Pathophysiology and prevention of acute renal failure associated with thoracoabdominal or abdominal aortic surgery
1987; Elsevier BV; Volume: 5; Issue: 3 Linguagem: Inglês
10.1016/0741-5214(87)90086-3
ISSN1097-6809
AutoresD. Craig Miller, Bryan D. Myers,
Tópico(s)Cardiac, Anesthesia and Surgical Outcomes
ResumoDespite many advances in vascular surgery over the last decade, the incidence and attendant mortality of postoperative acute renal failure (ARF) have not declined substantially.1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar This is especially true for patients having surgery for ruptured aneurysms1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar and, to a lesser extent, those requiring temporary total renal ischemia (TRI), for example, resection of thoracoabdominal (TAA) or suprarenal aortic aneurysms2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar and renal revascularization procedures. For example, 7% of patients having surgery for extensive TAAs sustained ARF, that required hemodialysis (a 5% incidence for those with normal preoperative renal function but 17% for patients with preoperative renal insufficiency).2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar Rigorous, multivariate statistical analysis in this article2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar identified preoperative renal insufficiency as the only independent, significant determinant of postoperative ARF. Interestingly, the apparent association between ARF and other variables, including extent of TAA, heart disease, aortic clamp time, age, rupture, and aortic dissection was not statistically significant.2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar It is also important to realize that modern methods of supportive care (including total parenteral nutrition, optimal hemodynamic monitoring, and aggressive hemodialysis) have not lowered the high mortality that accompanies this complication1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar, 2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar, 3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 6Myers BD Carrie BJ Yee RR Hilberman M Michaels AS. Pathophysiology of hemodynamically mediated acute renal failure in man.Kidney Int. 1980; 18: 495-504Crossref PubMed Scopus (34) Google Scholar, 7Hilberman M Myers BD Carrie G Derby G Jamison RL Stinson EB. Acute renal failure following cardiac surgery.J Thorac Cardiovasc Surg. 1979; 77: 880-888PubMed Google Scholar, 8Moran SM Myers BD. Course of acute renal failure studied by a model of creatine kinetics.Kidney Int. 1985; 27: 928-937Crossref PubMed Scopus (252) Google Scholar, 9Myers BD Hilberman M Spencer RJ Jamison RL. Glomerular and tubular function in non-oliguric acute renal failure.Am J Med. 1982; 72: 642-649Abstract Full Text PDF PubMed Scopus (24) Google Scholar; indeed, such supportive measures occasionally appear only to prolong the time before a seemingly inevitable cascade of multisystem failure supervenes (frequently punctuated by overwhelming sepsis), from which the patient ultimately dies. In the experience of Crawford et al.2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar with resection of TAA, fully 67% of patients (26 of 39) with ARF died within 90 days. Therefore it is clear that prevention of ARF in such circumstances is critical to improve the overall salvage rate for these patients. Because new knowledge concerning the fundamental pathophysiology of ARF in humans has recently become available and the development of effective renal protection methods in the future will require a more complete understanding of the kidney's response to (and recovery from) injury, this overview will focus on the pathophysiology of hemodynamically mediated ARF. This background will clarify the limitations inherent in clinical “renal protection” methods used empirically today and the rationale behind more effective “renal protection” techniques of the future. It has long been appreciated that the “filtration failure” characterizing postischemic oliguric ARF (glomerular filtration rate [GFR] depressed to less than 5% of normal) could not be fully explained on the basis of continued reduction of renal blood flow (RBF), since RBF was only depressed to 25% to 50% of normal.