|Year : 1998 | Volume
| Issue : 3 | Page : 237-246
|Prevention of Acute Renal Failure
Magdi M Hussein, Jacob M.V Mooij
Department of Nephrology and Dialysis, Al Hada Armed Forces Hospital, Taif, Saudi Arabia
Click here for correspondence address and email
|How to cite this article:|
Hussein MM, Mooij JM. Prevention of Acute Renal Failure. Saudi J Kidney Dis Transpl 1998;9:237-46
| Introduction|| |
According to figures from different parts of the world, the incidence of acute renal failure (ARF) varies from 66-254 cases per million populations per year , . ARF is hospital acquired in around 50% of the cases. Twenty-seven percent of all cases of ARF occur post-operatively. This indicates that ARF is iatrogenically induced at a high rate by modern medicine and prevention strategies are required to decrease its impact  . Classically, acute renal failure is divided into three main groups: prerenal, intrinsic renal and post-renal. Acute prerenal failure is defined as a rapidly reversible form of renal dysfunction associated with no significant renal tissue damage, which improves upon restoration of the renal perfusion  . There is a difference between prerenal and intrinsic acute renal failure since the latter is characterized by structural changes  . Therefore, It is thought that several cases in the transitional zone and Transplantation between prerenal azotemia and acute postischemic tubular necrosis might be prevented from progression to the stag of structural renal changes. Additionally, some strategies can be used for the prevention of some of the causes of intrinsic acute renal failure such as contrast-induced nephropathy and myohemoglobinuria.
We will first review the general concepts of intervention strategies to prevent acute renal failure, followed by a discussion of more specific measures in some frequently occurring syndromes.
| I. Optimal Volume Status and Circulation|| |
It might be expected that optimal hydration and renal perfusion prevents or mitigates any deleterious effect of an ischemic and/or toxic insult imposed on the kidney. This has been demonstrated in several groups of patients.
A. Patients with major surgery this has been particularly well illustrated in aortic aneurysm repair surgery  , and in surgery for obstructive jaundice  . It was shown that when volume replacement is optimal, abdominal aortic aneurysm surgery is not associated with postoperative renal insufficiency  . In patients with obstructive jaundice, there is usually depletion of the extracellular water reduction of the plasma volume  . Strict attention to pre-operative fluid balance and hydration, including intravenous fluid administration for 24 hrs prior to surgery, resulted in a lower incidence of postoperative renal failure ,, . This rule can be extended to any major surgery. In patients with pre-existing borderline renal perfusion, a minor hemodynamic change by anesthesia or blood loss may cause ischemic injury  . The role of optimal fluid administration has also been proven very useful in the prevention of post-operative anuria following kidney transplantation. The incidence of acute tubular necrosis (ATN) post-transplantation can be reduced from 30-40% to 5-15% with aggressive fluid expansion , .
B. Rhabdomyolysis and hemolysis it also has been repeatedly demonstrated that in the absence of hypovolemia/dehydration, and aciduria, myo-and/or hemoglobin have only minimal nephrotoxic effects. There is over-whelming support for vigorous intravenous fluid therapy, often together with NaHCO 3 and mannitol, in the treatment of myohemoglobinuric renal injury. In rhaddomyolysis, a fluid resusctitation of 12 liters per day (0.51 per hour) is recommended , together with alkalinization and mannitol infusion. Similar guidelines have been previously published in this Journal  .
C. Contrast-induced nephropathy: hydration with intravenous fluids prior to exposure to contrast medium has become the standard means of preventing radio-contrast induced nephropathy (RCIN). In patients undergoing cardiac angiography, a policy of 0.45% saline at a rate of I ml/kg hour from 12 hours prior to contrast medium administration to 12 hrs after the procedures has been recommended , .
