Acute Renal Failure

Acute Renal Failure
The kidney is an organ that primarily regulates volume and composition of the internal fluid environment; its excretory function is incidental to their regulatory function. In renal failure, this regulatory function is impaired.
Acute renal failure (ARF) is defined as a fall in the glomerular filtration rate (GFR) and the accumulation of nitrogenous wastes products (e.g., urea, creatinine, and potassium) in the serum and also disturbances in fluid, electrolyte, and acid-base balance; this condition may be oliguric or nonoliguric.


The term acute renal failure is used when the fall in GFR occurs relatively rapidly, and the BUN and creatinine levels increase over the course of days to weeks. In chronic renal failure, the GFR falls much more slowly, over months to years. Acute renal failure is a complex syndrome that occurs in a wide variety of settings with clinical manifestations ranging from a minimal elevation in serum creatinine to anuric kidney failure. Although the majority of cases are the result of acute tubular necrosis, the same clinical manifestations follow many different etiologies, especially sepsis and nephrotoxin exposure [1]. Outcomes range from recovery to death and include the development of chronic kidney disease and progression to dialysis dependency. A wide variation in the definition of ARF has made it difficult to compare information across studies and population. ARF is based on high serum creatinine, changes in urine output, or the need for dialysis [2]. Despite decades of experimental and clinical research, there has been little or no success in translating experimental therapy into clinical practice. Because of the use of creatinine-based definitions of ARF, the diagnosis of ARF has been made retrospectively and often by exclusion and usually without biopsy evidence. Consequently we know very little about the structural changes of early clinical ARF, including so-called prerenal ARF. However acute renal failure, more than any other ICU syndrome, has been defined different ways. Bellomo and collegues focused the importance of developing a consensus definition regarding acute or chronic renal failure [3]. The international Acute Kidney Injury Network (AKIN) proposed a change in nomenclature, and acute kidney injury (AKI) has become the preferred term to describe the syndrome of ARF, with “failure” related to patients who have AKI needing renal replacement therapy (RRT). An additional advance is a proposed grading of severity of AKI in 3 stages. This grading has been developed from an earlier 5-step grading captured in the acronym RIFLE (Risk, Injury, Failure, Loss and End stage) according to relative changes in the serum creatinine and urine output, which divided AKI into 3 severity based categories (Risk, Injury and Failure) and 2 categories reflecting persistence (Loss and End-stage kidney disease). The new 3-step staging breaches the conceptual gap between “minor” and more severe elevations of creatinine but omits the 2 outcome categories of loss and end-stage kidney failure. Individuals who receive RRT are automatically graded as stage 3 [4].
Acute renal failure is seldom a community-acquired disease but usually develops in hospitalized patients. It complicates 5% of all hospitalized patients [5]. Critically ill patients have the highest incidence of acute renal failure, more than 20%, and once they developed their mortality tend to increase five to sixth times more [6]. Renal failure is a common occurrence in the intensive care unit (ICU); it is frequently a part of a multitude of problems, which culminate in sepsis and multiple organ dysfunction/failure.
The causes of ARF traditionally are divided into 3 categories: prerenal, postrenal, and acute tubular necrosis [7,8]. This simple clinical classification of ARF remains useful, because it provides a logical basis for the diagnosis and treatment. The most common causes of ARF are prerenal failure with approximately 35% of cases and acute tubular necrosis (ATN) with 50% of cases. Obstruction accounts for the minority of cases (Table 16.1) [10].
Pseudorenal failure is a clinical condition characterized by an increase of the BUN or creatinine without a decrease in the GFR (Table 16.2). One should always

