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CARDIOVASCULAR ANESTHESIA

Intravascular Volume Replacement Therapy with Synthetic Colloids: Is There an Influence on Renal Function?

Joachim Boldt, MD^*, and Hans-Joachim Priebe, FRCA

*Department of Anesthesiology and Intensive Care Medicine, Klinikum der Stadt Ludwigshafen, Ludwigshafen, Germany; and Department of Anesthesia, University Hospital, Freiburg, Germany

Address correspondence and reprint requests to Prof. Dr. Joachim Boldt, Department of Anesthesiology and Intensive Care Medicine, Klinikum der Stadt Ludwigshafen, Bremserstr. 79, D-67063 Ludwigshafen, Germany. Address e-mail to BoldtJ{at}gmx.net

	Abstract

Top Abstract Introduction Development of Renal Failure Conclusions References

 

IMPLICATIONS: Articles on volume replacement published between 1981 and 2001 were analyzed. Albumin and gelatin do not predispose to development of kidney dysfunction. Modern hydroxyethyl starch (HES) solutions can be used safely in patients without kidney dysfunction even in large doses. Safety of HES in patients with preexisting altered kidney function still remains unclear.

	Introduction

Top Abstract Introduction Development of Renal Failure Conclusions References

 
Absolute or relative blood volume deficits often occur in patients undergoing surgery and in the intensive care unit (ICU). The preoperative medical status of the patient, medication, anesthesia, surgical trauma, and inflammatory reactions may all alter intravascular volume status. Appropriate intravascular volume replacement is a fundamental component of critical care management because failure to treat hypovolemia may lead to multiple organ dysfunction syndrome or death (1).

There is controversy as to whether crystalloids or colloids are preferred for intravascular volume replacement (2–5). However, because colloids with different physicochemical characteristics are now available in several countries, a colloid versus colloid debate has been added to the already existing crystalloid versus colloid fluid replacement controversy. When synthetic colloids (e.g., dextran [DEX], gelatin, or different hydroxyethyl starch [HES] solutions) are used, side effects may occur (6).

Development of renal insufficiency after the administration of synthetic colloids has been quoted as reason for avoiding them (7–12). More than a decade ago, a review on various fluid replacement therapies in septic shock concluded that only DEX appears to be associated with the development of renal dysfunction (13). A more recently published review asked whether HES is "safe or not" (14). In this review, several adverse effects of HES were discussed, mainly those on coagulation. Adverse effects on renal function were not mentioned. Finally, the most recent review on fluid resuscitation in trauma patients discussed the pros and cons of currently available solutions (15). No cause-effect relationship was postulated between the use of any of the colloid solutions and the development of renal dysfunction.

Against this background, it is surprising to find statements such as "renal toxicity of HES is now well recognized" (16) or that the administration of even small doses of HES causes tubular lesions in patients predisposed to renal insufficiency (17). Obviously, our current understanding in this area is limited. Accordingly, this overview will briefly outline the mechanisms and causes of acute renal failure (ARF) and review whether the use of colloid solutions could alter renal function.

	Development of Renal Failure

Top Abstract Introduction Development of Renal Failure Conclusions References

 
ARF is defined as an abrupt decline in renal function, as reflected by a sudden and sustained decline in glomerular filtration rate (GFR). A clinical or laboratory marker of ARF is not usually defined. Some define ARF as the need for hemofiltration or hemodialysis, and others, as a twofold increase in serum creatinine concentration (12). The causes of ARF are classified as prerenal (renal hypoperfusion), renal (intrinsic kidney diseases), and postrenal (obstructive uropathy) (18).

Prerenal azotemia is the most common form of ARF in surgery and ICUs (19). The common denominator is a (reversible) decrease in glomerular capillary pressure, which, in turn, is a major determinant of GFR. When perfusion and oxygenation of the proximal tubule become critically reduced, impaired sodium transport, altered cell-wall integrity, cell swelling, cellular calcium influx, and, ultimately, cell death will result. Cellular integrity can be damaged by various toxins (e.g., aminoglycosides, bilirubin, or contrast media).