D. Vigorous hydration is also being suggested to prevent cis-platinum-induced  and amphotericin-induced nephropathy  .
E. The administration of large volumes of fluid remains also the cornerstone in prevention of the tumour lysis syndrome, in combination with allopurinol and alkalinization in case of uric acid nephropathy  .
| II. Mannitol|| |
The theoretical considerations that would support the use of mannitol in impending or early renal failure are  .
a. Mannitol increases tubular flow, and thus helps washing out the sludged tubular cells and casts.
b. It decreases the swelling of tubular cells.
c. It causes renal vasodilatation.
d. As a hydroxyl radical scavenger, it can decrease oxidant stress.
However, the reports from clinical studies are controversial. For many years mannitol has been used as prophylactic measure in patients undergoing major vascular and cardiac operations as well as in surgery for obstructive jaundice. Most of the studies noted an increase in urine output, but without effect on GFR or incidence of postoperative ATN ,,, .
In preventing contrast-induced nephropathy, mannitol did not have a beneficiary effect in patients with chronic renal failure, and in patients undergoing cardiac catheterization. Mannitol in combination with hydration even increased the incidence of acute contrast nephropathy in diabetic patients compared to hydration alone , . Furthermore, there is no evidence that mannitol in its effect on preventing acute renal failure caused by amphotericin B, is superior to adequate hydration alone  .
However, in a randomized study comparing hydration alone with a combination of hydration and mannitol, the incidence of post-transplant ATN was significantly lower in the mannitol group, whether the patients were treated with cyclosporine or azathioprine  .
In addition, mannitol continues to be recommended for the treatment of severe hymolysis and rhabdomyolysis  .
Negative side-effects of mannitol include volume depletion and hypernatremia, and when retained, it can cause volume expansion, hyperoosmolality, metabolic acidosis, and even acute renal failure  .
In 1995, Lameire et al still recommended the use of prophylactic administration of mannitol in high-risk groups of patients  . However, Conger, in 1995, concluded that there was no significant beneficial effect of mannitol for prophylaxis of ARF, except in renal transplant surgery  .
| III. Loop Diuretics|| |
Oxygen utilization needed for active solute transport in the outer medulla contributes to the low oxygen tension in this area, which is already in a hypoxic state due to the counter current diffusion of oxygen (pO 2 of 10-20 mm Hg). Following an ischemic or toxic insult to the kidney, the oxygen tension in the medulla falls even further  . Loop diuretics, by inhibiting sodium and chloride reabsorption in the thick ascending limb (TAL) of the nephron, have the theoretical advantage of reducing oxygen demand, and might therefore protect the outer medulla against ischemic damage. In addition, promoting diuresis might wash out cell debris and relieve tubular obstruction.
However, clinical trials in humans have failed to show beneficial effects of diuretics for prophylaxis of acute renal failure ,, and even worsened the outcome in patients given radiocontrast media , .
Shilliday, et al recently concluded a prospective, double-blind, placebo-controlled, randomized study of 92 patients with acute renal failure  . They compared the effect of two different loop-diuretics (furosemide and torasemide, both 3 mg/kg body weight i.v. every 6 hours for 21 days) with placebo, while all the patients received at the same time lo-dose dopamine and mannitol. Although the urine output increased significantly during the first 24 hours in the patients receiving loop diuretics, this did not result in a significantly shorter duration of renal dysfunction, need for dialysis, or a lower mortality rate. The patients who responded to diuretics by increasing urine output were those with a lesser degree of renal failure and had lower apache score.
The reason for this negative effect of diuretics might be the fact that acute renal failure mostly occurs in the setting of a multiple-organ failure, of which the underlying disease primarily determines the outcome. However, the conversion of oliguric into non-oliguric ARF might be helpful in improving fluid balance, despite the lack of influence on outcome  .
| IV. Dopamine|| |
An extensive review on this subject was given by Denton, Chertow and Brady  . Dopamine augments renal blood flow (RBF), glomerular filtration rate (GFR), natriuresis and diuresis in healthy humans and experimental animals and limits ATP utilization and oxygen requirements in nephron segments at high risk for ischemic injury. Low dose of dopamine augments RBF, GFR and natriuresis in experimental models of ischemic and nephrotoxic ARF. The augmentation of RBF is caused by intrarenal vasodilatation, the natriuretic effect by attenuating tubular reabsorption of sodium, in large part by inhibiting Na-KATPase activity in proximal tubules, thick ascending limb (TAL) and cortical collecting tubules. Dopamine might prevent or limit further injury by improving RBF and oxygenation and increasing diuresis also by clearing debris from the tubular lumen. However, in controlled clinical trials, no preventive effect of the so called renal dose of dopamine (1-3 µg/Kg/min) has so far been found on the occurrence of ARF ,,,,, .