Table.1 Causes of acute renal failure hospital versus ICU

Acute tubular necrosis
Renal vascular disorders


Acute interstitial nephritis

Table.2 Causes of pseudorenal failure
Increased BUN
Increased creatinine
GI bleeding
Trimethroprim, cimetidine
Cefoxtin, acetone

consider these nonrenal factors as a potential explanation determining an increase of acute azotemia. Also, sometimes we may be in a situation where there is a decrease in the GFR with normal creatinine as in severe malnutrition or atrophic muscle disorders, or a decrease in GFR with normal BUN as in hepatic failure because of decreased urea synthesis.
Prerenal Azotemia
The reduction in GFR in prerenal failure is caused by abnormalities in glomerular perfusion. Prerenal ARF, by definition, is not associated with any intrinsic renal parenchymal disease and resolves rapidly when the underlying causes of renal hypoperfusion are corrected.
Although renal blood flow is reduced in prerenal failure, it remains adequate to provide enough oxygen and metabolic substrates to sustain the viability of the kidney. If prerenal ARF is not treated in a timely manner or is allowed to get progressively worse, ischemic injury to renal tubular cells ultimately occurs and precipitates ATN [9]. The pathophysiology and causes of prerenal azotemia is presented in Table.3. In the face of azotemia and oliguria, several markers are useful in order to differentiate prerenal azotemia versus ATN (Table.4). All those markers are useful in the absence of a prior diuretic administration, except for the fractional excretion of urea, which is not affected. It is also important to consider the causes of falsely high/low fractional excretion of sodium (Table.5). An abnormality of the routine urine analysis would suggest underlying acute or chronic renal disease. It is not unusual for the urinary sodium value to suggest a prerenal element, but the urine creatinine to suggest renal dysfunction or vice versa. If even one of many parameters suggests a prerenal element, any potential prerenal factors should be identified and reversed.
Prerenal azotemia is confirmed if the urine output improves and the azotemia resolves with the administration of isotonic fluids or improvement in the underlying condition, e. g., heart failure.

Table .3 Pathophysiology and causes of prerenal azotemia
Absolute decrease ECV
Decreased “effective” ECV “Third Spaced” volume
CHF/cirrhosis/nephrosis Abdominal catastrophes
Absolute decrease ECV

Table 16.4 Prerenal azotemia versus acute tubular necrosis (ATN)

Bun: Cr Ratio
Urine Osm (mOsm/l)
U:P Osm
Urine Na (mEq/l)
FE. Na (%)
FE. Urea (%)

Table 16.5 Falsely high/low fractional excretion of sodium
Contrast nephropathy acute glomerulonephritis
Congestive heart failure
Chronic azotemia

Postrenal Azotemia
Postrenal azotemia is a diagnosis that should not be missed, and it is generally done by anatomic exclusion (Table 16.6). All patients with early oliguric ARF should have a urinary catheter and an ultrasound done early in the course; if the patient is known to have only one kidney it will be better to do a CT scan or a retrograde pyelography.
Table 16.6 Postrenal azotemia
Stricture, stone, object
Hypertrophy, tumor
Neurogenic, tumor, clot
Stone, tumor, clot
Tumor, fibrosis

Acute Renal Failure
Although ATN is the most common cause of hospital-acquired ARF, one must consider the various intrinsic renal parenchymal or hemodynamic derangements responsible for ARF. These include diseases that primarily affect the glomerulus (glomerulonephritis), interstitium (interstitial nephritis), and blood vessels (vascular occlusion or vasculitis)  (Table.7).
Table 16.7 Acute renal failure
Glomerular disease
Glomerulonephritis intrarenal hemodynamics
Interstitial disease
Vascular disease
Tubular disease “ATN”
Fulminant glomerulonephritis due to bacterial endocarditis, staphylococcal septicemia, visceral abscesses, hepatitis B surface antigen, and Goodpasture syndrome, can be observed in a major intensive care unit. Once considered, these diagnoses are not difficult to make. The urinalysis will show dysmorphic red blood cells (those with multiple surface irregularities), red blood cell casts, and from moderate to heavy proteinuria. Hypertension is variably present. Blood cultures, serologic testing [antinuclear antibody, antineutrophilic cytoplasmic antibodies (ANCA), hepatitis B surface antigen, and antiglomerular basement membrane antibody], and a search for visceral abscess may be necessary. An early renal biopsy is usually helpful when acute glomerulonephritis causes ARF.
Alterations in glomerular hemodynamics are increasingly recognized as a cause of ARF. This situation includes afferent arteriolar vasoconstriction (hepatorenal syndrome) or efferent arteriolar vasodilation (angiotensin converting enzyme inhibitors). The latter is seen when renal blood flow is already compromised by diuretics, severe cardiac failure, or renal artery stenosis. In addition, less well defined derangements in intrarenal hemodynamics are likely responsible for the ARF in sepsis, potent vasodilators, and the nonsteroidal anti-inflammatory drugs
(NSAIDs). In these cases, the urinary sediment is nonrelevant, and the renal biopsy, if performed, tend to be normal. Recovery of renal function is expected, provided the offending drug is removed or the underlying condition is corrected (Table.8).
Table 16.8 ARF due to glomerular hemodynamics
Hepatorenal syndrome
ACE inhibitors

