Acute renal failure (ARF)
(Acute renal failure)
cute renal failure is the rapid decrease in renal function in days or weeks that causes accumulation of nitrogenous products in the blood (azotemia). It is often caused by severe trauma, illness or surgery, but is sometimes due to an intrinsic kidney disease of rapid progression. Symptoms include anorexia, nausea, and vomiting. If the condition is not treated, convulsions and coma may occur. Fluid alterations, electrolytes and acid-base balance develop rapidly. The diagnosis is based on laboratory tests of renal function, including serum creatinine. Urinary indices, urinary sediment analysis, and often imaging and other studies are needed to determine the cause. Treatment is directed to the cause,
In all cases of acute renal failure (ARF), creatinine and urea accumulate in the body over several days, and fluid and electrolytes are altered. The most serious of these alterations are hyperkalemia and fluid overload (possibly causing pulmonary edema). Retention of phosphates causes hyperphosphatemia. It is assumed that hypocalcemia is due to the fact that the diseased kidney no longer produces calcitriol , since hyperphosphatemia causes precipitation in the tissues of calcium phosphate. Acidosis occurs because the protons can not be excreted. With high uremia, coagulation may be affected, and pericarditis may occur. Urine excretion varies according to the type and cause of ARF.
Etiology
The causes of ARF (see Main causes of acute renal failure ) can be classified in
Prerenal
Renal
Posrenals
Azotemia azotemia is due to inadequate perfusion of the kidneys. The main causes are the depletion of extracellular fluid volume and cardiovascular diseases. Prerenal plaques cause 50-80% of FRA, but do not cause permanent renal damage (and thus are potentially reversible) unless hypoperfusion is so severe that it causes tubular ischemia. The hypoperfusion of a kidney by other functioning leads to an increased reabsorption of Na and water, which produces oliguria with urine of high osmolality and low Na content.
Kidney causes of ARF involve intrinsic disease or kidney damage. Kidney causes are responsible for 10 to 40% of cases. In general, the most common causes are prolonged renal ischemia and nephrotoxins (including radiopaque iodine contrast agents for IV use see Contrast Nephropathy ). These disorders can affect the glomeruli, tubules or interstitium. Glomerular diseases reduce the rate of glomerular filtration and increase the permeability of glomerular capillaries to proteins; May be inflammatory (glomerulonephritis) or the result of vascular damage by ischemia or vasculitis. Tubules can also be damaged by ischemia and clogged by cell debris, Deposition of proteins or crystals and cellular or interstitial edema. Tubular damage affects the reabsorption of Na, so this ion increases its concentration in the urine, a fact that is useful for diagnosis. Interstitial inflammation (nephritis) usually involves an immune or allergic phenomenon. These mechanisms of tubular damage are complex and interdependent, which makes the old popular term of acute tubular necrosis an inadequate description.
Posthumous azotemia (obstructive nephropathy - See also Obstructive uropathy ) is due to several types of obstruction in the collection and evacuation areas of the urinary tract, and is responsible for 5 to 10% of cases. Obstruction may also occur within the tubules when crystalline or proteinaceous material precipitates. This form of renal failure is often grouped with postnatal insufficiency because its mechanism is obstructive. The obstructed flow of the ultrafiltrate into the tubules or in more distal areas increases the pressure in the urinary space of the glomeruli, reducing the rate of glomerular filtration. The obstruction also affects the renal blood flow, Initially increasing the flow and pressure in the glomerular capillaries by reducing the resistance of the afferent artery. However, within 3 to 4 hours, renal blood flow declines, and by 24 hours has decreased to < 50% of normal due to increased resistance of renal vascularization. Renewascular resistance may take up to 1 week to return to normal after removal of a 24-hour blockage. To produce significant azotemia, obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in males. However, within 3 to 4 hours, renal blood flow declines, and by 24 hours has decreased to < 50% of normal due to increased resistance of renal vascularization. Renewascular resistance may take up to 1 week to return to normal after removal of a 24-hour blockage. To produce significant azotemia, obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in males. However, within 3 to 4 hours, renal blood flow declines, and by 24 hours has decreased to < 50% of normal due to increased resistance of renal vascularization. Renewascular resistance may take up to 1 week to return to normal after removal of a 24-hour blockage. To produce significant azotemia, obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in males. 50% of normal due to increased resistance of renal vascularization. Renewascular resistance may take up to 1 week to return to normal after removal of a 24-hour blockage. To produce significant azotemia, obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in males. 50% of normal due to increased resistance of renal vascularization. Renewascular resistance may take up to 1 week to return to normal after removal of a 24-hour blockage. To produce significant azotemia, obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in men. Obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in males. Obstruction at the level of the ureter requires that both ureters be affected, unless the patient has only one functioning kidney. Obstruction of the bladder outlet tract is probably the most common cause of cessation of sudden, and often total, urine output in males.