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar Furthermore, biopsy and autopsy studies revealed that the histologic appearance of the glomeruli was uniformly unremarkable; conversely, marked abnormalities in tubular morphology and interstitial edema were present, usually in a rather heterogenous pattern. These findings led Oliver et al.10Oliver J MacDowell M Tracy A. Pathogenesis of acute renal failure associated with traumatic and toxic injury, renal ischemia, nephrotoxic damage, and the ischemuric episode.J Clin Invest. 1951; 30: 1305-1351Crossref Google Scholar to propose that the cause of oliguria in ARF was intraluminal tubular obstruction due to tubulorrhexis with resultant transtubular back leak of tubular fluid; however, Oliver could not determine if any filtrate had actually entered the nephron in the first place. Subsequent work in animals (employing direct occlusion of renal arteries or administration of norepinephrine directly into the renal artery to induce 40 to 60 minutes of TRI) provided a suitable model of postischemic ARF, which has been studied extensively in terms of pretreatment with renal “protective agents.”11Waite RB White G Davis JH. Beneficial effects of verapamil on postischemic renal failure.Surgery. 1983; 94: 276-282PubMed Google Scholar, 12Lindner A Cutler RE Bell AJ Attenuation of nephrotoxic acute renal failure in the dog with angiotensin-converting enzyme inhibitor (SQ-20, 881).Circ Res. 1982; 51: 216-224Crossref PubMed Scopus (12) Google Scholar, 13Abbott WM Abel RM Beck CH. The reversal of renal cortical ischemia during aortic occlusion by mannitol.J Surg Res. 1974; 16: 482-487Abstract Full Text PDF PubMed Scopus (47) Google Scholar, 14Madias NE Harrington JT. Postischemic acute renal failure.in: Acute renal failure. WB Saunders, Philadelphia1983: 235-251Google Scholar, 15Hanley MJ Davidson K. Prior mannitol and furosemide infusion in a model of ischemic acute renal failure.Am J Physiol. 1981; 241: F556-F564PubMed Google Scholar, 16de Torrente A Miller PD Cronin RE Paulsen PE Erickson AL Schrier RW. Effects of furosemide and acetylcholine in norepinephrine-induced acute renal failure.Am J Physiol. 1978; 235: F131-F136PubMed Google Scholar, 17Mauk RH Patak RV Fadem SZ Lifschitz MD Stein JH. Effect of prostaglandin E administration in a nephrotoxic and a vasoconstrictor model of acute renal failure.Kidney Int. 1977; 12: 122-130Crossref PubMed Scopus (69) Google Scholar, 18Solez K D'Agostino RJ Stawowy L et al.Beneficial effect of propranolol in a histologically appropriate model of postischemic acute renal failure.Am J Physiol. 1977; 88: F163-F192Google Scholar Such “protected” experimental models of ARF are analogous to hemodynamically mediated, nonoliguric ARF in humans, which represents an attenuated form of postischemic ARF.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar Over the last decade, this nonoliguric type of ARF in humans has become more common than oliguric ARF; it is this nonoliguric form of ARF that is most frequently encountered after major vascular and cardiac surgery, assuming only a single ischemic renal insult occurs (pattern A of ARF in humans, vide infra). Investigators using these animal models have partially elucidated the complex pathophysiology of postischemic ARF.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar Tubular injury plays a key role; progressive tubular obstruction by necrotic cell debris, shed brush border, and casts lead to a rise in the upstream pressure, which in turn lowers the ultrafiltration pressure that governs the rate of formation of glomerular filtrate (Fig. 1).Second, transtubular back leak of filtrate across necrotic epithelium into the interstitium exacerbates the oligoanuria and further reduces inulin excretion. The magnitude of this transtubular back leak reflects the severity and extent of the initiating ischemic event, and restoration of tubular impermeability to inulin heralds renal recovery. Back leak is then followed by the third major factor, afferent arteriolar vasoconstriction, which further reduces the glomerular capillary hydraulic pressure and ultimately abolishes transcapillary ultrafiltration. The preglomerular vasoconstriction is believed to be mediated by the tubular injury. Acute intraluminal tubular obstruction per se has been shown recently to activate the intrarenal renin-angiotensin system. In unobstructed tubules, impaired resorption