Acute interstitial nephritis is usually due to allergies to drugs such as penicillins, cephalosporins, sulfonamides, diuretics, and NSAIDs. Patients will present with fever, rash, arthralgias, eosinophilia, and eosinophiluria (excepting NSAIDs) [11]. Other less frequent causes are pyelonephritis, multiple myeloma, uric acid nephropathy, and occasionally infiltrative disorders, such as lymphoma, leukemia, and sarcoidosis. Oxalate nephropathy may complicate acute ethylene glycol ingestion. The urine sediment is usually nonrelevant, but crystalluria, pyuria, and white blood cell casts can be seen, even in the absence of infection.
Vascular disease is a frequently overlooked cause of ARF. Malignant hypertension usually accompanied by retinopathy, thrombocitopenia, and microangiopathy can cause ARF. Microangiopathy and thrombocitopenia also accompany hemolytic uremic syndrome or thrombotic thrombocytopenic purpura (TTP). Renal infarction due to trauma, arterial embolus, or thrombosis can cause ARF with fever, hematuria, acute flank pain, ileus, leucocytosis, and an increased LDH . level. This syndrome often mimics an acute abdomen. Renal atherosclerotic or cholesterol microemboli commonly occur following aortic manipulation (surgery or catheterization), besides ARF, gastrointestinal bleeding (due to microinfarction), livedo reticularis of the lower extremities, patchy areas of ischemic necrosis in the toes, hypocomplementemia, and eosinophilia are common. Finally, renal vasculitis often causes ARF. These syndromes are identified by their multisystem manifestations, very active urine sediment (hematuria, pyuria, red and white blood cell casts, and proteinuria), and in the cases of Wegener’s and polyarteritis nodosa, the presence of ANCA in the serum (Tables.9-.12).
Acute tubular necrosis is the most common cause of hospital and ICU-acquired ARF, which is broadly divided into toxic and ischemic causes (Table.13). Drugs that induce renal damage and mechanisms can be reviewed in Table 16.14. Among the more common toxins causing ATN are the aminoglycoside antibiotics. Risk factors for aminoglycoside nephrotoxicity include volume contraction, age, hypokalemia, concomitant use of other nephrotoxins, and a short-dosing interval. After an initial loading dose, the maintenance dose should be adjusted based on the patient’s creatinine clearance. The routine use of peak and trough serum levels does not decrease the likelihood of ATN.
Table 16.9 Acute renal failure – vascular causes

• Hemolytic uremic syndrome/thrombotic thrombocytopenic purpura
• Renal vein thrombosis
• Renal artery embolism
• Vasculitis
• Cholesterol microemboli
• Malignant hypertension

Table 16.10 Renal artery embolism

Acute Azotemia
Increased LDH
Flank abdominal pain

Table 16.11 ARF. Cholesterol microemboli

• Eosinophilia/uria
• Intestinal ischemia/bleeding
• Livedo reticularis
• Myopathy
• Mononeuropathy

Table 16.12 ARF. Renal vasculitis

Wegener’s granulomatosis
Poliarteritis nodosa
Henoch Scholen purpura
Tissue Ig A
Pulse steroids
Cryoglobulinemia Cryos,
Steroids? Interferon? Cytox?
Hypersensitivity Vasculitis
Skin Bx

Table 16.13 Acute tubular necrosis

Suprarenal clamp

Table 16.14 Drugs that induce renal damage

Class of drug                                                                        Damage
Diuretics, ACE, ß-blockers                                                  Decrease in renal perfusion 
NSAID’S, contrast                                                                Impaired intrarenal homodyne
Aminoglycoside, amphot                                                   Tubular toxicity 
ß-Lactams, NSAIDs, furosemide, cimetidine                  Allergic interstitial nephritis 