Production of urine
Typically, the prerenal causes are manifested with oliguria, not anuria. Anuria usually occurs in obstructive uropathy or, less frequently, in bilateral renal artery occlusion, acute cortical necrosis, or rapidly progressing glomerulonephritis.
In most renal causes, a relatively preserved urine production of 1 to 2.4 L / day is usually present at the beginning. In acute tubular injury, urine production may have 3 phases.
Clinical Calculator: Kidney Failure Rate
The prodromal phase, usually with normal urine output, varies in duration depending on the cause (eg, amount of toxin ingested, duration and severity of hypotension).
The oliguric phase , with a typical production of between 50 and 400 mL / day, lasts on average about 10 to 14 days but can oscillate between 1 day and 8 weeks. However, many patients never present oliguria. Non-oliguric patients have lower morbidity and mortality and less need for dialysis.
In the posoliguric phase , urine excretion gradually returns to its normal value, but serum creatinine and urea concentrations may not decrease for several days. Tubal dysfunction may persist and manifests as loss of Na, polyuria (possibly massive) that does not respond to vasopressin , or hyperchloremic metabolic acidosis.
Signs and symptoms
At first, the only findings may be weight gain and peripheral edema. Often, the predominant symptoms are those of the underlying disease or those caused by surgical complications that precipitated renal deterioration. Later, as nitrogen products accumulate, uremia symptoms may appear, including anorexia, nausea, vomiting, weakness, myoclonus, convulsions, confusion, and coma. Asterixis and hyperreflexia may appear on the test. If there is uremic pericarditis, chest pain (which typically worsens on inspiration or in decubitus), pericardial rubbing, and signs of pericardial tamponade may occur. The accumulation of fluid in the lungs can cause dyspnoea and crackles in auscultation.
Other findings depend on the cause. Urine may be dark-colored (cola-colored) in glomerulonephritis or myoglobinuria. The bladder may be palpable if there is obstruction of the outflow tract. The costovertebral angle may be sensitive to touch if the kidney enlarges acutely.
Diagnosis
Serum Creatinine
Urinary sediment
Urinary Diagnostic Indices
Residual volume posmiction of the bladder, if an afterthought is suspected
An ARF is suspected when urine production declines, or urea nitrogen and creatinine in the blood increase. The assessment should determine the presence and type of ARF, and look for its cause. Blood tests usually include complete blood count, blood urea nitrogen, creatinine, and electrolytes (including Ca and phosphate). Urine tests include Na and creatinine concentration and microscopic analysis of the sediment. Early detection and treatment increase the likelihood of reversing renal failure and, in some cases, preventing it.
A progressive daily increase in serum creatinine is a diagnosis of ARF. Serum creatinine may increase to 2 mg / dL / day (180 μ mol / L / day), depending on the amount of creatinine produced, which varies with the lean body mass and total body water. An increase > 2 mg / dL / day suggests that there is excessive production due to rhabdomyolysis.
Urea nitrogen can increase by 10 to 20 mg / dL / day (3.6 to 7.1 mmol urea / L / day), but its determination in the blood can be misleading, as it frequently rises in response to Increased protein catabolism due to surgery, trauma, corticosteroids, burns, transfusion reactions, parenteral nutrition, or digestive or internal hemorrhage.
When creatinine is elevated, the 24-hour urine collection for creatinine clearance and the various formulas used to determine this value from serum creatinine are imprecise and are not used to estimate the glomerular filtration rate (GFR), since That increased serum creatinine is a late consequence of decreased GFR.