Who Is at Risk for Developing Renal Dysfunction?
Preexisting kidney and vascular disease, medication (e.g., angiotensin-converting enzyme [ACE] inhibitors), diabetes mellitus, unstable hemodynamics, hypothermia, hypoxia, and cardiopulmonary bypass are all contributing factors for the development of perioperative renal dysfunction (18–21). Critically ill ICU patients are at particular risk of developing renal dysfunction (22) related to hemodynamic instability, interference with the mediators of renal blood-flow autoregulation, or the use of substances that per se may impair renal function (e.g., catecholamines or aminoglycosides). After cardiac surgery with cardiopulmonary bypass, transient renal dysfunction develops in as many as 30% of patients (23), and ARF develops in 4%–15% (23,24). Because of a progressive decrease in GFR (25) and associated impaired renal compensatory mechanisms with increasing age, elderly patients are also prone to develop renal insufficiency (25,26).

How May Renal Function Be Altered by Intravascular Volume Replacement Solutions?
ARF induced by ischemia or cellular toxins is characterized by alterations in glomerular hemodynamics (18,21). A reduction in net transglomerular hydraulic pressure may be induced by an increase in proximal tubular pressure or a decrease in the hydraulic pressure in the glomerular capillary. In addition, impaired glomerular permeability and tubuloglomerular feedback activation may also lead to a reduction in GFR. Finally, back leakage of filtrate across a damaged tubular endothelium can further reduce renal excretory capacity.

The different plasma substitutes used for the treatment of hypovolemia show different physicochemical differences (Table 1). All colloids, including hyperoncotic human albumin (HA; 20% or 25%), may induce ARF by increasing the plasma colloid osmotic pressure (27). This has been termed "hyperoncotic ARF" (27). The dehydrated patient who receives considerable amounts of hyperoncotic colloids without additional crystalloids is especially at risk for developing hyperoncotic ARF.

DEX.
In humans without kidney dysfunction, 70% of IV-administered low-molecular-weight (LMW) DEX is excreted by the kidneys within 12 h (30). Older studies had linked the administration of (LWM) DEX to the development of ARF (31). The pathogenesis of DEX-related ARF appears to be multifactorial, including "hyperoncotic ARF," tubular obstruction, and direct toxicity (30,31). Renal biopsies or autopsies revealed proximal tubular cell swelling and vacuolation, termed "osmotic nephrosis" (30,32). However, these "osmotic nephrosis-like lesions" appear to be a rather unspecific phenomenon because this has also been demonstrated with substances such as mannitol, hypertonic glucose, and cyclosporin A (16). Moreover, its functional significance is questionable (30). Tubular obstruction may be another mechanism in the pathogenesis of ARF after DEX infusion (33). Clinical improvement has been documented when urine flow was increased by diuretics (34).

HES.
HES is a high polymeric glucose compound that is manufactured through hydrolysis and hydroxyethylation from the highly branched starch amylopectin. The different HES preparations are characterized by their mean molecular weight (Mw) (LMW HES, 70 kd; medium-molecular-weight [MMW] HES, 130–270 kd; high-molecular-weight HES, 450 kd), their concentration (3%, 6%, or 10%), and their degree of substitution (DS) (0.4, 0.5, 0.62, or 0.7). Current evidence indicates that the ratio of the C2/C6 hydroxyethylation also appears to be also very important for pharmacokinetic and other effects. Because the elimination of HES molecules varies with mean Mw, the DS, and the C2/C6 ratio, it is important to distinguish between the different HES preparations with regard to the different physicochemical characteristics (35).

Large HES molecules undergo hydrolytic cleavage by -amylase and are excreted in the urine, or they are phagocytosed by the reticuloendothelial system. The smaller HES molecules are eliminated by glomerular filtration. The higher the DS (0.62 and 0.7), the slower the metabolism and elimination of the molecule. It is a subject of continuing controversy as to whether the administration of HES may cause kidney dysfunction (9,11,12,17). Some histological studies have shown reversible swelling of renal tubular cells after the administration of certain HES preparations, most likely related to reabsorption of macromolecules (32). Swelling of tubular cells causes tubular obstruction and medullary ischemia, two important risk factors for the development of ARF (36).

Glomerular filtration of hyperoncotic colloid molecules causes a hyperviscous urine and a stasis of tubular flow, resulting in obstruction of the tubular lumen (37). The effective glomerular filtration pressure (P_eff) is P_eff = (P_cap - P_bow) - P_pla, where P_cap = hydrostatic capillary pressure, P_bow = hydrostatic pressure in Bowman’s space, and P_pla = plasma colloid osmotic pressure. An increase in plasma oncotic pressure by hyperoncotic colloids may be one reason for subsequent renal dysfunction (10,38). However, the precise mechanism by which HES may alter kidney function is unknown. There seems to be no relation between "osmotic nephrosis-like lesions" and kidney function (9). Whether the amount of administered HES is of importance when considering kidney dysfunction is also unknown.