Radiographic contrast agents may cause ARF in patients with pre-existing renal insufficiency, diabetes mellitus, poor left ventricular function, or when multiple diagnostic procedures are done in a 24-h period.
The volume of contrast used (>1. 5 ml/kg) appears directly related to nephrotoxicity. In patients at very high risk for contrast nephropathy, nonionic contrast may be slightly less nephrotoxic [12]. However, volume expanding these high-risk patients with intravenous crystalloids is a good prophylaxis [13]. Acetylcysteine appears to offer protection against contrast toxicity [14] though its use in very high-risk patients requires further study. Most cases of contrast nephrotoxicity are nonoliguric and resolve within a few days. Rarely, a patient will require dialysis.
Rhabdomyolysis is producing ARF at an increasing rate. Drugs (e.g., heroin, cocaine, and lovastatin) and major crush injuries have joined alcohol, seizures, and muscle compression as common causes. All have the potential of producing myoglobinuria and ARF, particularly if extracellular volume depletion or shock exists simultaneously. Hyperkalemia, hyperuricemia, hyperphosphatemia, and high levels of creatine-kinase, with low Bun/Cr ratio also result. Hypocalcemia occurs early; hypercalcemia appears during recovery [15]. Dark hemepositive urine without red blood cells is a major diagnostic clue. Prophylaxis against ATN depends on aggressive intravenous crystalloids administration. The addition of mannitol and bicarbonate (1/2 NS with 12.5 g/L of mannitol and 50 mEq/L of NaHCO3
/L at 250–500 ml/h) may be a useful adjunct.

Kidney ischemic insult occurs during prolonged hypotension, suprarenal aortic or renal artery occlusion (either with clot or clamp), and sepsis. The renal tubular cells are particularly susceptible to ischemic insults because their baseline balance between oxygen supply and demand is tenuous [16]; thus, whenever systemic or intrarenal blood flow decreases slightly, ischemic insult to the tubular cell may occur. This imbalance of oxygen supply and demand may help to explain the beneficial effects attributed to loop diuretics in some studies; by inhibiting active chloride and sodium transport in the ascending limb of the loop, these agents decrease metabolic work and, therefore, oxygen requirements.
More than 50% of all cases of oliguric ARF in the hospital are due to sepsis. This condition appears related to a simultaneous decrease in systemic vascular resistance, reducing renal plasma flow and GFR. ARF occurs independently of systemic hypotension. Fever, leucocytosis, and overt signs of sepsis may be absent. A mild alteration in mental status or respiratory alkalosis may be the only clinical clue. Oliguria and or azotemia in this setting should be considered occult septicemia unless disproved. The mechanisms of ATN in sepsis are shown in Table 16.15

Table 16.15 Mechanisms of acute tubular necrosis in sepsis

SIRS/SEPSIS induce ATN               

Ischemic renal injury + cytotoxic renal injury
Cytotoxic renal injury
Potential concomitant renal insults as nephrotoxic drugs, obstructive jaundice, rhabdomyolysis, contrast agent

Ischemic renal injury
Peripheral vasodilation: increased nitric oxide, prostacyclin, activation K-ATP channels
Intrarenal vasoconstriction: endothelin, TX A2, LTC4, LTD4
Microvascular injury: cytokines, activated leucocytes, PAF, intracapillary thrombosis

Sepsis and Renal Failure
The incidence of ARF is approximately 20–25% in patients suffering sepsis; with the condition of severe sepsis the incidence of ARF exceeds 50% [17,18]. The fundamental cause of ATN in sepsis, even in the absence of hypotension, is renal hypoperfusion and ischemic injury to proximal tubular cells. An important mechanism of renal hypoperfusion is the combined effect of arterial vasodilation and intrarenal vasoconstriction. Another mechanism is intrarenal microvascular injury caused by PMN- and complement-induced endothelial injury and intravascular thrombosis [19,20].
The intrarenal vasoconstriction associated with sepsis has been ascribed to the local release of endothelial-derived vasoconstrictors, including endothelin, thromboxane A2, and leukotrienes [21]. Renal hypoperfusion also increases renal susceptibility to superimposed nephrotoxic events, which are common in septic patients. Acute renal failure in sepsis is more often part of the multiorgan dysfunction syndrome (MODS) associated with sepsis. MODS is caused by diffuse microvascular injury, which leads to inadequate perfusion and hypoxia of the lung, heart, liver, and other organs.