Other laboratory findings are progressive acidosis, hyperkalemia, hyponatremia, and anemia. Acidosis in general is moderate, with an HCO 3 plasma content of 15 to 20 mmol / L. The potassium concentration in the serum rises slowly, but when the catabolism is very fast, it can increase by 1 or 2 mmol / day. Hyponatremia is usually moderate (serum Na of 125 to 135 mmol / L) and correlates with excess water. Normocytic and normocytic anemia is typical, with hematocrit of 25 to 30%.
Hypocalcemia is common, and may be marked in patients with myoglobinuric ARF, apparently because of the combined effects of calcium deposition on the necrotic muscle, decreased calcitriol production , bone resistance to PTH and Hyperphosphataemia. During recovery of FRA, hypercalcemia may occur as calcitriol production increases , bone begins to respond to PTH, and calcium deposits are mobilized from damaged tissues.
Determination of cause
Prerenal or postenal causes that can be easily reversed should be excluded first. Extracellular fluid volume and obstruction should be considered in all patients. The history of drug use should be accurately recorded and all potentially toxic drugs should be discontinued. Urinary diagnostic indices (see Urinary Diagnostic Indices for prerenal azotemia and acute tubular injury ) are useful for distinguishing prerenal azotemia from acute tubular injury, which are the most common causes of ARF in hospitalized patients.
The prerenal causes are often clinically evident. In this case, correction of the underlying hemodynamic abnormality should be attempted. For example, in hypovolemia, infusion of volume may be attempted; Diuretics and afterload reducing agents can be given in heart failure; And in hepatic impairment, octreotide may be given . The disappearance of the FRA confirms a prerenal cause.
The postrenal causes should be investigated in most cases FRA. Immediately after urination, an ultrasound of the bladder is performed at the foot of the bed (or, alternatively, a urinary catheter is placed) to determine the amount of residual urine in the bladder. A residual post-volume volume of > 200 mL suggests that there is an obstruction of the bladder outlet tract, although it may also be caused by weakness of the detrusor muscle or by a neurogenic bladder. The probe should be kept on the first day to monitor urine production hourly, but may be withdrawn once oliguria has been confirmed (if there is no obstruction of the bladder outlet) to reduce the risk of infection. A renal ultrasound is then performed to diagnose more proximal obstructions. However, sensitivity to obstruction is only 80-85% when ultrasound is used, because the collecting system is not always dilated, especially when the condition is acute, there is an intrarenal pelvis, the ureter is trapped In retroperitoneal fibrosis or neoplasia) or if the patient has concomitant hypovolemia. If the suspicion of obstruction is strong, noncontrast CT can establish its location and direct therapy. The ureter is trapped (as in retroperitoneal fibrosis or neoplasia) or if the patient has concomitant hypovolemia. If the suspicion of obstruction is strong, noncontrast CT can establish its location and direct therapy. The ureter is trapped (as in retroperitoneal fibrosis or neoplasia) or if the patient has concomitant hypovolemia. If the suspicion of obstruction is strong, noncontrast CT can establish its location and direct therapy.
The urinary sediment can provide clues about the etiology. In prerenal azotemia and sometimes in obstructive uropathy, a normal sediment appears. In renal tubular injury, the characteristic sediment has tubular cells, tubular cell cylinders and many granular cylinders (often with brown pigments). Urinary eosinophils suggest an allergic tubulointerstitial nephritis; The erythrocyte cylinders, glomerulonephritis or vasculitis.
The renal causes are sometimes suggested by clinical findings. Patients with glomerulonephritis (see Glomerulopathies ) often have edema, marked proteinuria (nephrotic syndrome) or signs of arteritis in the skin and retina, sometimes without a history of intrinsic kidney disease. Hemoptysis suggests granulomatosis with polyangeitis (formerly Wegener's granulomatosis) or Goodpasture's syndrome. Certain eruptions (such as erythema nodosum, cutaneous vasculitis, discoid lupus) suggest polyarteritis, cryoglobulinemia, SLE or Schönlein-Henoch purpura. Tubulointerstitial nephritis and drug allergies are suspected when there is a history of drug administration and a maculopapular or purpuric rash.
To further differentiate renal causes, titers of antistreptolysin-O and complement, antinuclear antibodies and anti-neutrophil cytoplasmic antibodies should be determined. If a diagnosis is not yet made, a renal biopsy may be performed (see Causes of acute renal failure according to laboratory results ).