In the study by Schortgen et al. (12) that considered septic patients and those in septic shock, ARF developed although the volume of administered HES (median dose, 31 mL/kg) had been less than the maximal dose recommended by the manufacturer (33 mL/kg). In a case report of a patient undergoing buccopharyngectomy, even a very small dose of 500 mL of HES (<10 mL/kg) was implicated as having caused ARF (17). Unfortunately, in several studies, the absolute amount of administered HES was not mentioned.

Studies Addressing Intravascular Volume Replacement Therapy and Renal Function
Using MEDLINE, we performed a search for human studies addressing intravascular volume replacement therapy and renal function. Key words entered were kidney, kidney function, kidney dysfunction, renal function, renal dysfunction, volume replacement, hydroxyethylstarch, dextran, gelatin, and volume therapy. Data analysis was restricted to the following kinds of publications: 1) English-language articles, 2) studies comparing the effects of different volumes of replacement strategies on renal function, and 3) only articles published between the years 1981 and 2001 (because overall perioperative anesthetic and surgical management before this time period cannot be compared with present management strategies). Not considered for analysis were review articles, case reports, and experimental and animal data, because animal data cannot necessarily be translated into clinical practice.

Fourteen studies were identified and analyzed (9,12,28,39–48) (Table 2). The first report suggesting adverse effects of HES on kidney function was a retrospective analysis in patients undergoing kidney transplantation who received HES with a high DS (0.62) (9). "Osmotic nephrosis-like lesions" were documented only in the HES-treated group. However, no adverse effects on graft function or serum creatinine concentration were observed 3 and 6 months after transplantation.

Five studies were performed in surgical patients to assess the influence of intravascular volume replacement therapy on perioperative renal function (28,42,44,47,48). Three of these studies included cardiac surgery patients and elderly patients who per se appear to be at risk to develop renal dysfunction (28,42,47). In all of these studies, HES with LMW and DS was infused. Renal function remained unchanged after HES administration in these studies.

A prospective, randomized study assessed the influence of different intravascular volume replacement regimens on renal function in elderly (>65 yr) and younger (<65 yr) patients with normal preoperative renal function undergoing major abdominal surgery (44). Six percent LMW HES (Mw, 70 kd; DS, 0.5), 6% MMW HES (Mw, 200 kd; DS, 0.5), or modified gelatin (Mw, 35 kd) was administered to maintain mean arterial blood pressure >65 mm Hg and central venous pressure between 10 and 14 mm Hg. Urinary ₁-microglobulin and N-acetyl-ß-glucosamidase concentrations, fractional sodium clearance, and creatinine clearance were measured to assess renal function. Colloids (1300–3000 mL) were infused until the first postoperative day. Neither gelatin nor the two HES preparations adversely affected renal function in these elderly surgical patients with normal preoperative renal function.

Five studies were performed with ICU patients (12,39,40,43,45). In three of these studies, HA was compared with synthetic colloids (HES and gelatin) (39,40,43). In none of these studies was any advantage of HA in comparison to an MMW HES with a low DS seen with regard to kidney function. One study comparing HES 200/0.62 and 3% fluid-modified gelatin demonstrated significant changes in kidney function after HES administration (12). In this multicenter, prospective study, patients with mild preexisting renal dysfunction who subsequently developed sepsis or septic shock were included. Median serum creatinine concentrations before volume administration were 143 and 114 mmol/L in the HES- and gelatin-treated groups, respectively. The slow degradable HES preparation, but not gelatin, was an independent risk factor for the development of ARF. However, despite a more frequent incidence of ARF in the HES-treated patients, mortality was not significantly different between groups. Whether HES preparations with different physicochemical characteristics (especially lower DS) also constitute a risk factor for the development of ARF under these circumstances is not known.

Data on the renal effects of repetitive doses of colloids are limited. Long-term (>5 days) administration of 10% HES 200/0.5 in critically ill ICU patients did not adversely affect renal function (as assessed by serum creatinine concentration, urine output, or need for hemofiltration) compared with a control group treated with 20% HA (43).

