases of AKI. Immediately after the patient has left the water, should be at the bedside ultrasonography be performed (or, alternatively, a urethral catheter is placed) to determine the residual urine in the bladder. A residual urine> 200 ml speaks for bladder outlet obstruction, although a Detrusormuskelschwäche or neurogenic bladder can produce an equally high residual urine volume. The catheter can be left on the first day to measure the hourly excretion, must to reduce the risk of infection but are removed when oliguria occurs – so if no bladder outlet obstruction is present. (Ed .:. N. D Even with bladder outlet obstruction, after ANV occur oliguria, which then changes into a polyuria, the catheter can and therefore should be longer than one day be left to account for the patient.) Renal ultrasonography is then performed to diagnose a more proximal obstruction. However, the sensitivity is compared with an obstruction during a sonography only 80-85%, because the pyelocaliceal system – especially in acute obstruction, when an intra-renal pelvis of the kidney is present or Ureterummauerung (eg for retroperitoneal fibrosis or neoplasm.), Or at the same time existing hypovolemia – is not always dilated. Is an obstruction highly probable, can be determined by a CT without a contrast agent, the cause of obstruction, and thus the therapy be initiated (n. D. Ed .: In ANV i.v. contrast administration is contraindicated). provide the urine sediment Can etiologic clues. A normal urinary sediment occurs in pre-renal azotemia and sometimes in obstructive uropathy. In a renal tubular damage the sediment characteristically tubular cells, tubular cell cylinder and many granular cylinder (often with brown pigmentation) contains. Eosinophil cells in urine speak of an allergic tubulointerstitiale nephritis, but the diagnostic accuracy of this finding is limited. Red blood cell casts show a glomerulonephritis or vasculitis, but may rarely occur with acute tubular necrosis .. Renal causes are sometimes suggested by clinical findings. Patients with glomerulonephritis often have edema, a pronounced proteinuria (nephrotic syndrome) or signs of cutaneous or retinal arteritis on, often without the history of intrinsic renal disease. Hemoptysis indicates granulomatosis with polyangiitis or Goodpasture’s syndrome. Certain rashes (z. B. erythema nodosum, cutaneous vasculitis, discoid lupus) indicate cryoglobulinemia, SLE or immunoglobulin-A-associated vasculitis. A tubulointerstitial nephritis, a drug allergy and possible microscopic polyangiitis, given a a history of medication and maculopapular rash or a purple. To further differentiate renal causes are antistreptolysin O and complement titer antinuclear antibodies and anti-neutrophil cytoplasmic antibodies are determined. If the diagnosis remains unclear, a renal biopsy should be performed (see Table: Causes of acute kidney injury based on laboratory results). Causes of acute kidney injury based on laboratory results of blood test result Possible diagnosis antiglomerular basement membrane antibody positive Goodpasture’s syndrome Antineutrophil cytoplasmic antibody positive vasculitis of small vessels (granulomatosis with polyangiitis or) microscopic angiitis antinuclear antibodies or antibodies to double-stranded DNA Positive SLE Antistreptolysin-O or antibodies to streptokinase or hyaluronidase positive post streptococcal glomerulonephritis CK or myoglobin significantly increased rhabdomyolysis Komplementtiter low acute proliferative glomerulonephritis, SLE, subacute bacterial endocarditis, Cholesterinembolus protein electrophoresis (serum) “Monoclonal spike” Multiple Myeloma uric acid levels Increases cancer or tumor lysis syndrome (leading to uric acid crystals) prerenal acute kidney injury Imaging Techniques In addition to renal ultrasonography may be occasionally other imaging tests useful. To investigate a ureteral obstruction which native CT is compared with the antegrade or retrograde urography preferred. (.. Editor’s note .: The KM-free CT extraluminal tumor is only in ureteral stones or suspected sense;.. Standard is initially retrograde urography) display In addition to its ability to soft tissue and calcium-containing stones, the CT X-ray can evidence not visible stones. Contrast agents should be avoided if possible. However Nierenarteriographie or venography can sometimes be indicated in case of suspected vascular causes. Magnetic