of tubular fluid by proximal tubular cells will result in increased solute delivery to the macula densa, a phenomenon known to lead to preglomerular vasoconstriction via a tubuloglomerular feedback mechanism. Thus the tubular obstruction and transtubular back leak that complicate acute tubular necrosis are the predominant causes of filtration failure and oligoanuria during the onset (hours) and early sustained phases (days) of ARF. Thereafter the extent to which preglomerular vasoconstriction persists will determine whether or not recovery ensues. Once recovery has begun, it takes many weeks before afferent arteriolar tone falls to normal levels. A progressive increase in GFR parallels the improvement in glomerular perfusion rate and ultrafiltration pressure.5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar This conceptual framework derived from animal studies has been recently corroborated at Stanford with the study of human ARF in patients undergoing suprarenal and infrarenal abdominal aortic reconstruction, resection of TAAs, and cardiac procedures. Previously it was not possible to estimate GFR because of back leak of filtered inulin out of the necrotic tubule. Back leak of p-aminohippuric acid (PAH) combined with impaired tubular secretion of this organic acid also invalidated the use of PAH clearance to determine the real renal plasma flow.4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 8Moran SM Myers BD. Course of acute renal failure studied by a model of creatine kinetics.Kidney Int. 1985; 27: 928-937Crossref PubMed Scopus (252) Google Scholar, 19Myers BD Chui F Hilberman M Michaels AS. Transtubular leakage of glomerular filtrate in human acute renal failure.Am J Physiol. 1979; 237: F319-F325PubMed Google Scholar With the use of mathematic models of creatinine kinetics and excretory dynamics of inulin and the differential clearance of macromolecules of graded size to probe the glomerular filter, some of these difficulties have been overcome.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 19Myers BD Chui F Hilberman M Michaels AS. Transtubular leakage of glomerular filtrate in human acute renal failure.Am J Physiol. 1979; 237: F319-F325PubMed Google Scholar These physiologic techniques, although too complex to describe in this brief review, have elucidated the course and pathophysiology of postischemic ARF in humans. This line of investigation has characterized three major clinical patterns of attenuated (protected) postischemic ARF in humans (Fig. 2 and Table I)3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar: pattern A (abbreviated ARF) occurs after an isolated ischemic insult to “protected” human kidneys, for example, renal ischemia during TAA resection after mannitol pretreatment.4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google ScholarTable ICharacteristic laboratory findings in studies of three patterns of human postischemic acute renal failureAbbreviated formOvert formProtracted formA1 (Maintenance phase)A2 (Recovery phase)B1(Maintenance phase)B2 (Recovery phase)C (Maintenance phase)Time after ischemia1 hr3 days7 days12 days21 daysNo. of patients159161010Cardiac index (1/min/mol2/L)NA2.52.43.1NAUrine flow rate (ml/min)3.3 ± 1.11.7 ± 0.31.6 ± 0.31.5 ± 0.10.6 ± 0.2Inulin clearance (ml/min/1.73 m2)23 ± 530 ± 312 ± 2*29 ± 35 ± 2*U/P inulin14 ± 416 ± 410 ± 122 ± 47 ± 1U/P osmolality1.15 ± 0.11.4 ± 0.11.1 ± 0.031.3 ± 0.11.0 ± 0.04Fractional Na excretion (%)13.0 ± 4.20.8 ± 0.25.1 ± 0.51.4 ± 0.68.1 ± 3.5*Indicates uncorrected for inulin back leak; assuming 50% back leak, corrected figures would be 24 and 10 ml/min/1.73 m2, respectively, for pattern B (maintenance phase) and pattern C, acute renal failure.NA = not available; U/P = urine to plasma ratio; Na = sodium.NOTE: Data are expressed as mean ± SEM and are from references 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 8Moran SM Myers BD. Course of acute renal failure studied by a model of creatine kinetics.Kidney Int. 1985; 27: 928-937Crossref PubMed Scopus (252) Google Scholar, 9Myers BD Hilberman M Spencer RJ Jamison RL. Glomerular and tubular function in non-oliguric acute renal failure.Am J Med. 1982; 72: 642-649Abstract Full Text PDF PubMed Scopus (24) Google Scholar.