Type Of Acute Renal Failure Research Articles

Prospective study on immune function in renal transplant patients during perioperative period: A prospective cohort study.

Delayed graft function (DGF) is a type of acute renal failure that is closely linked to the immune system. The objective of this study is to investigate immune trends during the perioperative period of renal transplantation and compare the variations between patients with DGF and immediate graft function (IGF). A total of 48 kidney transplant patients were enrolled. Parameters including stimulated adenosine triphosphatase concentrations (sATP), nonstimulated ATP concentrations, white blood cells, and lymphocyte count were assessed. Patients were categorized into the DGF or IGF group. Clinical information and changes in immune markers were compared. Receiver operating characteristic analysis was performed to determine the sensitivity and specificity in predicting DGF. Additionally, separate immune function analyses were conducted for the 3 infection cases. Following induction immunosuppressive therapy, white blood cells, and neutrophil count showed a significant initial increase followed by a gradual decline. Lymphocyte count, nonstimulated ATP concentrations, and sATP exhibited an initial significant decrease followed by a slow recovery. Immune markers between the DGF and IGF groups were significantly different at day 4 after renal transplantation. Only sATP levels at day 4 after renal transplantation (area under the curve = 0.731, sensitivity = 0.864, specificity = 0.684) demonstrated predictive value for DGF occurrence. Among the 3 infection cases, 2 cases exhibited persistently decreased sATP levels and died within the first month and 6 months, while the remaining case showed a recovery of sATP levels at D9 and survived. These findings indicate that sATP level can potentially serve as a biomarker reflecting the impact of immunosuppressants. Poor recovery of sATP may be associated with DGF, infection, or even mortality.

Tanshinone IIA analogue 15a inhibits NLRP3-mediated inflammation by activating mitophagy in macrophages to alleviate acute tubular necrosis.

Acute tubular necrosis (ATN) is a common type of acute renal failure. Recent studies have shown that NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis in macrophages plays a crucial role in the progression of ATN. Previously, we synthesized an anti-inflammatory compound 15a based on Tanshinone IIA (Tan IIA). In the present study, we found that compound 15a exhibited a greater inhibitory effect on NLRP3-mediated pyroptosis than Tan IIA in vitro. C57BL/6 and NLRP3-knockout (NLRP3-KO) mice were intraperitoneally injected with LPS or folic acid (FA) to develop ATN. In vitro, bone marrow-derived macrophages (BMDMs) were treated with LPS for 3h and then treated with ATP for 0.5h. We explored the mechanism by which compound 15a inhibited NLRP3 inflammasome in BMDMs as well as its renal protective effect against ATN in mice. We found that compound 15a exhibited a protective effect on mitochondria and reduced the production of mitochondrial reactive oxygen species (mtROS). Moreover, we revealed that compound 15a remarkably reduced the production of mtROS by promoting mitophagy, which resulted in the inhibition of NLRP3 inflammasome to alleviates ATN in mice. In summary, compound 15a inhibited NLRP3-mediated inflammation by activating mitophagy in macrophages to alleviate ATN. Our results identified compound 15a as a promising candidate for the treatment of NLRP3-driven ATN.

Acute Renal Failure in Children at the University Hospital of Brazzaville

Introduction: Acute renal failure (ARF) is a medical emergency that does not spare children. Its interest lies in the search for etiologies and management made difficult by the poor quality of hospital technical platform in Africa. Objectives: To improve the management of ARF in children, determine its prevalence, and identify the causes and factors associated with mortality. Patients and Methods: We reviewed the records of children from one month to 17 years hospitalized between January 2016 and December 2018 in every pediatric department at the University Hospital of Brazzaville and included those whose discharge diagnosis included the item “ARF”. Study variables were age, sex, source, (para)clinical signs, stage and type of ARF, etiology and evolutionary profile. Results: Included were 18952 hospitalized children out of whose 253 had ARF 1.3%. There were 145 (57.3%) boys and 108 (42.7%) girls with an average age of 71.5 months. The mean time to consultation was 8.1 days. ARF was at failure stage in 147 cases (58.1%). It was functional in 210 cases (83.0%), out of which 95.1% resulted from severe dehydration. No extra-renal treatment was performed. Lethality was 34.4%. Hypovolemic shock (56.3%), severe sepsis (18.4%) and severe malaria (14.9%) were the main causes. Young age, provenance of the child, severe dehydration, deep coma, oligoanuria, stage of failure, hyperkalemia, absence of an extra-renal purification center were factors associated with mortality (p Conclusion: The high prevalence of ARF and its lethality requires public health actions including proper management of dehydration and malaria but also the creation of an extra-renal purification center.