resonance angiography has been increasingly used for the diagnosis of renal artery stenosis and thrombosis of arteries and veins, as is used in the MRI gadolinium, which was considered safer than the iodinated contrast agents in angiography and contrast-enhanced CT. However, recent findings suggest that gadolinium in the pathogenesis of nephrogenic systemic fibrosis, a serious complication that occurs in patients with AKI, such as chronic kidney disease may be involved as well. Therefore gadolinium should be avoided in patients with reduced kidney function as possible. The determination of the kidney size by an imaging study may be useful, because a normal or enlarged kidney for reversibility speaks, whereas a small kidney suggests a chronic renal insufficiency. Prognosis Although a lot of damage with early diagnosis and treatment are reversible, the overall survival rate is still only about 50% because many patients suffer with AKI from serious underlying diseases (sepsis, respiratory failure). Death is more the result of these disorders generally, rather than a consequence of. AKI even the most survivors remains adequate renal function. About 10% requiring dialysis or transplantation-a-half now and the other in gradual deterioration of renal function. Therapy Immediate treatment of pulmonary edema and hyperkalemia dialysis, if necessary, to hyperkalemia, pulmonary edema, metabolic acidosis and uremic symptoms to control setting of drug therapy Usually restriction of water, sodium phosphate and potassium intake, but provision of sufficient protein intake may phosphate binder and sodium polystyrene sulfonate emergency treatment of life-threatening complications, must be addressed in the ICU immediately preferably. Pulmonary edema is with oxygen administration, i.v. Vasodilators (eg. As nitroglycerin), diuretics (often ineffective in AKI) treated or dialysis. The treatment of hyperkalemia with i.v. Infusion of a 10% calcium glucose solution, 10 ml; Dextrose, 50 g and insulin, 5-10 units. These drugs do not reduce total body potassium, so that a further (but slower acting) treatment is necessary (eg. As sodium polystyrene sulfonate, dialysis). Although the correction of metabolic acidosis with anion gap is controversial with sodium bicarbonate to correct a severe metabolic acidosis without anion gap (pH <7.20) is less controversial. The share non-anion can with i.v. are treated with sodium bicarbonate to a slow infusion (? 150 mmol of sodium bicarbonate in 1 L of 5% D / W at a speed of 50-100 ml / h). The use of the delta-delta gradient calculation, metabolic acidosis with normal anion, as well as metabolic acidosis with high anion gap yields a negative delta-delta gradient;.,. Sodium bicarbonate is added to increase the serum bicarbonate until the delta-delta gradient reaches zero. As variations of the buffer systems of the body and the rate of acid production are difficult to predict, it is not recommended, as a rule, to calculate the Bicarbonatbetrag required to achieve complete correction. Instead, bicarbonate is administered by continuous infusion, and the anion is monitored serially. Clinical Calculator: anion gap Delta Delta gradient Multicalc Clinical Calculator: is a pulmonary edema despite medical treatment anion hemodialysis or hemofiltration be initiated if severity electrolyte abnormalities can not be controlled otherwise (eg potassium> 6 mmol / l.): Anion gap in Hypo albumin states Clinical Calculator metabolic acidosis unresponsive uremic symptoms to treatment (eg. as vomiting that was attributed to uremia, asterixis, encephalopathy, pericarditis, seizures) urea and creatinine levels are probably not the best indicators for the start of dialysis in AKI. In asymptomatic patients who appear to be less seriously ill, in particular where the recovery of renal function is considered likely those on dialysis can be postponed until the onset of symptoms to the placement of a central venous catheter because of the associated potential complications thus, to vermeiden.Allgemeine measures this purpose, the determination of serum levels is recommended. Nephrotoxic drugs should be discontinued, and any medications that are excreted by the kidneys (eg. Digoxin, some antibiotics) to be adjusted. The daily fluid intake is limited to a volume corresponding to the urinary excretion of the previous day, plus

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