(Reprinted by permission of The New England Journal of Medicine, Myers BD, Moran SM. N Engl J Med 1986;314:97-105.) Open table in a new tab Pattern B (overt or sustained ARF) is associated with partial (or intermittent) renal ischemia lasting several days, as occasionally seen in patients with poor left ventricular function following cardiac surgery or resection of ruptured aneurysms.6Myers BD Carrie BJ Yee RR Hilberman M Michaels AS. Pathophysiology of hemodynamically mediated acute renal failure in man.Kidney Int. 1980; 18: 495-504Crossref PubMed Scopus (34) Google Scholar, 7Hilberman M Myers BD Carrie G Derby G Jamison RL Stinson EB. Acute renal failure following cardiac surgery.J Thorac Cardiovasc Surg. 1979; 77: 880-888PubMed Google Scholar Pattern C (protracted ARF) is the most severe form and tends to evolve into oliguric ARF. It is accompanied by extreme hyperreninemia, which probably prevents a decline in afferent arteriolar tone and hence limits kidney recovery, and is frequently fatal.5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar Persistent hemodynamic compromise resulting in ongoing partial renal ischemia is associated with pattern C ARF; frequently, a patient with pattern C ARF has sustained multiple, repetitive ischemic renal insults, for example, prolonged low cardiac output with intermittent hypotension following resection of a ruptured aneurysm (or a cardiac surgical procedure) in a patient who was initially in shock. Pattern C ARF in humans is analogous to the oliguric ARF after TRI in animals not protected with mannitol or vasodilator drugs.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar NA = not available; U/P = urine to plasma ratio; Na = sodium. NOTE: Data are expressed as mean ± SEM and are from references 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 8Moran SM Myers BD. Course of acute renal failure studied by a model of creatine kinetics.Kidney Int. 1985; 27: 928-937Crossref PubMed Scopus (252) Google Scholar, 9Myers BD Hilberman M Spencer RJ Jamison RL. Glomerular and tubular function in non-oliguric acute renal failure.Am J Med. 1982; 72: 642-649Abstract Full Text PDF PubMed Scopus (24) Google Scholar. (Reprinted by permission of The New England Journal of Medicine, Myers BD, Moran SM. N Engl J Med 1986;314:97-105.) Transtubular back leak is a prominent finding in patterns B and C ARF in humans3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 7Hilberman M Myers BD Carrie G Derby G Jamison RL Stinson EB. Acute renal failure following cardiac surgery.J Thorac Cardiovasc Surg. 1979; 77: 880-888PubMed Google Scholar and in a minority of patients with pattern A ARF who become markedly azotemic.4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar A substantial difference between patterns B and C ARF may be the extent of tubular obstruction,3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar as assessed in our studies3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar by the excretion kinetics of inulin. Peak inulin excretion time (and inulin transit time) is more prolonged in pattern C than pattern B ARF, indicating a lower velocity of tubular fluid flow in the former. This suggests a more homogeneous and generalized form of obstructive tubular injury in patients with pattern C ARF compared with the heterogeneous (or patchy) lesion in pattern B.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar All three patterns of ARF in humans probably involve afferent capillary vasoconstriction to varying degrees, but the mechanism responsible for acute hyperreninemia after transient TRI in patients with pattern A ARF4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar or in animals during partial renal ischemia (clamping of the descending thoracic aorta)20Joob AW Harman PK Kaiser DL Kron IL. The effect of renin-angiotensin system blockade on visceral blood flow during and after thoracic aortic cross-clamping.J Thorac Cardiovasc Surg. 1986; 91: 411-418PubMed Google Scholar, 21Gelman S Reves JG Fowler K Samuelson PN Lell WA Smith LR. Regional blood flow during cross-clamping of the thoracic aorta and infusion of nitroprusside.J Thorac Cardiovasc Surg. 1983; 85: 287-291PubMed Google Scholar, 22Roberts AJ Nora JD Hughes WA et al.Cardiac and renal responses to cross-clamping of the descending thoracic aorta.J Thorac Cardiovasc Surg. 1983; 86: 732-741PubMed Google Scholar may be related more to increased renal sympathetic