Protective effects of probucol in rats with postoperative acute renal failure*

Abstract Objective We investigated the protective effect of probucol in rats with acute renal failure caused by various ischemia-reperfusion injuries (IRIs) after surgery. Methods Forty male Sprague-Dawley rats were randomly divided into a sham operation group (S group), ischemia reperfusion group (IR group), probucol low-dose treatment group (probucol + IR group 1, P+ IR 1 group; probucol 250 mg/kg intragastric administration daily), and probucol high-dose treatment group (P + IR 2 group; probucol 500 mg/kg intragastric administration daily). Rats in the S and IR groups were intragastrically administered with warm water every day. After 1 week, the kidney IRI rat models were prepared, after which the rats were fed for another week, and blood, urine, and the kidney tissue specimens were retained. A series of biochemical indices, superoxide dismutase (SOD), and malondialdehyde in the serum and kidney tissues were detected, and pathological changes in renal tissue were observed. Results Twenty-four-hour urinary protein excretion, urinary NAGase, CysC, blood urea nitrogen (BUN), and creatinine were significantly lower in the P + IR 1 and P + IR 2 groups than in the IR group (P < 0.05). Superoxide dismutase in the serum and renal tissue increased significantly, malondialdehyde decreased significantly (P < 0.05), renal pathological injury was alleviated, and the kidney index improved significantly (P < 0.05). Conclusion Probucol can relieve various types of acute renal failure in postoperative rats.

Contrast-Induced Nephropathy Is Less Common in Patients with Good Coronary Collateral Circulation

Background/Aims: Contrast-induced nephropathy (CIN) is a typically reversible type of acute renal failure that develops after exposure to contrast agents; underlying endothelial dysfunction is thought to be an important risk factor for CIN. Although the mechanism of coronary collateral circulation (CCC) is not fully understood, a pivotal role of the endothelium has been reported in many studies. The aim of this study was to investigate whether there is a relationship between CCC and CIN. Methods: Patients with at least one occluded major coronary artery and blood creatinine analyses performed before and on the second day after angiography were included in the study. CIN was defined as a 25% or greater elevation of creatinine on the second day after exposure to the contrast agent. Collateral grading was performed according to the Rentrop classification. Patients were grouped according to whether they developed CIN or not, i.e., CIN(-) and CIN(+) group. Results: A total of 214 patients who met the inclusion criteria were included in the study. CIN was diagnosed in 43 patients (20.1%) in the study population. Good CCC was identified in 112 patients (65.5%) in the CIN(-) group, whereas it was identified in 13 patients (30.2%) in the CIN(+) group. In the CIN(-) group, good CCC was significantly more frequent (p < 0.001). Furthermore, collateral circulation was an independent predictor of CIN. Conclusion: Good collateral circulation was associated with a lower frequency of CIN, and poor collateral circulation was an independent predictor of CIN.

Acute Renal Failure in the Neonate.

Acute renal failure (ARF) is a common disorder in high-risk neonates. ARF may be oliguric or nonoliguric, the latter having a better prognosis. Risk factors for ARF include prematurity, respiratory and vascular disorders, heart failure, congenital uropathies, and the use of nephrotoxic drugs. Chemical analysis of urine and ultrasounds help differentiate the nature and the type of ARF: prerenal, intrinsic, or postrenal. Conservative management of prerenal forms of ARF consists in carefully restoring cardiac output and controlling fluid and electrolyte balances. Early relief of obstruction is mandatory in severe postrenal forms of ARF. Renal replacement therapy is often necessary when ARF is secondary to intrinsic renal damage: peritoneal dialysis is the treatment of choice. Hemodialysis and continuous venovenous hemofiltration may be used in specific cases. Overall prognosis of ARF depends on the nature and severity of the renal injury that has led to renal failure.

