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PubMedDate not supplied

Pattern of acute renal failure in a tertiary hospital in the United Arab Emirates.

Acute renal failure (ARF) is a challenging problem in nephrology. To evaluate the pattern, management and outcome of ARF in our tertiary hospital, we analyzed the data of all 81 patients admitted with or developing ARF in hospital between January 2002 and June 2003. The 45 men and 36 women of mean age 56.2 +/- 21 (range 13 to 91) years were managed either on the ward (n = 48; 59%) and or in the ICU (n = 33; 41%) 10% were direct admissions to the nephrology service with ARF, and 90% developed ARF in hospital. Thirty percent were referred by oncology services and 15% by general medicine. Sepsis was the cause of ARF in 36 (44%) patients, followed by drug nephrotoxicity in 11 (14%), and obstructive uropathy in 9 (11%). Comorbid conditions were hypertension in 28 (35%); diabetes in 27 (33%); chronic renal failure, 19 (23%); ischemic heart disease 19 (23%); and liver disease 12 (15%). The most common predisposing factor was hypotension in 42 (52%), dehydration in 32 (40%), and drug nephrotoxicity in 20 (25%). Sixty patients (74%) were managed conservatively, and 21 (26%) required renal replacement therapy. The length of hospital stay was 29.5 +/- 38.4 (range 2 to 279) days. Patient survival for those managed on the ward was 71% compared to 33% for ICU patients (P <.00001). Renal survival was 83% for ward patients, compared to 48% for those in the ICU (P <.001). This study showed that majority of ARF developed in-hospital with oncology patients constituting the greatest proportion. Sepsis was the leading cause of ARF and hypotension, the main predisposing factor. Patients treated in the ICU showed a worse prognosis for both patient and renal survival.

Acute Kidney Injury↗
PubMed2006

Factors related to post-liver transplantation acute renal failure.

Acute renal failure (ARF) after liver transplantation (OLT) is a common complication with severe impact on early and late prognosis of recipients. Factors predicting its incidence have not been fully identified due to the lack of a universal standard as well as the variance of data between transplant centers. To identify factors related to post-OLT ARF, we retrospectively collected materials on 89 patients, who underwent OLT from 1999 to 2001 in our center. Factors associated with post-OLT ARF were identified using univariate logistic regression. Significant factors were then entered into a multivariate logistic regression to identify factors independently associated with post-OLT ARF. Upon univariate analysis, intraoperative volume of blood transfusion (P = .041) and duration of operation (P = .005) were significant. ARF was associated with a poor prognosis (P < .001). Only duration of operation (P = .026) was an independent factor predicting the development of ARF. In conclusion, intraoperative volume of blood transfusion and duration of operation were factors contributing to post-OLT ARF in which the duration of the operation was an independent risk factor. The incidence of post-OLT ARF greatly increased recipient mortality in the early postoperative period.

Acute Kidney Injury↗
PubMed2003

Valvular heart operation is an independent risk factor for acute renal failure.

BACKGROUND: Acute renal failure (ARF) after cardiac operation with cardiopulmonary bypass is associated with a high mortality rate. The purpose of this study was to determine and quantify whether valvular heart operation is an independent risk factor for developing ARF. METHODS: We retrospectively analyzed 5,132 consecutive patients who underwent cardiac operation involving cardiopulmonary bypass between April 1997 and March 2001. Patients with significant renal impairment (preoperative serum creatinine > 200 micromol/L) were excluded. A multivariable logistic regression model was constructed to identify independent risk factors for the postoperative development of ARF. RESULTS: In 151 (2.9%) patients ARF developed before hospital discharge. The crude incidence of ARF for isolated coronary artery bypass grafting, isolated valve(s) operation, and valve(s) with coronary artery bypass grafting operation was 1.9%, 4.4%, and 7.5%, respectively (p < 0.001). The results of the logistic regression analysis found that valve operation with or without coronary artery bypass grafting was an independent risk factor for the development of postoperative ARF (odds ratio 2.68, 95% confidence interval 1.89 to 3.79; p < 0.001). Other independent predictors of ARF were increased preoperative serum creatinine levels, urgent or emergent operation, insulin-dependent diabetes, and increased cardiopulmonary bypass time. CONCLUSIONS: Valve operation is an independent risk factor for postoperative ARF. This risk is further increased by prolonged cardiopulmonary bypass.