In the early phase of ARF, dopamine coupled with furosemide, may be of benefit in improving azotemia and shortening the duration of ARF , . In a group of patients with congestive heart failure, a renoprotective action of dopamine in combination a loop diuretic (bumetanide) has been observed  . More randomized, controlled trials should be undertaken to confirm any preventive effect of dopamine alone or in combination with loop-diuretics  .
One should be aware that dopamine can give serious side effects, including gut ischemia and cardiac arrhythmias  .
| V. Calcium Channel Blockers|| |
Calcium channel blockers have been found to be beneficial in the prevention of acute tubular necrosis post-kidney transplant ,, . This is especially the case when the graft is preserved with solution containing diltiazem and the recipient receives the drug immediately post-transplant  . However, part of this effect of diltiazem might be due to interaction with cyclosporine metabolism, inducing higher cyclosporine levels and by this a higher level of immunosuppression  . Calcium channel blockers also ameliorate cyclosporine nephrotoxicity  . No significant effect of calcium channel blockers have been found in contrast-induced nephropathy  .
| VI. Atrial Natriuretic Peptides (ANP's)|| |
In experimental studies, ANP's have a well-documented protective effect in ischemic and toxic renal injuries, however, sometimes in doses causing systemic hypotension , . In humans, there is little convincing evidence that pretreatment with ANP's has any prophylactic value  . No preventive effect of atrial natriuretic peptides has been found against the occurrence of acute renal failure post cadaver kidney transplantation  . ANP's may worsen renal function post liver transplantation  .
| VII. Alkalinisation of Urine|| |
Alkalinisation of the urine has been generally found to have a positive effect in a wide range of acute renal failure. It increases the solubility of myoglobin and hemoglobin, uric acid and cystine, preventing the precipitation of these agents. The goal is achieving a urine pH of > 6.5 , . In addition, it provides a non-reabsorable solute, so increasing urine flow  . Besides this, there is non-specific protective action by solubilization of the Tamm-Horsfall protein. Precipitation of this protein might be necessary for the precipitation of other proteins such as the heme proteins. However, an alkaline urine pH will be deleterious in hyperphosphatemia, as might occur in the tumor lysis syndrome, leading to deposition of phosphate in the kidney and worsening the renal failure  .
| VIII. Prudent Use of Commonly Used Nephrotoxic Drugs|| |
A. Aminoglycosides are associated with nephrotoxicity in 10-20% of patients receiving them. Peak levels correlate with efficacy and trough levels with toxicity. A once-daily dose might take advantage of the concentration-dependent bactericidal effect as well as of less repeated exposure, so reducing nephrotoxicity , . Other risk factors for aminoglycoside toxicity include age, simultaneous administration of other nephrotoxicity entirely, is not to administer them  .
B. The use of NSAID's by their interference with prostaglandin synthesis, is associated with a significant risk of acute renal failure, accounting for 15.6% of drug-induced renal failure  , and doubling the risk for hospitalization for ARF  . Side-effects vary from reversible functional changes to severe complications such as interstitial nephritis and papillary necrosis. They should be used with caution in old age, dehydration, concurrent use of diuretics and ACE-inhibitors, pre-existing renal disease, heart failure, and diabetes mellitus. COX-2 specific drugs might offer an improved side-effects profile  .