Acute Renal Failure in the Elderly, over the Age of 75, in the Medical and Rehabilitation Hospital of Saint-Maurice (Paris - France)

Introduction: Acute renal failure (ARF) in the elderly is a common occurrence and will increase because of the aging population. Even though the elderly can develop any type of ARF, they are more exposed to iatrogenic ones due to polymedication. Objective: To determine the frequency of the ARF in the elderly over 75, and evaluate its impact on mortality. Methods: This is a retrospective study conducted in 2011 at the medical and Rehabilitation Hospital of Saint- Maurice. Were included, all patients aged 75 and over with an ARF, hospitalized during the study period. Results: Fifty-six patients of which 23 men (41%) and 33 women (59%) were included from a total of 209 patients; a frequency of 26.8%. The mean age was of 86.5 ± 6 years. The mean creatinine clearance level was of 17.2 ± 40.8 ml/min (MDRD). Twenty-eight of our patients were on diuretics i.e. 50%. The average hospital stay was of 78 days in patients with ARF against 33 days in those who did not have ARF. We recorded 8 deaths, including six in those with acute renal failure (10.7%). Conclusion: Acute renal failure in the elderly is a common disease that is a common morbid event. Prevention relies on the preservation of the extracellular volume and should be a marker for quality health care.

Bombs and rhabdomyolysis: War leads to the discovery of a new renal disease

In the Summer of 1940, the German Luftwaffe switched its bombing targets from English airfields and aircraft factories to cities, and in September 1940 large scale air raids on London began. Shortly afterwards, a new type of acute renal failure was noticed in some of those rescued from fallen buildings.

Acute kidney injury: how do we define it?

Over recent years, there has been welcome increased interest in acute kidney injury (AKI) and its association with patient outcome. The term AKI has replaced the term acute renal failure (ARF) and encompasses all types of ARF. New definitions and staging systems for AKI have been proposed, which have stimulated a multitude of different studies to evaluate their clinical utility. These recent advances need to be communicated to the wider health care community so that we are using a shared nomenclature. In 2009 the National Confidential Enquiry into Patient Outcome and Death AKI study ('Adding Insult to Injury') announced its findings and recommendations. The report recommended that the detection of AKI and its management should be improved. These recommendations along with the adoption of the new staging systems will potentially have an impact on clinical biochemistry departments and exert an increased demand on resources. Running in parallel with these initiatives is the quest to discover novel biomarkers to detect AKI, the development and introduction of which will require laboratory support.