Acute Kidney Injury↗
PubMed1999

Response to growth hormone therapy in experimental ischemic acute renal failure.

In acute renal failure (ARF), the gene and peptide expression of insulin-like growth factor-I (IGF-I) falls. Because IGF-I is regulated by growth hormone (GH) and because kidney GH receptor expression is also attenuated in ARF, the impaired IGF-I expression may partly reflect local GH resistance. Because IGF-I treatment accelerates recovery from ARF, we determined whether high-dose GH therapy could overcome this putative GH resistance, stimulate IGF-I production, and enhance recovery. Rats with ARF were given 2.5 mg GH or vehicle (V) over 2 days, beginning 24 hours before the onset of ARF. GH prevented weight loss but did not modify the course of ARF. Next we determined whether the failure of GH to modify kidney recovery could reflect a failure to stimulate renal IGF-I gene expression. Rats were treated with GH or V over an 18-hour period beginning 1 day after the induction of ARF. Hepatic IGF-I mRNA and serum IGF-I peptide levels rose significantly with GH treatment, but the low kidney IGF-I mRNA levels did not respond. We conclude that the failure of GH to enhance recovery from ARF is caused by impaired GH-stimulated renal IGF-I production, while the maintenance of body weight likely reflects the systemic effects of the increase in hepatic IGF-I production.

Acute Kidney Injury↗
PubMed1996

Acute renal failure secondary to solid tumor renal metastases: case report and review of the literature.

Renal metastases from solid tumors to both kidneys rarely result in acute renal failure (ARF). We present a case of squamous cell pulmonary carcinoma responsible for ARF due to (1) extensive (50% to 75%) bilateral parenchymal infiltration and replacement accompanied by tissue destruction, (2) widespread vascular invasion and thrombosis resulting in ischemia, and (3) histological evidence for foci of distal intratubular obstruction and pyelonephritis. Five additional cases, including one pulmonary cancer, causing ARF from extensive tissue replacement and destruction are reviewed. In a separate case, ARF resulted from lymphatic metastases rather than from parenchymal destruction or obstruction. Common findings in all six reported cases include bilaterally enlarged kidneys and progressive oligoanuria despite correction of prerenal or postrenal conditions. In our patient and in one other prior reported case, extrarenal obstruction was not considered important because invasive therapeutic procedures were unsuccessful in reversing ARF. In one case, irradiation of kidney tumor resulted in reversal of ARF. These cases emphasize the rare potential for solid tumors to metastasize to both kidneys and result in irreversible oligoanuric ARF. A high level of suspicion is required, and an early diagnosis may result in reversible ARF if the tumor is amenable to chemotherapy or irradiation.

Acute Kidney Injury↗
PubMed1998

Feasibility of noninvasive mechanical ventilation in the treatment of acute respiratory failure in postoperative cancer patients.

PURPOSE: Patients with cancer who require mechanical ventilation have high mortality rates. Although oncological patients have multiple clinical problems, including nutritional and immunological deficiencies, added complications from mechanical ventilation by themselves may be life-threatening and may further compromise the ability of these patients to recover from an episode of acute respiratory failure (ARF). Noninvasive mechanical ventilatory support (NIMV) using positive-pressure-ventilation delivered through a mask has gained popularity for the treatment of ARF and may limit some mechanical ventilation complications. The purpose of this study was to prospectively evaluate NIMV in cancer patients with ARF. MATERIALS AND METHODS: All patients admitted to the surgical intensive care unit (SICU) at The University of Texas M.D. Anderson Cancer Center from August 1, 1994, to April 15, 1996, with hypoxemic or hypercapnic ARF were eligible for this study. NIMV was delivered with the BiPAP S/T-D (Respironics, Murrysville, PA) device. The initial settings were adjusted to achieve a tidal volume of 5 to 7 mL/kg and a SaO2 greater than 0.90. Demographic data, duration of therapy, and need for endotracheal intubation were recorded for each patient. RESULTS: Sixty patients were included in this study. There were 21 women (35%) and 39 men. The primary cancer sites of these patients were gastrointestinal (25 patients), genitourinary (15), hematological (8), lung (6), sarcoma (4), and skin (2). Fifty-three patients (88%) had hypoxemic ARF and 7 had hypercapnic ARF. The mean duration of NIMV was 1.83 days (range, 1 to 5 days) with a median of 2 days. Forty-two patients (70%) were weaned from NIMV and were spared endotracheal intubation. The remaining 18 patients deteriorated and ultimately required intubation and assisted mechanical ventilation. No complications related to the use of NIMV were seen in this study population. CONCLUSIONS: NIMV was effective in the treatment of ARF in cancer patients at our institution substantially decreasing the need for intubation. This ventilatory technique is a viable option for cancer patients with ARF.