Studies by the image
In addition to renal ultrasound, other imaging studies are sometimes useful. To evaluate a ureteral obstruction, contrast-enhanced CT is preferred over antegrade and retrograde urography. In addition to its ability to delineate soft tissue structures and calcium stones, CT can also detect non-radiopaque stones.
If possible, contrast agents should be avoided. However, arteriography or renal venography may sometimes be indicated if the clinical findings suggest a vascular cause. Magnetic resonance angiography was widely used for the diagnosis of renal artery stenosis as well as arterial and venous thrombosis because it used gadolinium, which was believed to be much safer than iodinated contrast agents of angiography and Of CT with contrast. However, recent evidence indicates that gadolinium may participate in the pathogenesis of systemic nephrogenic fibrosis, a serious complication occurring only in patients with ARF. Therefore, if possible, gadolinium should be avoided in such patients.
It is useful to know the size of the kidney through imaging because an organ of normal or increased size favors the reversibility of the picture, whereas a small kidney suggests chronic renal failure.
Forecast
Although many causes are reversible if they are diagnosed and treated early, the overall survival rate remains at 50% because many patients with ARF have major underlying disorders (sepsis, respiratory failure). In general, death is usually a result of these disorders rather than the FRA itself. Most patients who survive have an adequate kidney function. Approximately 10% require dialysis or transplantation; Half of them immediately and the rest as kidney function deteriorates.
Treatment
Immediate treatment of pulmonary edema and hyperkalemia
Dialysis as needed to control hyperkalemia, pulmonary edema, metabolic acidosis, and uremic symptoms
Adjustment of medication regimen
In general, restriction of water intake, Na, phosphate and K, but with adequate protein supply
Possibly, phosphate binding agents and Na polystyrene sulfonate
Emergency treatment
Complications that endanger the patient's life should be treated, preferably in an intensive care unit. Pulmonary edema (see Edema of the lung ) is treated with O 2 , IV vasodilators (such as nitroglycerin) and diuretics (which are often not effective in ARF). Hyperkalemia (see Hyperkalemia ) is treated as needed with IV infusion of 10 mL of 10% Ca gluconate, 50 g of dextrose and 5 to 10 units of insulin. These drugs do not reduce total body K, so a subsequent (slower acting) treatment is initiated with 30 g Na polystyrene sulfonate either orally or rectally. Since the correction of metabolic acidosis with an anionic gap with NaHCO 3 is controversial, It is more acceptable to correct the non-anionic hiatus portion of severe metabolic acidosis (pH < 7.20), which can be treated with diluted NaHCO 3 as a slow infusion ( ≤ 150 mEq of NaHCO 3 in 1 L of 5% , At a rate of 50 to 100 mL / hour). The portion of the metabolic acidosis without an anion gap is determined by calculating the above-normal anion gap and then subtracting this value from the decrease of NaHCO 3 to the value of 24 mmol / L. NaHCO 3 is administered to increase the serum HCO 3 by this difference. Since the variation in body damping systems and rate of acid production are difficult to predict, It is generally not recommended to calculate the amount of NaHCO 3 needed to achieve a complete correction. Instead, NaHCO 3 is administered in a continuous infusion, and the anion gap is monitored serially.
The hemodialysis (see Hemodialysis ) or hemofiltration (see hemofiltration and hemodialysis continuous ) start when
Severe anomalies of the electrolytes can not be controlled in any other way (eg K > 6 mmol / L)
Pulmonary edema persists despite pharmacological treatment
Metabolic acidosis does not improve with treatment
Uremic symptoms (eg, vomiting attributable to uremia, asterixis, encephalopathy, pericarditis, seizures)
Blood urea nitrogen and creatinine concentrations are probably not the best guidelines for initiating dialysis in patients with ARF. In asymptomatic patients who are not severely ill, especially in those who are considered likely to regain renal function, dialysis may be delayed until symptoms appear, thus avoiding the placement of a central venous route with associated complications.
General measures
All nephrotoxic drugs should be discontinued and doses adjusted for all renal excretion drugs (eg, digoxin, some antibiotics); Determination of serum concentrations may be useful.
Daily water intake is restricted to a volume equal to the previous day's urine output plus measured extrarenal losses (eg, vomiting), plus 500 to 1,000 mL per day to compensate for non-measurable losses. It can be further decreased if there is hyponatremia, or increased if there is hypernatremia. Although weight gain indicates excess fluid, water intake is not decreased if serum Na remains normal; Instead, the consumption of Na is restricted.