Kontrastmittel-induzierte Nephropathie

Contrast media induced nephropathy is a common complication, particularly in high risk patients, such as patients with chronic kidney disease (CKD) and diabetes. The majority of studies show an increased in-hospital mortality and an unfavourable long-term prognosis after manifestation of contrast media induced nephropathy. The course and the potential risk factors of this type of acute renal failure are known. Therefore, an effective prophylaxis should allow to prevent this complication. In low risk patients oral or intravenous volume expansion is probably sufficient combined with the withdrawal of non-steroidal anti-inflammatory drugs. In high risk patients additional prophylactic measures are needed but their efficacy is not clearly defined. Therefore, heterogeneous recommendations exist. Hydration reduces (afferent) renovasoconstriction, the tubuloglomerular feedback, the tubulotoxic effects of contrast media (via dilution) and the oxygen radical formation. The optimal composition, timing and amount of fluid which should be administered to the patients remain unclear. Most studies show that intravenous administration of volume is more effective than oral fluid intake. The majority of studies found a benefit of isotonic sodium bicarbonate in comparison to isotonic saline solutions, even if meta-analyses displayed only a positive trend for sodium bicarbionate due to the heterogeneity of the data. Controversies exist for N-acetylcysteine, vitamin C, fenoldopam, theophylline or statins. Due to low cost and low side effects, N-Acetylcysteine is widely used. Theophyllin (given intravenously 30 minutes before contrast media injection) is renoprotective, particularly in intensive care unit patients. Very important is the reduction of contrast media volume (if possible <30 ml for diagnostic procedures and <100 ml for interventions). Iso-osmolar and low-osmolar contrast media may have a comparable low risk for the induction of contrast media induced nephropathy. This risk is probably higher after intra-arterial as compared to intravenous administration of contrast media. Controversies exist with respect to the reduction of contrast media induced nephropathy and mortality by prophylactic hemodialysis or hemofiltration. A possible benefit of these procedures consists probably for patients with advanced chronic kidney disease (stage 5). With the further increase of investigations using contrast media, with the further increase in vascular interventions, in age and comorbidities of the patients one may suggest that the problem of contrast media induced nephropathy will further increase, despite all prophylactic procedures so far recommended.

Features and management of drug-induced renal failure

Our series on serious ADRs focusses on rare but potentially fatal drug reactions and how to recognise and avoid them. This article considers the different types of acute renal failure and the drugs commonly implicated. Copyright © 2006 Wiley Interface Ltd

Spectrum of Acute Renal Failure and Factors Predicting Its Outcome in an Intensive Care Unit in India

Identification of factors causing acute renal failure (ARF) and its associated poor prognosis in critically ill patients can help in planning strategies to prevent ARF and to prioritize the utilization of sparse and expensive therapeutic modalities. Most of the studies in such patients have been done in the developed world, and similar data from the developing world is sparse.We analyzed 45 consecutive patients who developed ARF in the intensive care unit (ICU) during a 12-month period. Demographic and detailed biochemical profile, previous chronic illness, precipitating factors, number of failed organs, type of ARF (oliguric/nonoliguric), and need for and type of renal replacement therapy (RRT) received were recorded at the time of admission to ICU and during the course of illness. The mean age of these patients was 43.1 years, with 75.6% being males. Hypotension, sepsis, and use of nephrotoxic drugs were common precipitating factors for ARF in these patients. However, multiple precipitating factors were present in the majority (80%): 81.5% had at least one organ failure prior to development of ARF, 71.1% had oliguria, and 71.1% required RRT. Intermittent hemodialysis was the most common form of RRT given. Patient mortality was 64.4%, with 15 of the 16 surviving patients becoming dialysis independent. We observed an increase in mortality from 0% to 100%, depending on the number of failed organs from one to six. On comparing the predictor outcomes between survivors and nonsurvivors by multivariate analysis, only the number of failed organs at the time of ARF (2.6 ± 0.9 vs. 4.5 ± 0.8) and serum albumin <3.0 g/dL were found to be statistically significant.To conclude, ARF in critically ill patients is multifactorial in origin and carries a high mortality. Mortality in these patients increases with increasing numbers of failed organs and with a serum albumin of <3.0 g/dL.

Review article: hepatorenal syndrome--definitions and diagnosis.

Hepatorenal syndrome (HRS) is a severe complication of cirrhosis that develops in the final phase of the disease. Two types of HRS exist. Type 1 is defined by a rapid reduction of renal function and in type 2 HRS the reduction of renal function is slowly progressive. Type 1 HRS is diagnosed when the serum creatinine level increases by more than 50% of the baseline value to above 133 micromol/L. According to the International Ascites Club, HRS is defined by the presence of five criteria: (1) severe cirrhosis; (2) glomerular hypofiltration; (3) no other functional or organic causes; (4) failure of plasma volume expansion; (5) no proteinuria. Additional diagnostic criteria may be present. The diagnosis of HRS may be difficult in patients with severe cirrhosis. Other types of acute renal failure may occur. For example, ischaemic or toxic tubular necrosis or sepsis may cause renal failure in these patients. Furthermore, uncontrolled HRS may lead to ischaemic tubular necrosis; thus, these patients must be managed as soon as possible in an intensive care unit.