Acute Disease↗
PubMed1998

Perioperative renal dysfunction and cardiovascular anesthesia: concerns and controversies.

In patients with renal disease undergoing cardiovascular surgery, perioperative management continues to be a challenge. Traditional answers have turned into new questions with the introduction of new agents and the redesign of old techniques. For ARF prevention, early recognition of pending deleterious compensatory changes is critical. Theoretically, therapeutic intervention designed to prevent ischemic renal failure should be designed to preserve the balance between RBF and oxygen delivery on one hand and oxygen demand on the other. Maintenance of adequate cardiac output distribution to the kidney is determined by the relative ratio of renal artery vascular resistance to systemic vascular resistance. Indeed, it should not be surprising to learn that norepinephrine (despite its vasoconstricting effect) has been reported to have no deleterious renal effects in patients with low systemic vascular resistance. Until recently, strategies for the treatment of ARF have been directed to supportive care with dialysis (to allow tubular regeneration). Various therapeutic maneuvers have been introduced in an attempt to accelerate the recovery of glomerular filtration, including dialysis, nutritional regimens, and new pharmacologic agents. A recent small prospective trial of low-dose dopamine in the prophylaxis of ARF in patients undergoing abdominal aortic aneurysm repair showed no benefit in those patients receiving dopamine. Conversely, the effects of intravenous atrial natriuretic peptide in the treatment of patients with ARF appear to offer benefit in patients with oliguria. Among 121 patients with oliguric renal failure, 63% of those who received a 24-hour infusion of atrial natriuretic peptide required dialysis within 2 weeks compared with 87% who did not. Whether this effect will be borne out in the future remains to be determined. The administration of epidermal growth factor after induction of ischemic ARF in rats has been shown to enhance tubular regeneration and accelerate recovery of kidney function. Human growth factor administration has been shown to increase GFR 130% greater than baseline in patients with chronic renal failure, but no data for clinical ARF have been reported. In addition, there have been significant improvements in dialysis technology in the treatment of ARF. Modern dialysis uses bicarbonate as a buffer as opposed to acetate, which reduces cardiovascular instability, and has more precise regulation of volume removal. Dialysate profiles and temperatures improve hemodynamics and reduce intradialytic hypotension. Techniques of hemodialysis without anticoagulation have reduced bleeding complications. Finally, dialysis membranes activate neutrophils and complement less with the biocompatible membranes used today that reduce recovery time and dialysis treatment. Evidence indicates that activation of complement and neutrophils by older dialysis membranes caused a greater incidence of hypotension, adding to ischemic renal injury. It remains to be determined whether early and frequent dialysis with biocompatible membranes, as well as other therapeutic interventions, will increase the survival of patients with perioperative ARF.

Acute Kidney Injury↗
PubMed2004

[Acute renal failure in critically-ill children. A preliminary study].