C. Despite their major benefits in patients with hypertension, proteinuria and congestive heart failure. ACE-inhibitors are associated with acute renal failure in circumstances where renal blood supply is compromised, as in renal artery stenosis, in addition to situations characterized by volume and/or sodium depletion. Other risk factors include cardiac failure, pre-existing chronic renal failure, combined therapy with NSAID's, and diabetes mellitus , .
| IX. Future Developments?|| |
The pathophysiology of acute renal failure is characterized by persistent medullary hypoxia, caused by intrarenal vasoconstriction and medullary vascular congestion. In addition, there is increased ischemic and toxic injury to tubular cells, resulting in sublethal injury, apoptosis and necrosis  . Pathogenetic mechanisms include imbalance of endothelin and nitric oxide (NO), increased leucocyteendothelial adhesion, loss of polarity of NaK-ATPase and of integrin molecules on tubular cells. Other factors possibly involved are depletion of ARP, increase of cytosolic calcium, activation of phospholipase A2, and formation of reactive oxygen species  .
The result is back flow of glomerulus filtrate through the tubules into the interstitium and loss of cell-matrix adhesion, leading to exfoliation of epithelial cells and aberrant intra-tubular cell-cell adhesion causing intra-tubular obstruction.
Blocking the overproduction of endothelin or its effect has been reported to improve renal function following ischemic or toxic injuries  .
The action of NO is complicated as it counteracts, by the "endothelial nitric oxide synthetase" (eNOS), the vascoconstrictive action of endothelin. However, when there is an overwhelming production of NO by cytokine "inducible" nitric oxide synthetase (iNOS), it contributes to septic shock. Specific inhibition of iNOS might be an option for therapy-resistant septic shock  .
The clustering of tubular cells inside the lumen might be prevented by monoclonal inter-cellular adhesion molecules (ICAM-1) and by the arginine-glycine-aspartic acid (RGD) peptides, which bind to integrins and therefore can prevent the adhesion of tubular cells together. Experimental studies using these options have given promising results ,, .
There is also a potential role for the administration of growth factors in the prophylaxis and treatment of acute renal failure, as they stimulate epithelial cell regeneration , . Franklin et al, gave Insulin-like growth factor I (UGF-I) and placebo to 54 patients prior to aorta and renal artery surgery, which resulted in a better preserved post-operative renal function in the patients who received IGF-I  .
The role of scavengers of reactive oxygen species in patients with acute renal failure remains uncertain.
| Specific Preventive Strategies for Some Frequently Occurring Syndromes|| |
A. Radiocontrast-medium induced contrast nephropathy (RCIN)
Risk factors for radiocontrast-medium induced nephropathy (RCIN) includes: renal insufficiency, diabetes mellitus, congestive heart failure, volume depletion, and the dose of the contrast agent  . Patients without renal insufficiency are at very low risk to develop contrast-induced nephropathy 95% to 10%), even if they are diabetic. The risk begins clearly to increase with a serum creatinine of greater than 1.2 mg/dl (135 µmol/L). Approximately 20% of patients with a serum creatinine of 2.0 mg/dl (226µmol/L) are liable to develop RCIN. Diabetes mellitus is a risk factor for RCIN, but without renal insufficiency, the risk is similar to the non-diabetic group. The combination of diabetes and renal insufficiency increases the risk for RCIN at least two folds, compared to that expected with renal insufficiency alone  .
The volume of contrast media was also found to be a significant risk factor. When the contrast volume was assessed against the estimated creatinine clearance (contrast volume: creatinine clearance ratio), the risk of nephropathy was 61% for patients with a ratio > 6.0, but only 1% with a ratio < 6.0. This ratio can be used to calculate an upper limit for contrast volume and might reduce the chance of renal failure  .
The type of contrast (low versus high osmolality agents) is important in patients with serum creatinine levels greater than 1.6 mg/dl (180 µmol/l) alone or combined with diabetes mellitus , . In patients with pre-existing renal failure a 40% reduction in the incidence of RCIN has been observed when using low osmolality contrast  .
The main pathogenetic factors of RCIM include medullary ischemia based on hemodynamic changes and direct toxicity to tubular cells. Activation of the tubuloglomerular feedback (TGF) mechanism and release of the biological mediators endothelein and adenosine have recently been identified as pathogenetic factors  .