Vasoactive mediators and renal haemodynamics in exertional heat stroke complicated by acute renal failure.

Although vasoactive substances may be important in the pathogenesis of some types of acute renal failure (ARF), their potential role in exertional heat stroke (ExHS) with ARF has not been explored. To evaluate whether changes in concentration of individual vasoactive mediators correlated with alterations in renal function and haemodynamics in patients with ExHS and ARF. Prospective case-control study. Systemic and renal haemodynamics, circulating vasoactive hormones and urinary vasodilator metabolites were determined in 12 military recruits who developed ExHS with ARF but without other organ failure during a three-year period. The control group consisted of 12 recruits who performed similar exercise under the same conditions without developing ExHS. There were significant elevations in circulating pressor hormones (catecholamines, renin, aldosterone and endothelin-1 (ET-1)) and significant decreases in the vasodilatory hormone prostaglandin E(2) (PGE(2)) in the acute phase of ExHS with ARF when compared to ExC. There was also a significant rise in nitric oxide metabolites (NOx) in the acute phase of ExHS. All of these abnormalities in circulating hormones returned to normal range during the recovery phase of ExHS. The ERPF correlated positively with GFR and urinary PGE(2) and negatively with plasma catecholamines, renin, ET-1 and NOx. The changes in the plasma levels of these hormones, together with enhanced NO production, may both contribute to the pathophysiology of ARF in ExHS.

Beneficial Effect of Pentoxifylline on Cisplatin-Induced Acute Renal Failure in Rabbits

Pentoxifylline (PTX) has been reported to inhibit TNF-α production and prevent several types of acute renal failure. This study was undertaken to determine the effect of PTX on the cisplatin-induced acute renal failure in rabbits. Rabbits received a single injection of cisplatin (5 mg/kg, i.p.) with or without PTX pretreatment (30 mg/kg, i.v.). Alterations in renal function, apoptotic cell death, and TNF-α mRNA expression were measured at 24 or 48 h after cisplatin injection. Cisplatin caused an increase in BUN and serum creatinine levels, a reduction in GFR, and an increase in fractional Na+ excretion. Such changes were significantly attenuated by PTX pretreatment (30 mg/kg, i.p.) 30 min before and 24 h after cisplatin injection. Morphological evaluation showed that cisplatin injection induced diffuse proximal tubular necrosis and the effect was reduced by PTX pretreatment. Cisplatin induced apoptotic cell death in renal cortex and the effect was significantly prevented by PTX. Treatment of opossum kidney cells with cisplatin resulted in cell death, which was significantly prevented by PTX. The increase in lipid peroxidation and the decrease in renal blood flow induced by cisplatin were not affected by PTX. The expression of TNF-α mRNA was increased after cisplatin injection and the effect was inhibited by PTX pretreatment. These results suggest that cisplatin-induced acute renal failure in rabbits is associated with an induction of TNF-α-mediated apoptosis, and that PTX may exert a protective effect against cisplatin nephrotoxicity by inhibiting TNF-α production.

Positive effect of the induction of p21WAF1/CIP1 on the course of ischemic acute renal failure