Other Causes of Acute Renal Failure
Acute renal failure in pregnancy has declined markedly from years 1950 to 1990, from approximately 1/1,390 pregnancies to 1/20,000 pregnancies. It is generally associated with volume depletion (hyperemesis gravidarium, hemorrhage), preeclampsia or eclampsia (with a higher incidence of RCN), HELLP syndrome, acute fatty liver of pregnancy, and idiopathic postpartum renal failure.
Acute renal failure caused by nonsteroidal anti-inflammatory drugs is associated with the presence of certain risk factors such as true hypovolemia, cardiac failure, cirrhosis with ascites, and sepsis when the effective arterial blood volume is decreased; and with advanced age, chronic renal insufficiency, and diabetes when the effective arterial blood volume is normal.
Patients in ICU are at high risk for developing ATN [18].  These patients include postoperative and sepsis [22,23]. Postoperative ARF is associated with substantial increase in morbidity, length of stay in ICU and in hospital, and poor outcome (Table 16.16).
Other causes of acute renal failure in the ICU are consequences of osmotic nephropathy, i.e. with substances that are added as vehicles to drug formulations such as propylene glycol and sucrose. Other causes of osmotic nephropathy include mannitol, methanol, or ethylene glycol.

Table 16.16 Risk factors for acute tubular necrosis after surgery

Preoperatives variables
Chronic renal disease: creatinine >2mg/dl
Advanced age
Emergency surgery
Cardiac dysfunction
Diabetes mellitus
 Atherosclerotic vascular disease
Obstructive jaundice

Type of surgery

AAA repair
Post operatives variables

Cardiac dysfunction
Re-do surgery
Number of transfusions
Angiography within 24 h of surgery

Prevention of Acute Renal Failure
Because the risk and the mortality of ARF are high in critically ill patients [24,25], prevention is the better therapy. The most common risk factor is extracellular volume depletion. Volume expansion can minimize the risk of ARF from radiographic contrast agents, cisplatin, and NSAIDs. Mannitol appears to at least partially abrogate the ARF caused by rhabdomyolysis and cisplatin but not that caused by contrast agents. Limiting the dose and simultaneous exposure appears important in avoiding contrast, aminoglycoside, and cisplatin toxicity. Alkali may limit the nephrotoxicity of myoglobinuria and uric acid. Allopurinol should be used before chemotherapy, whenever tumor lysis is anticipated. Adjusting dosing interval for changes in Ccr is important to prevent aminoglycoside toxicity. Correcting hypokalemia and expanding ECV are also helpful. Positive end-expiratory pressure (PEEP), as well as high intrathoracic pressure associated with mechanical ventilator support, may compromise cardiac output and renal perfusion. If possible, PEEP should be minimized and ECV should be expanded in high-risk patients. There are animal data to suggest that high caloric nutrition may increase the risk of ARF. However, the benefits of nutritional support seem to far outweigh this risk. It appears to improve renal tubular cell regeneration and survival in patients, particularly those with several complications. Whenever possible, enteral nutrition is preferred.
Acute Renal Failure Oliguric Versus Nonoliguric
Converting oliguria to nonoliguria appears helpful. Nonoliguric patients have fewer complications, a decreased dialysis requirement, and in some studies improved survival [26] (Table 16.17). Conversion to a nonoliguria condition can often be accomplished by repleting intravascular volume (if deficient) and using high-dose loop diuretics (e.g., 200 mg i.v. of furosemide or continuous infusions at a rate of 10–40 mg/h). The diuretic may have the additional advantage of decreasing tubular cell metabolic activity, thus lessening the oxygen requirement. A renal vasodilatory dose of dopamine (0.5–2.0 µgr/Kg/min) is sometimes helpful in stimulating urine volume. However, in a recent placebo controlled trial in critically ill patients, low-dose dopamine failed to improve renal function [27]. Neither furosemide nor dopamine have any utility as prophylaxis prior to major surgery.