Volume repletion with its attendant down regulation of renal vasoconstriction mechanisms is the goal of prevention , . Other measures include discontinuation of diuretics 24 hours before contrast medium and the use of low osmolality contrast media in high-risk patients (patients with the combination of renal insufficiency and diabetes mellitus; hospitalized patients who have multiple risk factors). The administration of dopamine  and of theophylline, a nonselective adenosine receptor antagonist, might be considered , . The role of calcium channel blockers is uncertain.
Dialysis when instituted as soon as possible following the exposure to contrast is effective in removing the contrast medium, but it may not influence the incidence of RCIN in high-risk patients  .
B. Myo-and Haemoglobinuria
Pathogenetic factors of my-and haemoglobin associated nephropathy include vasoconstriction, heme protein cast formation, and direct tubular cytotoxcity of the heme proteins (due to iron-induced oxidant stress)  .
Although no prospective trials have confirmed this, retrospective analyses by Better et al in patients with extensive rhabdomyolysis provide overwhelming support for the use of vigorous intravenous therapy (12 liters per day)  . In the crush syndrome, the therapy should begin as soon as a trapped limb is freed, with immediately 1.5 liter of normal saline intravenously.
In addition, alkalinisation of the urine is recommended by systemic sodium bicarbonate to reach a urine pH of >6.5, which will increase the solubility of the heme proteins. Some of the bicarbonate's protection stems from its serving as a non-reabsorbable anion, which promotes diuresis  .
C. Acute Tumour Lysis Syndrome
The acute tumour lysis syndrome occurs prior to and after chemotherapy and irradiation of hematological malignancies. It consists of hyperuricemia, hyerphosphatemia, hyperkalemia, hypocalcemia, and acute renal failure.
The pathogenesis of renal failure in the acute tumor lysis syndrome is crystallization uric acid in the tubular lumina causing intratubular obstruction. When there is also massive phosphate release, intra-renal precipitation of calcium phosphate contributes to renal failure.
The mainstay for preventing renal failure in this syndrome is producing a large urine output of 3-4 liters per day, during and for 3-4 days after chemotheraphy, which washes out the excess uric acid and phosphate. In addition, the production of uric acid can be reduced by allopurinol in a dose of 400-600 mg per day for 2 days prior to chemotherapy, followed by 300 mg/day for one week  . Lower doses of allupurinol should be given to children and patients with pre-existing renal insufficiency. However, the large aquantities of hypoxanthine and xanthine, which are formed during allopurinol therapy, can occasionally cause nephropathy.
Urine alkalinisation is important to increase the solubility of uric acid, which has a pK of 5.4. However, this will at the same time accelerate the precipitation of calcium phosphate, so it cannot be recommended as a routine measure to prevent renal impairment  .
Sepsis is characterized by massive vasodilatation resulting in relative hypovolemia and hypotension. Additionally, there is extravasation of fluid in the third space, worsening these two parameters.
The lower limit of the range of autoregulation of the renal perfusion pressure is often above the one achieved in patients with septic shock. In addition, normal renal autoregulation is often lost if critically ill patients  . Vigorous fluid substitution is the first therapeutic measure to correct the hypovolemia and hypotension, often with invasive monitoring , . However, in sepsis much of the fluid is extravasated causing oedema. In addition, vasopressing catecholamines are often required. Despite their attendant risk of renal vasoconstriction and a reduction in RBF, both laboratory studies and clinical data suggest that RBF and renal function usually improve when renal perfusion pressure is augmented during shock ,, .
As mentioned earlier, dopamine is being commonly used in a "renal dose" to improve urine output. Despite its scientific rationale, no prospective randomized study has so far shown a reduction in the incidence of renal impairment ,,, .