The p21 protein is found in the nucleus of most cells where it modulates cell cycle activity. At low levels, p21 stabilizes interactions between D cyclins and their cyclin-dependent kinases (cdks), but at high levels after induction by several different stress pathways, it causes cell cycle arrest. The p21 mRNA is induced in murine kidney after several types of acute renal failure, including cisplatin administration, ischemia-reperfusion, and ureteral obstruction. We reported that after cisplatin injection, mice with a p21 gene deletion developed much more severe renal damage than wild-type mice. To dissociate the effects of cisplatin-induced DNA damage and subsequent initiation of DNA damage-dependent cell death pathways from effects of acute renal failure, we have now examined mice after ischemia-reperfusion, a model of renal failure not associated with genotoxin-induced DNA damage early after the injury. Wild-type and p21(-/-) mice were made ischemic by clamping both renal hila for 30 or 50 minutes. At various times after reflow, mortality and parameters of renal function and morphology were quantified. Also, the nuclear proteins p21 and proliferating cell nuclear antigen (PCNA) were localized in kidney sections by immunohistochemistry. Kidney function was more impaired and mortality increased significantly in p21(-/-) mice as compared with p21(+/+) mice. We found more cell cycle activity, indicated by increased number of mitotic cells and nuclear PCNA-positive cells, in kidney of p21(-/-) mice. In this study, p21(-/-) mice were more susceptible to ischemia-induced acute renal failure, with similarly elevated levels of parameters of cell cycle activity. We propose that the increased and inappropriate cell cycle activity in kidney cells is responsible for the increased kidney impairment and mortality.

Antibodies to both ICAM-1 and LFA-1 do not protect the kidney against toxic (HgCl2) injury

The role of inflammatory leukocytes in acute renal failure (ARF) remains controversial and appears largely uninvestigated in toxic (in contrast to ischemic) ARF. Female Wistar rats were injected with monoclonal antibodies (mAbs) directed to both the leukocyte function-associated antigen 1 (LFA-1) and the intercellular adhesion molecule 1 (ICAM-1). Doses (6 mg/kg of each mAb) were given 24 hours prior to the induction of acute tubular necrosis (ATN) by mercuric chloride administration (2 mg/kg, subcutaneously, day 0) and subsequently every 48 hours. Control rats similarly received either control antibody (12 mg/kg) or vehicle prior to and following the induction of ATN. Renal function was also measured from male Lewis rats that were similarly treated with anti-adhesion antibodies during exposure to 30 minutes of unilateral renal ischemia. Injected antibodies were demonstrated on peripheral blood leukocytes (flow cytometrical detection of mouse anti-LFA-1) and on endothelium (immunohistochemical staining of mouse anti-ICAM-1) and were measured in serum (enzyme-linked immunosorbent assay). Macrophages and T cells were prominent in the kidney of control treatment rats after HgCl2 injection, but anti-adhesion treatment clearly had prevented their infiltration. Notwithstanding, renal tubular injury was equally pronounced in all mercuric chloride treatment groups and so was the decline in renal function (serum creatinine, proteinuria). Tubular epithelial cell proliferation seemed slightly less pronounced and delayed in anti-adhesion treated rats. Kidneys from ischemia exposed rats were, however, functionally protected by identical anti-ICAM-1/anti-LFA-1 treatment. Prevention of cellular infiltration by mAbs to LFA-1 and ICAM-1 has no effect on renal morphology, function, or regeneration following mercuric chloride-induced ARF in the rat. This result contrasts with the functional protection of the rat kidney to ischemia/reperfusion injury by virtue of an identical antibody treatment protocol. Resolving that controversy should bring better insight in fundamental processes underlying different types of ARF, and will be the subject of further study.

Up-Regulation of Galectin-3 in Acute Renal Failure of the Rat

Galectin-3, a multifunctional beta-galactoside-binding lectin, is known to participate in development, oncogenesis, cell-to-cell attachment, and inflammation. We studied to determine whether galectin-3 is associated with cell injury and regeneration in two types of acute renal failure (ARF), namely ischemic and toxic ARF. In ischemia/reperfusion renal injury in rats (bilateral renal pedicles clamped for 40 minutes), galectin-3 mRNA began to increase at 2 hours and extended by 6.2-fold at 48 hours (P: < 0.01 versus normal control rats), and then decreased by 28 days after injury. In addition, a significant negative correlation between galectin-3 mRNA expression and serum reciprocal creatinine was shown at 48 hours after injury (n = 13, r = -0.94, P: < 0.0001). In folic acid-induced ARF, galectin-3 mRNA was found to be up-regulated at 2 hours after injury and increased levels continued until at least 7 days post-injury. In immunohistochemistry, at 2 hours following reperfusion, galectin-3 began to develop in proximal convoluted tubules. From 6 hours up to 48 hours, galectin-3 was also found in proximal straight tubules, distal tubules, thick ascending limbs, and collecting ducts. In later stages of regeneration, galectin-3 expressions were found in macrophages. In conclusion, we demonstrated that galectin-3 expressions were markedly up-regulated in both ischemic and toxic types of ARF. Galectin-3 may play an important role in acute tubular injury and the following regeneration stage.