nervous activity during surgical manipulations of the aorta and renal pedicles13Abbott WM Abel RM Beck CH. The reversal of renal cortical ischemia during aortic occlusion by mannitol.J Surg Res. 1974; 16: 482-487Abstract Full Text PDF PubMed Scopus (47) Google Scholar, 21Gelman S Reves JG Fowler K Samuelson PN Lell WA Smith LR. Regional blood flow during cross-clamping of the thoracic aorta and infusion of nitroprusside.J Thorac Cardiovasc Surg. 1983; 85: 287-291PubMed Google Scholar than to postischemic tubular damage (as in patterns B and C). Recovery from ARF (especially pattern B or C) might possibly be enhanced by pharmacologic amelioration of the hyperreninemic state, although this remains to be demonstrated. To date pretreatment with angiotensin-converting enzyme (ACE) inhibitors has provided only incomplete protection from postischemic ARF in animal models of TRI.14Madias NE Harrington JT. Postischemic acute renal failure.in: Acute renal failure. WB Saunders, Philadelphia1983: 235-251Google Scholar It does appear, however, to attenuate experimental nephrotoxic ARF.12Lindner A Cutler RE Bell AJ Attenuation of nephrotoxic acute renal failure in the dog with angiotensin-converting enzyme inhibitor (SQ-20, 881).Circ Res. 1982; 51: 216-224Crossref PubMed Scopus (12) Google Scholar In contrast to the satisfactory animal models reflecting pattern A ARF in humans, it should be emphasized that research efforts investigating the pathophysiology and treatment of postischemic ARF have been limited by the lack of a suitable animal model that simulates human pattern B or C ARF.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 6Myers BD Carrie BJ Yee RR Hilberman M Michaels AS. Pathophysiology of hemodynamically mediated acute renal failure in man.Kidney Int. 1980; 18: 495-504Crossref PubMed Scopus (34) Google Scholar, 9Myers BD Hilberman M Spencer RJ Jamison RL. Glomerular and tubular function in non-oliguric acute renal failure.Am J Med. 1982; 72: 642-649Abstract Full Text PDF PubMed Scopus (24) Google Scholar The majority of renal protection techniques used clinically today are based on empiricism,1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar, 2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar, 3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 23Ochsner JL Mills NL Gardner PA. A technique for renal preservation during suprarenal abdominal aortic operations.Surg Gynecol Obstet. 1984; 159: 388-390PubMed Google Scholar but some methods have been tested either in humans24Hilberman M Maseda J Stinson EB et al.The diuretic properties of dopamine in patients following open heart operations.Anesthesiology. 1984; 61: 489-494Crossref PubMed Scopus (64) Google Scholar or in experimental models of TRI or prolonged partial renal ischemia.11Waite RB White G Davis JH. Beneficial effects of verapamil on postischemic renal failure.Surgery. 1983; 94: 276-282PubMed Google Scholar, 12Lindner A Cutler RE Bell AJ Attenuation of nephrotoxic acute renal failure in the dog with angiotensin-converting enzyme inhibitor (SQ-20, 881).Circ Res. 1982; 51: 216-224Crossref PubMed Scopus (12) Google Scholar, 13Abbott WM Abel RM Beck CH. The reversal of renal cortical ischemia during aortic occlusion by mannitol.J Surg Res. 1974; 16: 482-487Abstract Full Text PDF PubMed Scopus (47) Google Scholar, 14Madias NE Harrington JT. Postischemic acute renal failure.in: Acute renal failure. WB Saunders, Philadelphia1983: 235-251Google Scholar, 15Hanley MJ Davidson K. Prior mannitol and furosemide infusion in a model of ischemic acute renal failure.Am J Physiol. 1981; 241: F556-F564PubMed Google Scholar, 16de Torrente A Miller PD Cronin RE Paulsen PE Erickson AL Schrier RW. Effects of furosemide and acetylcholine in norepinephrine-induced acute renal failure.Am J Physiol. 1978; 235: F131-F136PubMed Google Scholar, 17Mauk RH Patak RV Fadem SZ Lifschitz MD Stein JH. Effect of prostaglandin E administration in a nephrotoxic and a vasoconstrictor model of acute renal failure.Kidney Int. 1977; 12: 122-130Crossref PubMed Scopus (69) Google Scholar, 18Solez K D'Agostino RJ Stawowy L et al.Beneficial effect of propranolol in a histologically appropriate model of postischemic acute renal failure.Am J Physiol. 