Intake of Na and K is minimized, except in patients with previous deficiencies or gastrointestinal losses. Adequate diet should be provided, with a daily protein intake of approximately 0.8 g / kg. If oral or enteral nutrition is impossible, the parenteral route is used; However, in IVF IV nutrition increases the risk of fluid overload, hyperosmolarity, and infections. Calcium (carbonate, acetate) salts or synthetic phosphate-free substances before meals help maintain serum phosphate levels < 5 mg / dL ( < 1.78 mmol / L). If K is needed to maintain serum K < 6 mmol / L in the absence of dialysis (eg, if other therapies, such as diuretics, They fail to decrease K), a cation exchange resin, Na polystyrene sulfonate, is administered in doses of 15 to 60 g orally or rectally, 1 to 4 times per day, as a suspension in water or in a Syrup (eg, 70% sorbitol). A permanent bladder catheter is rarely needed and should be used only if necessary, because of the increased risk of urinary infection and urosepsis.
In many patients, relief of an obstruction produces intense and even dramatic diuresis as a physiological response to the expansion of the ECC during obstruction that does not compromise volume. However, polyuria accompanied by excretion of large amounts of Na, K, Mg and other solutes may cause hypokalemia, hyponatremia, hypernatremia (if no free water is supplied), hypomagnesemia or marked contraction of ECC volume with peripheral vascular collapse. In this posoliguric phase, it is essential to closely monitor fluid and electrolyte balance. Excessive salt and water administration after release of an obstruction may prolong diuresis. When a posoliguric diuresis occurs, the volume of the urine is replaced with saline at 0,
Prevention
FRA can be prevented by maintaining a normal fluid balance, blood volume and blood pressure in patients with major trauma, burn or bleeding, and those who are undergoing major surgeries. Infusion of isotonic saline and blood may be helpful. The use of contrast agents should be minimal, especially in the highest risk groups (eg, the elderly and those with pre-existing renal impairment, volume depletion, diabetes, or heart failure). If contrast agents are required, the risk can be lowered by minimizing the volume of IV contrast agent, non-ionic, low osmolality or iso-molecular agents, avoidance of NSAIDs, and normal saline at 1 mL / kg / H IV for 12 hours prior to the study. The infusion before and after administration of isotonic NaHCO 3 contrast has also been successfully used in place of physiological solution. N- acetylcysteine has been used in doses of 600 mg orally twice daily for the day before and the day of administration of contrast IV to prevent nephropathy, but reports of its efficacy are controversial.
Before initiating cytolytic therapy in patients with certain neoplastic diseases (lymphoma, leukemia), treatment with either rasburicase or allopurinol should be considered together with an increase in urinary flow by administration of oral fluids or IV to reduce the formation of crystals Of urates. It has been recommended to make urine more alkaline (with oral NaHCO 3 or IV, or acetazolamide), but this treatment is controversial because it can also induce precipitation of urinary calcium phosphate and crystalluria, which can make the ARF worse.
The renal vasculature is very sensitive to endothelin, a potent vasoconstrictor that reduces renal blood flow and glomerular filtration rate. Endothelin is implicated in progressive renal damage, and its receptor antagonists have been used successfully to slow or even slow the progression of experimental renal disease. Antiendothelin antibodies and endothelin receptor antagonists are being studied as potential kidney protectors in ischemic ARF.
Key concepts
The causes of ARF may be prerenal (eg, renal hypoperfusion), renal (eg, direct effects on the kidney) or postrenal (eg, obstruction of the urinary tract distal to the kidneys).
In FRA, consider the loss of ECL volume and nephrotoxins, obtain urinary diagnostic indices, and measure the residual volume of the bladder to identify an obstruction.
Avoid the use of intravenous contrasts in diagnostic imaging studies.
Initiate hemodialysis or hemofiltration as needed based on pulmonary edema, hyperkalemia, metabolic acidosis, or uremic symptoms that do not respond to other treatments.
Minimize the risk of acute renal failure in patients at risk by maintaining normal fluid balance, avoiding nephrotoxins (including contrast agents) when possible, and taking precautions such as administration of liquids or medications when it is necessary to use a contrast agent Or cytolytic therapy.