OBJECTIVE: To analyze the characteristics of acute renal failure (ARF) in critically-ill children and develop a protocol for a multicenter study. METHODS: A prospective, descriptive study was performed in four pediatric intensive care units (PICU) over 5 months. Epidemiological, clinical and laboratory data from children aged between 7 days and 16 years with ARF were analyzed. Premature neonates were excluded. RESULTS: There were 16 episodes of ARF in 14 patients and 62.5 % were male (mean 6 SD age: 50 +/- 49 months). The incidence of ARF was 2.5 % of PICU patients. The most frequent primary diseases were nephro-urological (50 %) and heart disease (31 %). The main risk factors for ARF were hypovolemia (44 %) and hypotension (37 %). Six patients (37.5 %) developed ARF following surgery (cardiac surgery in four, kidney transplantation in one and urological surgery in one). Furosemide was used in 13 patients (as continuous perfusion in nine), inotropes in nine and renal replacement therapy in 12. Medical complications were found in 94 % and some organic dysfunction was found in 81 %. The length of stay in the PICU was 21 +/- 21 days. The probability of death according to the Pediatric Risk of Mortality was 14 +/- 8 %. Five patients died (36 % of the patients and 31.2 % of ARF episodes). CONCLUSIONS: The incidence of ARF in critically-ill children is low but remains a cause of high mortality and prolonged stay in the PICU. Mortality was caused not by renal failure but by multiple organ failure.

Acute Kidney Injury↗
PubMed1980

Pathophysiology of hemodynamically mediated acute renal failure in man.

A tubular injury characterized by intraluminal obstruction and transtubular backleak of glomerular filtrate occurs in experimental acute renal failure (ARF) in animals. To determine whether these alterations also occur in human ARF, we studied 44 patients developing nonoliguric ARF following cardiac surgery. The delay in appearance of i.v. administered inulin in urine (Tu) was used as a measure of tubular fluid flow rate. Tu was not longer in 13 ARF patients than it was in control subjects (7.2 vs 9.0 min), suggesting that at least a subpopulation of tubules was widely patent. The fractional urinary dextran clearance profile (thetaD; radii, 20 to 40 A) was then determined in 20 patients with sustained ARF in whom inulin clearance averaged 11 +/- 1 ml/min/1.73 m2. A mass conservation model, which assumes that thetaD in Bowman's space in ARF is the same as that measured in controls, when applied to the experimental observations revealed that, on the average, 42% of filtered inulin was lost by transtubular backleak. A similar fractional inulin backleak (38%) persisted in 11 additional patients in whom ARF had begun to recover and in whom inulin clearance averaged 26 +/- 3 ml/min/1.73 m2. These findings suggest that in hemodynamically-mediated and nonoliguric ARF, (1) tubular obstruction is not homogeneous, and (2) backleak of glomerular filtrate contributes to but does not fully account for depression of inulin clearance.

Acute Kidney Injury↗
PubMed1985

Specific defects in insulin-mediated muscle metabolism in acute uremia.

The mechanisms underlying the abnormal insulin-mediated muscle glucose metabolism occurring in acute uremia (ARF) have not been identified. To characterize the defects, insulin dose-response curves for glucose uptake, glycogen synthesis, glucose oxidation, glycolysis, and lactate release were measured in incubated rat epitrochlearis muscles. ARF did not affect insulin sensitivity, but decreased the responsiveness to insulin of glucose uptake, glycogen synthesis, and glucose oxidation. Glycogen synthesis was subnormal at all levels of insulin and at the maximal insulin concentration; it was 54% lower in muscles of ARF compared to control rats. This inhibition of glycogen synthesis in ARF could be caused by a 23% decrease in the total activity of muscle glycogen synthase and the percentage of enzyme in the activated form. Glycogen phosphorylase activity was unchanged by ARF. ARF also increased the ratio of muscle lactate release to glucose uptake at concentrations of insulin from 10 to 10(4) microU/ml. In the absence and presence of insulin, muscle protein degradation was increased by ARF. In individual muscles incubated with insulin, the rate of proteolysis was correlated with the ratio of lactate release to glucose uptake (r = + 0.82; P less than 0.01). From the insulin dose-response relationships and changes in enzyme activities, we conclude that ARF increases protein degradation in muscle and causes abnormal insulin-mediated glucose metabolism. The abnormalities in glucose metabolism are caused by changes in post-receptor events.

Animals↗
PubMed2002

GGA proteins associate with Golgi membranes through interaction between their GGAH domains and ADP-ribosylation factors.