The most important strategy in acute renal failure related to sepsis remains the treatment of the underlying disease. Trials with different monoclonal antibodies developed against cytokines involved in sepsis have been so far disappointing. However, there are experimental promising results from experimental studies of newly developed antibodies against inter-cellular adhesion molecules (UCAM-1)  and with No-inhibitors  .
| References|| |
|1.||Liano F, Pascual J. Epidemiology of acute renal failure: a prospective, multi-center, community-based study. Madrid Acute Renal Failure Study Group. Kidney Int 1996;50(3):811-8. |
|2.||Abraham G, Gupta RK, Senthiselvan A, van der Meulem J, Johny KV. Cause and prognosis of acute renal failure in Kuwait: a 2-year prospective study. J Trop med Hyg 1989;92(5):325-9. |
|3.||Lameire N, Verbeke M, Vanholder R. Prevention of clinical acute tubular necrosis with drug therapy. Nephrol Dial Transpl 1995;10(11):1992-2000. |
|4.||Bush HL Jr, Huse JB, Johnson WC, O'Hara ET, Nabseth DC. Prvention of renal insufficiency after abdominal aortic aneurysm resection by optimal volume loading. Arch Surg 1981;116:1517-24. [PUBMED] |
|5.||Diamond T, Parks RW. Perioperative management of obstructive jaundice. Br J Surg 1997;84(2):147-9. |
|6.||Sitges-Serra A, Carulla X, Piera C, et al. Body water compartments in patients with obstructive jaundice. Br J Surg 1992;79:553-6. [PUBMED] |
|7.||Parks RW, Diamons T, McCrory DC, Johnston GW, Rowlands BJ. Prospective study of postoperative renal function in obstructive jaundice and the effect of perioperative depomine. Br J Surg 1994; 81(3):437-9. |
|8.||Fogarty BJ, Parks RW, Rowlands BJ, Diamond T. Renal dysfunction in obstructive jaundice. Br J Surg 1995;82(7):877-84. |
|9.||Byrick RJ, Rose DK. Pathophysiology and prevention of acute renal failure. The role of the anaesthetist. Can J anaesth 1999;37(4pt 1):457-67. |
|10.||Carlier M, Squifflet JP, Pirson Y, et al. Confirmation of the crucial role of the recipient's maximal hydration on early diuresis of the human cadaver renal allograft. Transplantation 1983;36(4):455-6. |
|11.||Willims CD, Dawidson IJ, Dickerman R, Drake D, Sandor ZF, Trevino G. Intraoperative blood volume expansion induces primary function after renal transplantation: a study of 96 paired cadaver kidneys Transplant Proc 1991;23(1 pt 2):1338-9. |
|12.||Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhadomyolysis. N Engl J Med 1990;322(12):825-9. |
|13.||Zager RA. Rhabdomyolysis and myohemoglobinuric acute renal failure. Kidney Int 1996;49(2):314-26. |
|14.||Sheikh IA, Shaheen FA, El-Aqeil NA, AlKhader A, Karsuwa S. Acute renal failure due to rhabdomyolysis following human stampde. Saudi J Kidney Dis Transplant 1994;5(1):17-22. |
|15.||Solomon R, Wener C, Mann D, D'Elia J, Silva P. Effects of saline, mannitol, and furosemide to prevent acute decrease in renal function induced by radio contrast agents. N Engl J Med1994;31(21):1416-20. |
|16.||Solomon R. Contrast-medium-induced acute renal failure. Kidney Int 1998;53:230-42. [PUBMED] [FULLTEXT]|
|17.||Ries F, Klastersky J Nephrotoxocity induced by cancer chemotherapy with special emphasis on cisplatin toxicity. Am J Kidney Dis 1986;8(5):368-79. |
|18.||Branch RA. Prevention of amphotercin Binduced renal impairement. A review on the use of sodium supplementation. Arch Intern Med 1988;148(11):2389-94. |