Only one study investigated nonsurgical, non-ICU patients. The renal effects of 20% HA, dextran 70, and polygeline were evaluated in cirrhotic patients with ascites undergoing paracentesis in whom volume was given IV to maintain hemodynamics (41). Six days after paracentesis, serum creatinine concentration had remained unchanged in the HA-treated group but had increased slightly in the DEX-treated (mean increase 0.06 mg/dL) and the gelatin-treated (mean increase 0.11 mg/dL) patients. However, differences between groups were not statistically significant.

Study Limitations
Almost all studies have serious methodologic limitations. First, end points of intravascular volume therapy are often not exactly defined. Either fixed amounts were administered or criteria for volume administration were very vague (e.g., "to maintain stable hemodynamics") (28).

Second, in most studies, renal function was assessed by rather insensitive variables (e.g., urine output or serum creatinine concentration). More sophisticated markers of renal dysfunction (e.g., kidney-specific proteins such as ₁-microglobulin or N-acetyl-ß-D-glucosamidase) were measured in only two studies (44,48). In both studies, HES 200/0.5 did not adversely affect kidney function.

Third, in most studies, the effect of different solutions on variables of renal function, rather than on outcome, was assessed. Those studies that investigated patient outcome did not find significant differences between different treatment groups (39–41,43,44,47,48).

Fourth, the differences in physicochemical properties between the various synthetic colloids have mostly been neglected in metaanalyses on volume replacement strategies (3–5). Because of the large variations in physicochemical properties between individual colloids (35), it is not appropriate to allocate all colloids collectively to a "colloid group" when evaluating their effects on renal function. Rapidly degradable HES preparations (DS 0.4 or 0.5) appear to have less risk for impairing renal function than HES with a high DS (0.62 or 0.7).

Fifth, unfortunately a control group is often missing in whom only crystalloids as a noncolloid plasma substitute were administered for intravascular volume therapy. Finally, we have to learn to distinguish different kinds of patients when comparing different volume replacement strategies. It is inappropriate to compare volume-replacement therapy in burned, cardiac surgery, and septic patients, because the underlying diseases markedly differ, and, subsequently, the different solutions may have different effects on renal function.

	Conclusions

Top Abstract Introduction Development of Renal Failure Conclusions References

 
There are several reasons why kidney function may worsen in the perioperative period or in the intensive care setting. These include the use of definite nephrotoxic substances or potentially nephrotoxic substances [e.g., ACE inhibitors (49) or volatile anesthetics (50)]. ARF can be prevented best by preserving organ perfusion, which, in turn, is achieved by maintaining the effective circulating volume and, hence, cardiac output.

Albumin, gelatin, and HES are the most frequently used colloids for intravascular volume replacement. Astonishingly, information on the influence of different volume replacement strategies is fairly incomplete. Albumin and gelatin do not seem to predispose to the development of ARF, although large, well controlled studies are lacking, especially in patients with deteriorated kidney function. Although HES can be used safely even in large doses in patients without altered kidney function (42), the effect of intravascular volume therapy with different HES preparations on renal function in those patients who show altered kidney function before the use of HES or who are at increased risk to develop kidney dysfunction still remains unclear. In patients with increased serum creatinine concentrations (>2–3 mg/dL), HES should be used cautiously. However, there is no study that defines a "critical" serum creatinine concentration that would contraindicate the use of HES. Nevertheless, other colloid intravascular volume-replacement regimens (gelatin or albumin) or crystalloids should be used in this situation until other data are available. The dehydrated patient who receives considerable amounts of (hyperoncotic) colloids is especially at risk for developing (hyperoncotic) ARF. Thus, it may be advisable (although not evidence based) to administer colloids in addition to, rather than in lieu of, crystalloids.

In reviewing the literature on HES and kidney function, the general recommendation that "HES should be avoided in ICUs and during the perioperative period" (17) cannot be supported. All HES preparations are not created equally. There are large differences in physicochemical properties between the first-generation HES (Mw, 450 kd; DS, 0.7 [Hetastarch]) and the newest, third-generation HES solution (Mw, 130 kd; DS, 0.4). Although promising results with this rapidly degradable HES preparation have been published regarding patients with moderate to severe kidney dysfunction showing no deterioration in kidney function (51), large, well controlled, prospective studies demonstrating no adverse effects of this HES preparations on kidney function in the critically ill are missing.

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