1977; 88: F163-F192Google Scholar, 20Joob AW Harman PK Kaiser DL Kron IL. The effect of renin-angiotensin system blockade on visceral blood flow during and after thoracic aortic cross-clamping.J Thorac Cardiovasc Surg. 1986; 91: 411-418PubMed Google Scholar, 21Gelman S Reves JG Fowler K Samuelson PN Lell WA Smith LR. Regional blood flow during cross-clamping of the thoracic aorta and infusion of nitroprusside.J Thorac Cardiovasc Surg. 1983; 85: 287-291PubMed Google Scholar, 22Roberts AJ Nora JD Hughes WA et al.Cardiac and renal responses to cross-clamping of the descending thoracic aorta.J Thorac Cardiovasc Surg. 1983; 86: 732-741PubMed Google Scholar, 25Coles JG Wilson GJ Sima AF et al.Intraoperative management of thoracic aortic aneurysm: experimental evaluation of perfusion cooling of the spinal cord.J Thorac Cardiovasc Surg. 1983; 85: 292-299PubMed Google Scholar, 26Lim KH Weiss M Connolly M Rose D Jacobowitz I Cummingham Jr., J Can dimethyl sulfoxide (DMSO) prolong the ischemic tolerance of the spinal cord.J Am Coll Cardiol. 1986; 7 ([Abstract]?): 162AGoogle Scholar An important fundamental and widely appreciated element of renal protection involves intravenous volume expansion (or replacement) before and after periods of TRI or renal oligemia. This tenet, coupled with the ability today to monitor and optimize systemic hemodynamics carefully in the operating room and in the intensive care unit, has probably had the greatest clinical impact in terms of minimizing ischemic renal injury.1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar, 2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar, 3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar It is equally important to avoid repetitive episodes of hypovolemia and hypotension after the initial damage, since the autoregulatory behavior of the renal circulation is lost in experimental postischemic ARF.27Kelleher SP Robinette JB Conger JD. Sympathetic nervous system in the loss of autoregulation in acute renal failure.Am J Physiol. 1984; 246: F379-F386PubMed Google Scholar Thus RBF becomes essentially pressure dependent; transient hypotension produces recurrent renal ischemia, which can then induce new episodes of tubular necrosis and/or impede healing of established damage. Such factors can presage the evolution into pattern C ARF and oliguria in humans, as noted above (Fig. 2). Paradoxically, hemodialysis (by inducing volume depletion) can be responsible for such repeated episodes of hypotension. With careful serial monitoring of creatinine clearance and urinary solute excretion, the number of dialysis treatments can be minimized. Because the renal circulation in ARF is unresponsive to norepinephrine,27Kelleher SP Robinette JB Conger JD. Sympathetic nervous system in the loss of autoregulation in acute renal failure.Am J Physiol. 1984; 246: F379-F386PubMed Google Scholar this vasoconstrictor drug can be used to prevent dialysis-induced hypotension without fear of the preexistent renal hypoperfusion becoming worse.3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar Because intravenous sodium nitroprusside (SNP) is used frequently during aortic cross-clamping to control proximal hypertension and unload the left ventricle (particularly when partial cardiopulmonary bypass or a shunt is not employed2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar), a word of caution is necessary. An elegant experiment with microspheres in dogs undergoing descending thoracic aortic cross-clamping has demonstrated conclusively that SNP administration normalized proximal hemodynamics at the expense of reducing substantially (the already low) distal mean aortic pressure (MAPd), cortical RBF (cRBF), and juxtamedullary RBF (jmRBF).21Gelman S Reves JG Fowler K Samuelson PN Lell WA Smith LR. Regional blood flow during cross-clamping of the thoracic aorta and infusion of nitroprusside.J Thorac Cardiovasc Surg. 1983; 85: 287-291PubMed Google Scholar SNP reduced MAPd by an additional 52% to 55%, cRBF by an additional 66%, and jmRBF by 77%. Distal spinal cord blood flow also fell. Although these experimental data pertain more to patients undergoing resection of descending thoracic aortic aneurysms (partial renal ischemic injury instead of TRI), these potential adverse effects of SNP may be relevant because even during resection of extensive thoracoabdominal aneurysms, some degree of renal perfusion via collateral arterial (ureteric and capsular) vessels and retrograde via the renal venous system is present. Another useful intraoperative adjunct is selective profound renal hypothermia,1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar, 2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar, 23Ochsner JL Mills NL Gardner PA. A technique for renal preservation during suprarenal abdominal aortic operations.Surg Gynecol Obstet. 