Resources in this articleStudies by the image
In addition to renal ultrasound, other imaging studies are sometimes useful. To evaluate a ureteral obstruction, contrast-enhanced CT is preferred over antegrade and retrograde urography. In addition to its ability to delineate soft tissue structures and calcium stones, CT can also detect non-radiopaque stones.
If possible, contrast agents should be avoided. However, arteriography or renal venography may sometimes be indicated if the clinical findings suggest a vascular cause. Magnetic resonance angiography was widely used for the diagnosis of renal artery stenosis as well as arterial and venous thrombosis because it used gadolinium, which was believed to be much safer than iodinated contrast agents of angiography and Of CT with contrast. However, recent evidence indicates that gadolinium may participate in the pathogenesis of systemic nephrogenic fibrosis, a serious complication occurring only in patients with ARF. Therefore, if possible, gadolinium should be avoided in such patients.
It is useful to know the size of the kidney through imaging because an organ of normal or increased size favors the reversibility of the picture, whereas a small kidney suggests chronic renal failure.
Forecast
Although many causes are reversible if they are diagnosed and treated early, the overall survival rate remains at 50% because many patients with ARF have major underlying disorders (sepsis, respiratory failure). In general, death is usually a result of these disorders rather than the FRA itself. Most patients who survive have an adequate kidney function. Approximately 10% require dialysis or transplantation; Half of them immediately and the rest as kidney function deteriorates.
Treatment
Immediate treatment of pulmonary edema and hyperkalemia
Dialysis as needed to control hyperkalemia, pulmonary edema, metabolic acidosis, and uremic symptoms
Adjustment of medication regimen
In general, restriction of water intake, Na, phosphate and K, but with adequate protein supply
Possibly, phosphate binding agents and Na polystyrene sulfonate
Emergency treatment
Complications that endanger the patient's life should be treated, preferably in an intensive care unit. Pulmonary edema (see Edema of the lung ) is treated with O 2 , IV vasodilators (such as nitroglycerin) and diuretics (which are often not effective in ARF). Hyperkalemia (see Hyperkalemia ) is treated as needed with IV infusion of 10 mL of 10% Ca gluconate, 50 g of dextrose and 5 to 10 units of insulin. These drugs do not reduce total body K, so a subsequent (slower acting) treatment is initiated with 30 g Na polystyrene sulfonate either orally or rectally. Since the correction of metabolic acidosis with an anionic gap with NaHCO 3 is controversial, It is more acceptable to correct the non-anionic hiatus portion of severe metabolic acidosis (pH < 7.20), which can be treated with diluted NaHCO 3 as a slow infusion ( ≤ 150 mEq of NaHCO 3 in 1 L of 5% , At a rate of 50 to 100 mL / hour). The portion of the metabolic acidosis without an anion gap is determined by calculating the above-normal anion gap and then subtracting this value from the decrease of NaHCO 3 to the value of 24 mmol / L. NaHCO 3 is administered to increase the serum HCO 3 by this difference. Since the variation in body damping systems and rate of acid production are difficult to predict, It is generally not recommended to calculate the amount of NaHCO 3 needed to achieve a complete correction. Instead, NaHCO 3 is administered in a continuous infusion, and the anion gap is monitored serially.
The hemodialysis (see Hemodialysis ) or hemofiltration (see hemofiltration and hemodialysis continuous ) start when
Severe anomalies of the electrolytes can not be controlled in any other way (eg K > 6 mmol / L)
Pulmonary edema persists despite pharmacological treatment
Metabolic acidosis does not improve with treatment
Uremic symptoms (eg, vomiting attributable to uremia, asterixis, encephalopathy, pericarditis, seizures)
Blood urea nitrogen and creatinine concentrations are probably not the best guidelines for initiating dialysis in patients with ARF. In asymptomatic patients who are not severely ill, especially in those who are considered likely to regain renal function, dialysis may be delayed until symptoms appear, thus avoiding the placement of a central venous route with associated complications.
General measures
All nephrotoxic drugs should be discontinued and doses adjusted for all renal excretion drugs (eg, digoxin, some antibiotics); Determination of serum concentrations may be useful.
Daily water intake is restricted to a volume equal to the previous day's urine output plus measured extrarenal losses (eg, vomiting), plus 500 to 1,000 mL per day to compensate for non-measurable losses. It can be further decreased if there is hyponatremia, or increased if there is hypernatremia. Although weight gain indicates excess fluid, water intake is not decreased if serum Na remains normal; Instead, the consumption of Na is restricted.