ADP-ribosylation factors (ARFs) are a family of small GTPases that are involved in various aspects of membrane trafficking events. These include ARF1-ARF6, which are divided into three classes on the basis of similarity in the primary structure: Class I, ARF1-ARF3; Class II, ARF4 and ARF5; and Class III, ARF6. Previous studies identified a novel family of potential ARF effectors, termed GGA1-GGA3, which interact specifically with GTP-bound ARF1 and ARF3 and are localized to the trans-Golgi network (TGN) or its related compartment(s) (GGA is an abbreviation for Golgi-localizing, gamma-adaptin ear homology domain, ARF-binding protein). In the present study we have shown that ARF proteins belonging to the three classes, ARF1, ARF5 and ARF6, can interact with all GGA proteins in a yeast two-hybrid assay, in vitro and in vivo. Segmentation of GGA proteins and isolation of GGA mutants defective in ARF binding have revealed that a limited region within the GGA homology domain, which is conserved in the GGA family, is essential for ARF binding. Expression in cells of GTPase-restricted mutants of ARF1 and ARF5 blocks dissociation of GGA proteins from membranes induced by brefeldin A. However, neither of the ARF mutants recruits GGA mutants defective in ARF binding. On the basis of these observations, we conclude that at least ARF1 (Class I) and ARF5 (Class II) in their GTP-bound state cause recruitment of GGA proteins on to TGN membranes. In contrast, on the basis of similar experiments, ARF6 (Class III) may be involved in recruitment of GGA proteins to other compartments, possibly early endosomes.

ADP-Ribosylation Factors↗
PubMed2003

Acute renal failure in the surgical setting.

Acute renal failure (ARF) is an unwelcome complication of major surgical procedures that contributes to surgical morbidity and mortality. Acute renal failure associated with surgery may account for 18-47% of all cases of hospital-acquired ARF. The overall incidence of ARF in surgical patients has been estimated at 1.2%, although is higher in at-risk groups. Mortality of patients with ARF remains disturbingly high, ranging from 25% to 90%, despite advances in dialysis and intensive care support. Appreciation of at-risk surgical populations coupled with intensive perioperative care has the capacity to reduce the incidence of ARF and by implication mortality. Developments in understanding the pathophysiology of ARF may eventually result in newer therapeutic strategies to either prevent or accelerate recovery from ARF. At present the best form of treatment is prevention. In this review the epidemiology, pathophysiology, diagnosis, treatment and possible prevention of ARF will be discussed.

Acute Kidney Injury↗
PubMed2000

A trial of thyroxine in acute renal failure.

UNLABELLED: A trial of thyroxine in acute renal failure. BACKGROUND: Acute renal failure (ARF) remains a serious medical problem with a high mortality rate. Efforts to shorten the course of ARF might reduce this mortality. Since thyroxine has been shown in experimental models to shorten the course of ARF, we designed a trial to determine if a defined course of thyroxine would alter the course or change the mortality of clinical ARF. METHODS: A prospective, randomized, placebo-controlled, double-blind trial of thyroxine was carried out in patients with ARF. End points were the percentage requiring dialysis, the percentage recovering renal function, time to recovery, and mortality. RESULTS: Fifty-nine patients were randomized to receive either thyroxine or placebo. The groups were well matched in terms of basal and entry creatinines, age, sex, APACHE II scores at entry, and percentage oliguric. Baseline thyroid functions, including T3, T4, rT3, and thyroid stimulating hormone (TSH) levels, were equal between the two groups and typical of patients with euthyroid sick syndrome. Thyroxine resulted in a progressive and sustained suppression of TSH levels in the treated group, but had no effect on any measure of ARF severity. Mortality was higher in the thyroxine group than the control group (43 vs. 13%) and correlated with suppression of TSH. CONCLUSIONS: In contrast to the beneficial effects seen in experimental ARF, thyroxine has no effect on the course of clinical ARF and could have a negative effect on outcome through prolonged suppression of TSH. Critically ill euthyroid sick patients should not be replaced with thyroid hormone.

APACHE↗
PubMed2000

Expression of apoptosis regulatory proteins in tubular epithelium stressed in culture or following acute renal failure.