Differential expression of renal adenosine A 1 receptors induced by acute renal failure

The distribution of renal adenosine A 1 receptors was investigated in rats with glycerol- or mercuric chloride (HgCl 2)-induced acute renal failure. Receptors were localised by autoradiography using [ 3H]8-cyclopentyl-1,3-dipropylxanthine ([ 3H]DPCPX), a selective A 1 adenosine receptor antagonist. In saline-injected control animals, significant labelling with [ 3H]DPCPX was detected in glomeruli, the inner stripe of outer medulla, and the inner medulla. Sixteen hours following induction of glycerol-induced acute renal failure (ARF), a 34% increase in labelling in glomeruli was noted compared to saline-injected controls, and by 48 hr, glomerular labelling had increased by 200%. In addition, 48 hr following glycerol injection, significant labelling was now detected in the cortical labyrinth and medullary rays whilst, in the inner medulla, labelling had decreased by 34%. By contrast to glycerol-induced ARF, the only significant change noted 48 hr following induction of HgCl 2-induced ARF was a 39% decrease in labelling in the inner medulla. It is concluded that glycerol-induced ARF results in differential expression of renal adenosine A 1 receptors with increased expression in the cortex and reduced expression in the inner medulla. Increased density of A 1 receptors in glomeruli may account, at least in part, for the increased renal vasoconstrictor response to adenosine and depressed glomerular filtration rate noted previously in this type of acute renal failure.

Cause of Acute Tubular Necrosis Affects Its Prognosis

<h3>Background:</h3> Acute tubular necrosis (ATN) is the most common type of acute renal failure in hospitalized patients and is associated with a high morbidity and mortality. The cause of ATN can be divided into nephrotoxic, ischemic, or mixed. <h3>Objective:</h3> To test the hypothesis that the cause of ATN affects its clinical outcome. <h3>Methods:</h3> The study compares clinical outcomes of patients enrolled in the placebo arm of a multicenter, randomized, double-blinded, placebo-controlled trial of anaritide (Auriculin, synthetic atrial natriuretic peptide, Scios, Mountain View, Calif) in patients with well-defined ATN. Patients were divided prospectively into groups according to the cause of ATN: pure nephrotoxic, pure ischemic, or mixed nephrotoxic and ischemic. Outcomes of interest were dialysis-free survival and all-cause mortality on day 14 and day 21. The causal groups were compared with respect to the prevalence of several comorbidities suspected of affecting the clinical outcomes. <h3>Results:</h3> Mortality was 10% in the nephrotoxic group and 30% in the ischemic group on day 21. Dialysis-free survival was 66% in the nephrotoxic group and 41% in the ischemic group on day 21. Outcomes in the mixed and ischemic groups were similar. Compared with the nephrotoxic group, there was a significantly higher prevalence of cardiogenic shock, hypotension, sepsis, and respiratory failure and a tendency toward a higher prevalence of acute hepatic dysfunction in the ischemic group. Diabetes mellitus was more prevalent in the nephrotoxic group. Among patients with ischemic ATN, dialysisfree survival improved significantly and mortality tended to decline with advancing age. <h3>Conclusions:</h3> Among patients with ATN, those in whom renal ischemia was causative had significantly higher mortality and lower dialysis-free survival than those whose ATN was purely nephrotoxic in origin. This difference in clinical outcomes was associated with a higher prevalence of serious comorbidities in the ischemic ATN group. Advancing age was associated with improved dialysisfree survival and a tendency toward reduced mortality in patients with ischemic ATN. Arch Intern Med. 1997;157:1833-1838