Intake of Na and K is minimized, except in patients with previous deficiencies or gastrointestinal losses. Adequate diet should be provided, with a daily protein intake of approximately 0.8 g / kg. If oral or enteral nutrition is impossible, the parenteral route is used; However, in IVF IV nutrition increases the risk of fluid overload, hyperosmolarity, and infections. Calcium (carbonate, acetate) salts or synthetic phosphate-free substances before meals help maintain serum phosphate levels < 5 mg / dL ( < 1.78 mmol / L). If K is needed to maintain serum K < 6 mmol / L in the absence of dialysis (eg, if other therapies, such as diuretics, They fail to decrease K), a cation exchange resin, Na polystyrene sulfonate, is administered in doses of 15 to 60 g orally or rectally, 1 to 4 times per day, as a suspension in water or in a Syrup (eg, 70% sorbitol). A permanent bladder catheter is rarely needed and should be used only if necessary, because of the increased risk of urinary infection and urosepsis.
In many patients, relief of an obstruction produces intense and even dramatic diuresis as a physiological response to the expansion of the ECC during obstruction that does not compromise volume. However, polyuria accompanied by excretion of large amounts of Na, K, Mg and other solutes may cause hypokalemia, hyponatremia, hypernatremia (if no free water is supplied), hypomagnesemia or marked contraction of ECC volume with peripheral vascular collapse. In this posoliguric phase, it is essential to closely monitor fluid and electrolyte balance. Excessive salt and water administration after release of an obstruction may prolong diuresis. When a posoliguric diuresis occurs, the volume of the urine is replaced with saline at 0,
Prevention
FRA can be prevented by maintaining a normal fluid balance, blood volume and blood pressure in patients with major trauma, burn or bleeding, and those who are undergoing major surgeries. Infusion of isotonic saline and blood may be helpful. The use of contrast agents should be minimal, especially in the highest risk groups (eg, the elderly and those with pre-existing renal impairment, volume depletion, diabetes, or heart failure). If contrast agents are required, the risk can be lowered by minimizing the volume of IV contrast agent, non-ionic, low osmolality or iso-molecular agents, avoidance of NSAIDs, and normal saline at 1 mL / kg / H IV for 12 hours prior to the study. The infusion before and after administration of isotonic NaHCO 3 contrast has also been successfully used in place of physiological solution. N- acetylcysteine has been used in doses of 600 mg orally twice daily for the day before and the day of administration of contrast IV to prevent nephropathy, but reports of its efficacy are controversial.
Before initiating cytolytic therapy in patients with certain neoplastic diseases (lymphoma, leukemia), treatment with either rasburicase or allopurinol should be considered together with an increase in urinary flow by administration of oral fluids or IV to reduce the formation of crystals Of urates. It has been recommended to make urine more alkaline (with oral NaHCO 3 or IV, or acetazolamide), but this treatment is controversial because it can also induce precipitation of urinary calcium phosphate and crystalluria, which can make the ARF worse.
The renal vasculature is very sensitive to endothelin, a potent vasoconstrictor that reduces renal blood flow and glomerular filtration rate. Endothelin is implicated in progressive renal damage, and its receptor antagonists have been used successfully to slow or even slow the progression of experimental renal disease. Antiendothelin antibodies and endothelin receptor antagonists are being studied as potential kidney protectors in ischemic ARF.
Key concepts
The causes of ARF may be prerenal (eg, renal hypoperfusion), renal (eg, direct effects on the kidney) or postrenal (eg, obstruction of the urinary tract distal to the kidneys).
In FRA, consider the loss of ECL volume and nephrotoxins, obtain urinary diagnostic indices, and measure the residual volume of the bladder to identify an obstruction.
Avoid the use of intravenous contrasts in diagnostic imaging studies.
Initiate hemodialysis or hemofiltration as needed based on pulmonary edema, hyperkalemia, metabolic acidosis, or uremic symptoms that do not respond to other treatments.
Minimize the risk of acute renal failure in patients at risk by maintaining normal fluid balance, avoiding nephrotoxins (including contrast agents) when possible, and taking precautions such as administration of liquids or medications when it is necessary to use a contrast agent Or cytolytic therapy.