BACKGROUND: While tubular cell death is a characteristic of acute renal failure (ARF), the molecular mechanisms that modulate this cell death are unclear. Cell fate in acute renal failure hinges on a balance of survival and mortality factors in a changing environment. We further explored this issue by studying selected cell death-related proteins in experimental renal failure. METHOD: The expression of genes that promote (c-myc, Bax, BclxS) or protect (Bcl2, BclxL) from cell death was studied by Northern blot, Western blot, and immunohistochemistry in murine kidneys following ARF induced by folic acid or in renal tubular epithelial cells (MCT) stressed in culture. RESULTS: Renal mRNA levels encoding for c-myc and BclxL were elevated in ARF while the Bcl2/Bax ratio was decreased (Bcl2 decreased and Bax increased; P < 0.05). Protein levels of BclxL increased and Bcl2 protein decreased. Expression of tumor necrosis factor (TNF-alpha), a mediator of ARF, was also increased. Immunohistochemistry further demonstrated that BclxL was increased in some tubuli and absent in others, while Bcl2 expression decreased diffusely. Bax staining was also patchy among tubuli and individual cells in the tubular wall and lumen. As a relative deficit of survival factors is present in ARF, MCT epithelium were deprived of serum survival factors. This resulted in apoptosis, decreased Bcl2/Bax and BclxL/Bax ratios (P < 0.05) and sensitization to TNF-alpha-induced apoptosis (P < 0.05). The latter was prevented by enforced overexpression of BclxL (P < 0.01). TNF-alpha increased the mRNA levels encoding for c-myc and decreased BclxL expression. Neither MCT cells nor the kidney expressed BclxS. CONCLUSIONS: A relative deficit of survival factors likely contributes to changes in levels of BclxL and Bax in ARF. These deficits predispose to cell death induced by persistent lethal factors such as TNF-alpha that is increased in ARF and a potential source of increased c-myc, a downstream facilitator of cell death. These findings implicate members of the Bcl2 family of proteins as regulators of tubular cell death in ARF and single them out as potential therapeutic targets.

Acute Kidney Injury↗
PubMed2003

Renal dysfunction and serious infections after open-heart surgery.

BACKGROUND: Infections and sepsis are important determinants of mortality in patients with renal dysfunction. We studied the influence of preoperative renal function or postoperative acute renal failure (ARF) on the frequency of infections after open-heart surgery. METHODS: This was a retrospective analysis of 24,660 patients undergoing open-heart surgery from 1993 to 2000. Primary outcome was occurrence of serious infections after open-heart surgery; secondary outcome was hospital mortality. RESULTS: Overall incidence of infections after open-heart surgery was 3.3%. The infection rate was higher in patients with lower preoperative creatinine clearance, ranging between 2.2% and 10.0%. Regarding postoperative ARF, the frequency of infections was 58.5% in those patients requiring dialysis vs. 23.7% in those with ARF not requiring dialysis (P < 0.001); within each subgroup, however, the infection rates were similar regardless of the baseline renal function. In patients who did not develop ARF by either of our definitions, the infection rate was 1.6%. By multivariate analysis, preoperative renal function was an independent risk factor associated with infections [odds ratio (OR) for preoperative creatinine>1.2 mg/dL, 1.3; CI, 1.1 to 1.6]. The relationship between preoperative renal function and infection prevailed even after excluding the patients with postoperative ARF. The overall morality was 2.2%; the mortality in patients with serious infection was 31.7%. CONCLUSION: Both preoperative renal dysfunction and postoperative ARF influence the frequency of serious infections after open-heart surgery. The infection rate was higher in patients with postoperative ARF regardless of the baseline renal function. However, preoperative renal dysfunction portended higher risk of infection, independent of the influence of postoperative ARF.

Acute Kidney Injury↗
PubMed2006

Urinary biochemistry and microscopy in septic acute renal failure: a systematic review.