Table 16.17 Oliguric versus nonoliguric renal failure


Hospital days
32 (84)
15 (28)
GI bleeding
15 (39)
10 (19)
16 (42)
11 (20)
Neuro changes
19 (50)
16 (30)
19 (50)
14 (26)

Standards of Care in Renal Failure
Unfortunately, there are no specific therapies for most causes of ARF. The management of patients with oliguria or anuria needs standardization of procedures such as:
      Assessment and correction of any respiratory or circulatory impairment
      Exclude obstruction of the urinary tract
      Establish underlying cause(s)
      Manage any life-threatening consequences of renal dysfunction
      Obtain a drug history and alter prescriptions appropriately
      Correct bleeding disorders
      Prevent and/or treat infection
Dialysis Modalities in the Intensive Care Unit
Intermittent hemodialysis has been the standard therapy for many years because it is efficient, widely available, and generally well tolerated. However hemodialysis is not without potential complications, bleeding (due to heparinization) and hypotension being the most severe. The bleeding can usually be avoided by using citrate as an alternative anticoagulant. Hypotension often can be modified by fluid removal (ultrafiltration). However, the hypotension of hemodialysis is, at least in part, due to the use of bioincompatible (cellulose) dialysis membranes. Complement activation and alterations in immune function are observed when hemodialysis is performed with these dialyzers. Recent studies have established that hypotension and complement activation can be reduced by the use of more compatible polysulfone, polyacrylonitrile, or polymethylmethacrylate dialysis membranes. Most importantly, survival is improved when ARF patients are dialyzed with these biocompatible membranes in some studies [28] while in others survival did not improve, but morbidity decreased. However, the use of biocompatible membranes is recommended for ARF patients requiring hemodialysis. Peritoneal dialysis requires no anticoagulation, and its slow continuous ultrafiltration rates are well suited to patients with baseline hypotension and/or poor cardiac output. However, its utility is limited after abdominal surgery and in severe catabolic patients because of relatively slow solute removal. Continuous extracorporeal techniques for solute and fluid removal are valuable in hemodynamically unstable patients, particularly those with multiple organ failure.
During the past decade, a number of advances have been made in the field of renal replacement therapy. Clinicians have gained a better appreciation of the need for early and aggressive management of patients with renal failure in the ICU [29].
Appropriate modality and decision making at the bedside requires an understanding of the clinical spectrum of renal failure in the ICU. Uncomplicated renal failure refers to an acute and transient decline in glomerular filtration rate without clinically apparent complications. Dialytic support often is not required in patients with uncomplicated ARF or may be performed for a single indication, such as hyperkalemia. In complicated ARF, however, multiple metabolic and volume status perturbations are present; the patient is often oliguric, and the renal failure may be present in association with multiorgan dysfunction/failure. The threshold for initiation of dialysis and the choice of dialytic modality differ depending on the associated complications and comorbid conditions. Many nephrologists avoid dialysis initiation for as long as possible and the reasons are because dialysis procedure itself has associated risks (hypotension, arrythmias, vascular access) and the concern that dialysis may delay recovery of renal function [30]. This contention is supported by animal data in which hypotension resulted in recurrent renal ischemia and by human studies that showed a decline in the GFR during and after the intermittent hemodialysis session [31–33].
In the critically ill patient ARF usually does not occur in isolation from other organ system dysfunction and therefore providing dialysis can be viewed as a form of renal support for multiorgan dysfunction rather than renal replacement.
In the presence of oliguric renal failure, administration of a large volume of fluid to patients with MODS may lead to impaired oxygenation. In such a setting, early intervention with extracorporeal therapies for management of fluid balance may significantly impact the function of other organs, even in the absence of traditional indices of renal failure such as marked azotemia.
Renal Support Versus Renal Replacement
In renal support the purpose is to support other organs, ; the timing of intervention is based on individualized need; the indications for dialysis is broad and the dialysis dose is targeted for overall support. In contrast, the purpose of renal replacement therapy is to replace renal function; , the timing of intervention is based on the levels of biochemical markers; the indications of dialysis are narrow and the dialysis dose is extrapolated from end-stage renal disease.
Different modalities of renal replacement therapies and comparisons are represented in Tables.18, .19.