1984; 159: 388-390PubMed Google Scholar a technique we have used routinely for 8 years in over 50 patients who required temporary interruption of RBF (the majority of whom were undergoing resection of TAAs). Cold (4° to 5° C) hyperosmolar crystalloid solution (with or without mannitol, heparin, or methyl prednisolone1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar, 23Ochsner JL Mills NL Gardner PA. A technique for renal preservation during suprarenal abdominal aortic operations.Surg Gynecol Obstet. 1984; 159: 388-390PubMed Google Scholar) is infused into the isolated segment of aorta via a 14-gauge catheter and a pressure bag system or directly into the renal ostia with hand-held cannulas (identical to those used to infuse cardioplegia directly into the coronary ostia). A 1000 ml bolus is infused initially, which can be followed by subsequent 500 ml reperfusions if necessary. Because oxygen consumption falls by 7% for each Celsius degree that temperature is reduced, the metabolic needs of the tubular cells are reduced by almost 50% at 30° C. Crawford et al.2Crawford ES Crawford JL Safi HJ et al.Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients.J Vasc Surg. 1986; 3: 389-404Crossref PubMed Google Scholar used this technique for the left kidney in many of their patients undergoing TAA resection; they attempted to reduce the kidney temperature to 15° C in 70 patients but accomplished this goal in only half of the cases because the volume of fluid administered was excessive or a drop in core temperature limited the amount of cold solution that could be given. Mannitol is used almost universally as a renal protective agent, and its effects have been investigated extensively.1Abbott WM Renal failure complicating vascular surgery.in: Complications in vascular surgery. Grune & Stratton, New York1980: 363-377Google Scholar, 3Myers BD Moran SM. Hemodynamically mediated acute renal failure.N Engl J Med. 1986; 314: 97-105Crossref PubMed Scopus (238) Google Scholar, 4Myers BD Miller DC Mehigan JT et al.Nature of the renal injury following total renal ischemia in man.J Clin Invest. 1984; 73: 329-341Crossref PubMed Scopus (88) Google Scholar, 5Moran SM Myers BD. Pathophysiology of protracted acute renal failure in man.J Clin Invest. 1985; 76: 1440-1448Crossref PubMed Scopus (81) Google Scholar, 6Myers BD Carrie BJ Yee RR Hilberman M Michaels AS. Pathophysiology of hemodynamically mediated acute renal failure in man.Kidney Int. 1980; 18: 495-504Crossref PubMed Scopus (34) Google Scholar, 7Hilberman M Myers BD Carrie G Derby G Jamison RL Stinson EB. Acute renal failure following cardiac surgery.J Thorac Cardiovasc Surg. 1979; 77: 880-888PubMed Google Scholar, 8Moran SM Myers BD. Course of acute renal failure studied by a model of creatine kinetics.Kidney Int. 1985; 27: 928-937Crossref PubMed Scopus (252) Google Scholar, 9Myers BD Hilberman M Spencer RJ Jamison RL. Glomerular and tubular function in non-oliguric acute renal failure.Am J Med. 1982; 72: 642-649Abstract Full Text PDF PubMed Scopus (24) Google Scholar, 13Abbott WM Abel RM Beck CH. The reversal of renal cortical ischemia during aortic occlusion by mannitol.J Surg Res. 1974; 16: 482-487Abstract Full Text PDF PubMed Scopus (47) Google Scholar, 15Hanley MJ Davidson K. Prior mannitol and furosemide infusion in a model of ischemic acute renal failure.Am J Physiol. 1981; 241: F556-F564PubMed Google Scholar Mannitol is purported to attenuate the reduction of renal cortical blood flow that occurs before, during, and after renal ischemia, while increasing glomerular ultrafiltration pressure, thereby increasing GFR. Mannitol also increases the velocity of proximal tubular fluid (filtrate) flow, thereby flushing necrotic tubular debris from nephrons, preventing or relieving tubular obstruction.15Hanley MJ Davidson K. Prior mannitol and furosemide infusion in a model of ischemic acute renal failure.Am J Physiol. 