BACKGROUND: Biochemistry and microscopy of urine are widely published diagnostic activities in patients with acute renal failure (ARF). However, their scientific basis in patients with septic ARF has not been assessed systematically. METHODS: We performed a systematic review of MEDLINE, EMBASE, CINHAL, and PubMed databases and bibliographies of retrieved articles for all studies describing urinary biochemistry, indices, and microscopy in patients with septic ARF. RESULTS: We identified 27 articles (1,432 patients). Because of substantial heterogeneity, no formal quantitative analysis could be performed. Urinary biochemistry or derived indices were reported in 24 articles (89%), and microscopy, in 7 articles (26%). The majority were small single-center reports and had serious limitations. For example, only 52% of patients were septic, only 54% of patients had ARF, many studies failed to include a control group, time from diagnosis of sepsis or ARF to measure of urinary tests was variable, and there were numerous potential confounders. Urinary sodium, fractional excretion of sodium, urinary-plasma creatinine ratio, urinary osmolality, urinary-plasma osmolality ratio, and serum urea-creatinine ratio showed variable and inconsistent results. Low-molecular-weight proteinuria was described in only 22% of articles. A few reports of urinary microscopy described muddy brown/epithelial cell casts and renal tubular cells in patients with septic ARF, whereas others described normal urinary sediment. CONCLUSION: The scientific basis for the use of urinary biochemistry, indices, and microscopy in patients with septic ARF is weak. More research is required to describe their accuracy, pattern, and time course in patients with septic ARF.

Acute Kidney Injury↗
PubMed1988

Guanine nucleotide-binding proteins that enhance choleragen ADP-ribosyltransferase activity: nucleotide and deduced amino acid sequence of an ADP-ribosylation factor cDNA.

Three (two soluble and one membrane) guanine nucleotide-binding proteins (G proteins) that enhance ADP-ribosylation of the Gs alpha stimulatory subunit of the adenylyl cyclase (EC 4.6.1.1) complex by choleragen have recently been purified from bovine brain. To further define the structure and function of these ADP-ribosylation factors (ARFs), we isolated a cDNA clone (lambda ARF2B) from a bovine retinal library by screening with a mixed heptadecanucleotide probe whose sequence was based on the partial amino acid sequence of one of the soluble ARFs from bovine brain. Comparison of the deduced amino acid sequence of lambda ARF2B with sequences of peptides from the ARF protein (total of 60 amino acids) revealed only two differences. Whether these are cloning artifacts or reflect the existence of more than one ARF protein remains to be determined. Deduced amino acid sequences of ARF, Go alpha (the alpha subunit of a G protein that may be involved in regulation of ion fluxes), and c-Ha-ras gene product p21 show similarities in regions believed to be involved in guanine nucleotide binding and GTP hydrolysis. ARF apparently lacks a site analogous to that ADP-ribosylated by choleragen in G-protein alpha subunits. Although both the ARF proteins and the alpha subunits bind guanine nucleotides and serve as choleragen substrates, they must interact with the toxin A1 peptide in different ways. In addition to serving as an ADP-ribose acceptor, ARF interacts with the toxin in a manner that modifies its catalytic properties.

ADP-Ribosylation Factors↗
PubMed1992

ADP-ribosylation factor, a small GTP-binding protein, is required for binding of the coatomer protein beta-COP to Golgi membranes.

The coatomer is a cytosolic protein complex that reversibly associates with Golgi membranes and is implicated in modulating Golgi membrane transport. The association of beta-COP, a component of coatomer, with Golgi membranes is enhanced by guanosine 5'-[gamma-thio]triphosphate (GTP[gamma S]), a nonhydrolyzable analogue of GTP, and by a mixture of aluminum and fluoride ions (Al/F). Here we show that the ADP-ribosylation factor (ARF) is required for the binding of beta-COP. Thus, beta-COP contained in a coatomer fraction that has been resolved from ARF does not bind to Golgi membranes, whereas binding can be reconstituted by the addition of recombinant ARF. Furthermore, an N-terminal peptide of ARF, which blocks ARF binding to Golgi membranes, inhibits GTP[gamma S]- as well as the Al/F-enhanced binding of beta-COP. We show that Golgi coat protein binding involves a sequential reaction where an initial interaction of ARF and GTP[gamma S] with the membrane allows subsequent binding of beta-COP to take place in the absence of free ARF and GTP[gamma S]. The fungal metabolite brefeldin A, which is known to prevent the association of coat proteins with Golgi membrane, is shown to exert this effect by interfering with the initial ARF-membrane interaction step.

ADP-Ribosylation Factors↗