Table.18 Renal replacement therapy

Hemodialysis (IHD)
Ultrafiltration (SCUF)
Ultrafiltration (IUF)
Peritoneal (CPD)
Peritoneal (IPD)
Hemofiltration (CAVH, CVVH)
Hemodialysis (CHD)
Hemodiafiltration (CA/CVVHDF)

Table.19 Comparison of renal replacement therapies

Pore size
C ur (ml/m) (L/D)

Continuous renal replacement therapy offer some advantages:
  •  Improve hemodynamic stability
  • Allow an optimal fluid balance during gradual urea removal
  • Permits a supply of virtually unlimited amounts of alimentation

The main disadvantages are:
  • Patient immobilization
  • Side effect from lactate-containing dialysate formulas
  • Risk for hypophosphatemia, hypomagnesemia, and hypokalemia

Evidence-Based Selection of Dialysis Modality
Unfortunately, there is no consensus regarding the timing, duration, frequency, and amount of dialysis to be administered for patients with ARF in the ICU. In practice, the modality choice is dictated by the experience of the provider and the availability of various modalities, tailored to the needs of each patient. However, continuous renal replacement therapy is indicated for patients with hemodynamic instability associated with sepsis and multiorgan failure, patients in need of aggressive nutritional support, and in patients with oliguria and volume overload resistant to diuretics. In regards to the membrane of choice, biocompatible membranes seem to be associated with improved renal recovery [34–36] and specifically polyacrylonitrile membrane is more efficient in clearing certain cytokines such as tumor necrosis factor, and interleukin (IL)-1ß and IL-6, when compared with a polysulfone or polyamide membrane. Nevertheless, human studies have shown the ability to remove cytokines during CCRT [37–40].
When considering dialysis modalities, it is important to remember that patients with ARF tend to have fluctuating body fluid composition and varying urea generation rates. Nevertheless, a number of factors are related to the dialysis dose delivered. Ronco et al. have shown that in patients treated with hemofiltration techniques, a filtration rate of 35 ml/h/kg was associated with improved 15-day survival [41,42].
According to intermittent versus continuous therapy, the data from retrospective analyses conflict with some studies that show a survival advantage and other studies that show CCRT has no advantages over conventional dialysis. A review of multiple studies showed that no survival advantage was conferred with the use of continuous therapies [43]. Although there is no definitive evidence that CCRT is superior to intermittent hemodialysis, it may be inherently invalid to make such a broad comparison. It might be more appropriate to categorize patients into subgroups. Patients with heart failure may have different outcomes with CCRT than patients with sepsis or trauma. Similarly, patients with end-stage liver disease who do not have a transplant have a poor outcome irrespective of the treatment modality used.
There are also new emerging dialysis techniques developing as continuous coupled plasma filtration and adsorption for the management of SIRS and sepsis [40].
1. Acute renal failure affects one fourth of intensive care unit patients and significantly increases morbidity and mortality, particularly in the setting of multiorgan failure and refractory hypotension.
2. Early recognition and treatment of acute renal failure may limit progression of renal dysfunction and complications.
3. Causes of acute renal failure in this setting are usually multifactorial, but often include decreased effective renal perfusion and exogenous or endogenous nephrotoxins.
4. Use of continuous renal replacement therapy provides excellent metabolic control and is particularly useful for managing volume status in critically ill patients.
5. Continuous renal replacement therapy is preferable to intermittent hemodialysis in hemodynamically unstable patients.
6. Replacement fluid composition must be individualized for each patient and adjusted as needed.

Oliguria and renal dysfunction are common in critically ill patients. In most cases the kidney is an innocent bystander affected secondarily by the primary disease process. Circulation must be corrected before any other specific intervention is started. The cause of renal dysfunction must be determined and if possible treated. There are considerable differences in opinion and practice patterns regarding indications for dialysis in the intensive care unit setting. Renal replacement therapy should be started and tailored according to the degree of biochemical derangement and the patient’s underlying condition. Most ICU patients die WITH acute renal failure, NOT FROM acute renal failure.

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