|19.||Llameire N. Acute tumour lysi syndrome and the kidney (Editorial) Neth J Med 1994;45:193-7. |
|20.||Gubern JM, Sancho JJ, Simo J, Sitges-Serra A. A randomized trial on the effect of mannitol on postoperative renal function in patients with obstructive jaundice. Surgery 1988;103-39-44. |
|21.||Conger JD. Interventions in clinical acute renal failure: what are the data? Am J Kidney Dis 1995;26(4):565-76. |
|22.||Thadhani R, Pascual M, Bonventre JV. Acute renal failure. N Engl J Med 1996;334(22):1448-60. |
|23.||Dunsworth TS, Mauro LS. Drug Intelligence and Clinical Pharmacy 1988;22:327-8. |
|24.||van Valenbrg PL, Hoitsma AJ, Tiggeler RG, et al. Mannitol as an indispensable constituent of an intra-operative of acute renal failure after renal cadaveric transplantation. Transplantation 1987;44(6):784-8. |
|25.||Lieberthal W. Biology of acute renal failure: therapeutic implications. Kidney Int 1997;52:1102-15. |
|26.||Weinstein JM, Heyman S, Brezis M. Potential deleterious effect of furosemide in radio-contrast nephropathy. Nephron 1992;62(4):413-5. |
|27.||Shiliday IR, Quinn KJ, Allison ME. Loop diuretics in the management of acute renal failure: a prospective, double-blind, placebo-controlled, randomized study. Nephrol Dial Transpl 1997;12:2592-6. |
|28.||Denton MD, Chertow GM, Brady HR. "Renal-dose" dopamine for the treatment of acute renal failure: scientific rationale, experimental studies and clinical trials. Kidney Int 1996;50:4-14. [PUBMED] |
|29.||Chertow GM, Sayegh MH, Allgren RL, Lazarus JM. Is the administration of dopamine associated with adverse or favorable outcomes in acute renal failure? Auriculin Anartide Acute Renal Failure Study Group. Am J Med 1996;101(1):49-53. |
|30.||Harper L, Savage CO. The use of dopamine in acute renal failure. Clin Nephrol 1997;47(5):347-9. |
|31.||Conger J. Prophylaxis and treatment of acute renal failure by vasoactive agents: the fact and the myths. Kidney Int 1998;53(Suppl 64):S23-6. |
|32.||Lumlertgul D, Keoplung M, Sirprija V, Moollaor P, Suwangool P. Furosemide and dopamine in malarial acute renal failure. Nephron 1989;52(1):40-4. |
|33.||Varriale P, Mossavi A. The benefit of lowdose dopamine during vigorous diuresis for congestive heart failure associated with renal insufficiency: Does it protect renal function? Clin Cardiol 1997;20(7):627-30. |
|34.||Neumayer H, Kunzendorf U, Schreibeer M. Protective renal transplantaion. Kidney Int Suppl 1992;36:S87-93. |
|35.||Davidson I, Ar'rahab A. Calcium antagonists prevent cyclosporine A-induced nephrotoxicity. Inflammopharmacology 1993:2(2):159-76. |
|36.||Smits P, Huysmans F, Hoissma A, Tan A, Koene R. The effect of alpha-human atrial natriuretic peptide on the incidence of acute renal failure in cadaveric kidney transplantation. Transplant Int 1989;2:73-7. |
|37.||Kuse ER, Meyer M, Constatntin R, et al. Urodilatin (INN:ulartide). A new peptide in the treatment of acute kidney failure following liver transplantation. Anaesthesist 1996;45(4):351-8. |
|38.||Swan SK. Aminoglycoside nephrotoxicity. Semin Nephrol 1997;17(1):27-33. |
|39.||Mattie H. Efficacy and nephrotoxicity of aminoglycosides. In De Broe ME and Verpooten GA (Eds): Preventionin nephrology. Kluwer Academic Publishers. Dordrecht (The Netherlands) 1991;55-63. |
|40.||Delmas PD. Non-steroidal antiinflammatory drugs and renal function. Br J Rheumatol 1995;34(Suppl 1):25-8. [PUBMED] [FULLTEXT]|