1981; 241: F556-F564PubMed Google Scholar Its free radical scavenger effects may also be influential in attenuating postischemic ARF. The mechanisms of action of furosemide15Hanley MJ Davidson K. Prior mannitol and furosemide infusion in a model of ischemic acute renal failure.Am J Physiol. 1981; 241: F556-F564PubMed Google Scholar, 16de Torrente A Miller PD Cronin RE Paulsen PE Erickson AL Schrier RW. Effects of furosemide and acetylcholine in norepinephrine-induced acute renal failure.Am J Physiol. 1978; 235: F131-F136PubMed Google Scholar (which is also widely used clinically), vasodilatory prostanoids (PGE1)17Mauk RH Patak RV Fadem SZ Lifschitz MD Stein JH. Effect of prostaglandin E administration in a nephrotoxic and a vasoconstrictor model of acute renal failure.Kidney Int. 1977; 12: 122-130Crossref PubMed Scopus (69) Google Scholar and catecholamines (dopamine HCl),24Hilberman M Maseda J Stinson EB et al.The diuretic properties of dopamine in patients following open heart operations.Anesthesiology. 1984; 61: 489-494Crossref PubMed Scopus (64) Google Scholar and beta adrenergic blockers18Solez K D'Agostino RJ Stawowy L et al.Beneficial effect of propranolol in a histologically appropriate model of postischemic acute renal failure.Am J Physiol. 1977; 88: F163-F192Google Scholar are less clearly elucidated, but their effect probably is mediated by reducing vascular resistance in the renal microvasculature and by increasing the rate of tubular fluid flow, thereby preventing tubular obstruction and increasing ultrafiltration pressure. Results with ACE inhibitors (captopril or MK-422 [enalapril])12Lindner A Cutler RE Bell AJ Attenuation of nephrotoxic acute renal failure in the dog with angiotensin-converting enzyme inhibitor (SQ-20, 881).Circ Res. 1982; 51: 216-224Crossref PubMed Scopus (12) Google Scholar, 14Madias NE Harrington JT. Postischemic acute renal failure.in: Acute renal failure. WB Saunders, Philadelphia1983: 235-251Google Scholar, 20Joob AW Harman PK Kaiser DL Kron IL. The effect of renin-angiotensin system blockade on visceral blood flow during and after thoracic aortic cross-clamping.J Thorac Cardiovasc Surg. 1986; 91: 411-418PubMed Google Scholar and angiotensin competitive blockers (saralasin)20Joob AW Harman PK Kaiser DL Kron IL. The effect of renin-angiotensin system blockade on visceral blood flow during and after thoracic aortic cross-clamping.J Thorac Cardiovasc Surg. 1986; 91: 411-418PubMed Google Scholar in models of TRI, prolonged partial renal ischemia, or nephrotoxic injury have been conflicting. Nevertheless, because primary or secondary hyperreninemia plays an important role in all three patterns of ARF in humans (especially in terms of late recovery of RBF and GFR in patients with pattern B or C ARF), this avenue of research is attractive and merits additional effort. Similarly, preliminary experimental data supporting the renal protective effects of verapamil, a calcium channel blocker, when infused directly into the renal arteries before reperfusion deserve further investigation.11Waite RB White G Davis JH. Beneficial effects of verapamil on postischemic renal failure.Surgery. 1983; 94: 276-282PubMed Google Scholar We have used intraarterial verapamil before renal reperfusion in patients requiring a period of TRI since 1982 without any untoward effects; although uncontrolled and retrospective, our limited clinical experience has been highly satisfactory. Verapamil, 5 mg, diluted in 50 ml of water with 5% dextrose is flushed directly into each renal artery ostium (or renal artery bypass graft) immediately before reperfusion. Other potentially promising methods include the use of hydroxyl and oxygen-free radical scavengers (dimethyl sulfoxide, superoxide dismutase, and mannitol) for end-organ protection before or during ischemic injury, but dimethyl sulfoxide and superoxide dismutase have been evaluated mostly in terms of spinal cord protection26Lim KH Weiss M Connolly M Rose D Jacobowitz I Cummingham Jr., J Can dimethyl sulfoxide (DMSO) prolong the ischemic tolerance of the spinal cord.J Am Coll Cardiol. 1986; 7 ([Abstract]?): 162AGoogle Scholar and myocardial preservation during ischemia. Additional experimental and clinical investigation of this class of agents may be rewarding, especially in the context of preventing reperfusion injury.
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