|41.||Evans JM, McGregor E, McMahon AD, et al. Non-steroidal anti-inflammatory drugs and hospitalization for acute renal failure. AJM 1995;88(8):551-7. |
|42.||Vane JR, Botting RM. Mechanism of action of aspirin-like drugs. Semin Arthiritis Rheum1997;26(6 Suppl 1):2-10. |
|43.||Bridoux F, Hazzan M, Pallot JL, et al. Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis. Nephrol Dial Transpl 1992;7(2):100-4. |
|44.||Textor SC. Renal failure related to angiotensin-coverting enzyme inhibitors. Semin Nephrol 1997;17(1):67-76. |
|45.||Ketteler M, Cetto C, Kirdorf M, et al. Nitric oxide in sepsis syndrome: potential treatment pf septic shock by nitric oxide synthase antagonists. Kidney Int 1998;53(Suppl 64):S27-30. |
|46.||Linas SL, Whitterburg D, Parsons PE, Repine JE. Ishcemia increase neutrophilretention and worsens acute renal failure: role of oxygen metabolites and ICAM I. Kidney Int 1995;48(5):1584-91. |
|47.||Goligorsky MS, Kessler H, Romanov VI. Molecular mimiery of integrin ligation: therapeutic potential of arginine-glycyineaspartic acid (RGD) peptides. Nephrol Dial Transpl 1998;13(2):254-63. |
|48.||Wang S, Hirschberg R. Role of growth factors in the prophylaxis and treatment of acute renal failure. Kidney Int 1997;12(8):1560-3. |
|49.||Hammerman MR. Potential role of growth factors in the prophylaxis and treatment of acute renal failure. Kidney Int 1998;53(Suppl 64):S19-22. |
|50.||Franklin SC, Moulton M, Sicard GA, Hammerman MR, Miller SB. Insulin-like growth factor I preserves renal function postoperatively. Am J Physiol 1997;272: F257-9. [PUBMED] [FULLTEXT]|
|51.||Barett BJ, Parfrey PS. Prevention of nephrotoxicity induced by radiocontrast agents. N Engl J Med 1994;331(21):144950. |
|52.||Altmann DB, Zwas D, Spatz A, et al. Use of the contrast volume to estimated creatinine clearance ratio to predict renal failure after angiography. J Intervent Cardiol 1997;10(2):113-9. |
|53.||Rudnick MR, Goldfarb S, Wexler L, et al. Nephroxicity of ionic and nonimic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study. Kidney Int 1995;47(1):254-61. |
|54.||Deray g, Jacobs C. Are low osmolality contrast media less neprotoxic? Nephrol Dial Transpl 1996;11(6):930-1. |
|55.||Barrett BJ, Carlisle EJ. Metaanalysis of the relative nehrotoxicity of high-and lowosmolality iodinated contrast media. Radiology 1993;188(1):171-8. |
|56.||Morcos SK, El Nahas AM. Advances in the understanding of the nephrotoxicity of radiocontrast media. Nephron 1998;78(3):249-52. |
|57.||Katholi RE, Taylor GJ, McCann WP, et al. Nephrotoxicity from contrast media: attenuation with theophylline. Radiology 1995;195(1):17-22. |
|58.||Lehnert T, Keller E, Gondolf K, et al. Effect of haemodialysis after contrast medium administration in patients with renal insufficiency. Nephrol Dial Transpl 1998;13(2):358-62. |
|59.||ersten AD, Holt AW. Vasoactive drugs and the importance of renal perfusion pressure. New Horiz 1995;3(4):650-61. |
|60.||Klahr S, Miller SB. Current concepts: acute oliguria. N Engl J Med 1998;338(10):671-5. |
|61.||Martin C, Eon B, Saux P, Aknin P, Gouin F. Renal effects of noerpinephrine used to treat septic shock patients. Crit Care Med 1990;18(3):282-5. |
Magdi M Hussein
Department of Nephrology and Dialysis, Al Hada Armed Forces Hospital, P.O. Box 1347, Taif
| Article Access Statistics|
| Viewed||2867 |
| Printed||63 |
| Emailed||0 |
| PDF Downloaded||462 |
| Comments ||[Add] |