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PubMed1989

Water immersion induced alterations of atrial natriuretic peptide in patients with non-inflammatory acute renal failure.

Water immersion induced alterations of plasma atrial natriuretic peptide (ANP), circulating plasma volume (PV), plasma sodium and potassium and mean blood pressure (MAP) were examined in 12 patients with non-inflammatory acute renal failure (ARF) and in 15 healthy subjects. In patients with ARF a significantly elevated basal ANP (139 +/- 13 pg/ml versus 75 +/- 4 pg/ml in normals) and elevated MAP (112 +/- 3.5 mmHg versus 87 +/- 2 mmHg in normals) were found. Water immersion induced a significant increase in plasma ANP in both groups, which was significantly more marked in healthy subjects (152 +/- 13 pg/ml) than in patients with ARF (86 +/- 13 pg/ml). Water immersion was accompanied by a significantly more marked reduction of MAP (23 +/- 3 mmHg) and plasma sodium (6.1 +/- 0.6 mmol/l) in patients with ARF than in normals (12.7 +/- 1.5 mmHg and 4.2 +/- 0.1 mmol/l respectively). In contrast to healthy subjects, in patients with ARF water immersion did not induce enhanced diuresis. In patients with ARF a significantly more marked increase in plasma volume was found than in normals. Data obtained in this study seem to prove preservation of the physiological regulatory mechanism of ANP secretion in ARF patients but reduction of ANP release induced by central volume expansion. The importance of elevated basal plasma values in the maintenance of ARF has not been proven.

Acute Kidney Injury↗
PubMed2005

The safety of gadolinium in patients with stage 3 and 4 renal failure.

BACKGROUND: Although there is a well-documented risk of acute renal failure (ARF) with the iodinated contrast agents, intravenous gadolinium-based contrast agents are considered non-nephrotoxic and have been widely used for magnetic resonance imaging (MRI). However, debate continues regarding the safety issue of gadolinium, especially in patients with kidney failure. Therefore, we aimed to evaluate the safety of gadolinium in patients with stage 3 and 4 renal failure as well as risk factors for nephrotoxicity. METHOD: We retrospectively analysed 473 patients with chronic renal failure who underwent angiographic MRI procedures in our centre from February 1999 to March 2005 in whom gadolinium was used as the sole contrast agent at a dose of 0.2 ml/kg. Among them, 91 patients with stage 3 or 4 renal failure according to K/DOQI definition, who had available data in their files, were enrolled in the study. The ARF was defined as an increase of at least 0.5 mg/dl in serum creatinine level over baseline after using gadolinium. RESULTS: Eleven of 91 (52 males, 39 females; median age 59 years; median estimated glomerular filtration rate (eGFR) 33 ml/min/1.73 m2) patients developed ARF (12.1%). The median eGFR was lower in patients with ARF than in those who did not develop ARF. The risk factors for ARF were baseline eGFR, older age, diabetic nephropathy and low baseline haemoglobin and albumin levels. Baseline eGFR and diabetic nephropathy were determined as the independent risk factors in regression analysis. CONCLUSIONS: An ARF can occur after gadolinium-based contrast agents in patients with moderate to severe chronic renal failure. Risk factors for ARF after gadolinium toxicity include diabetic nephropathy and low GFR.

Acute Kidney Injury↗
PubMed1977

The families of patients with acute rheumatic fever or glomerulonephritis in Trinidad.

The families of 21 patients with acute rheumatic fever (ARF) and 44 patients with acute glomerulonephritis (AGN) in Trinidad were examined in their homes. The ARF and AGN families were equally large and crowded and they lived in the same largely rural areas. However, only 22% of the ARF family members had skin infections in contrast to 61% of the AGN family members. Sixty-eight per cent of skin infections in ARF families and 69% of skin infections in Agn families yielded group A streptococci. Throat cultures were positive in 19% of ARF family members and 25% of AGN family members. Thirty-two per cent of 51 group A strains isolated from ARF family members (29 from throat, 22 from skin) were M11 or "M41" strains which were associated with ARF during the study, while only 8% were M1, T4 (MNT or 60) or M55 strains which were associated with AGN. In contrast, 49% of 171 group A strains isolated from Agn family members (64 from throat, 107 from skin) were M1, T4 (MNT or 60) or M55 while only 10% were M11 or "M41." Serum antibody titers were similar in both groups: antistreptolysin-0 titers were not markedly increased in either while anti-hyaluronidase and/or antideoxyribonuclease-B titers were increased in both. Evidence of subclinical AGN was found equally often in both groups: 6% of each had abnormal urine and 4% of each had decreased serum complement while 2% of the ARF and 3% of the AGN family members had both abnormal urine and decreased serum complement.

Adolescent↗
PubMed1996

Structure and intracellular localization of mouse ADP-ribosylation factors type 1 to type 6 (ARF1-ARF6).

ADP-ribosylation factors (ARFs) are a family of small GTP-binding proteins that are proposed to be involved in the formation of coated transport vesicles. Although six ARF sequences have been reported in mammals to date, it has been unclear how many ARF members are present in a single organism. In this study, we provide the first direct evidence by cDNA cloning for the presence of all six ARF members in mouse. These proteins are highly conserved across mammalian species and Northern blot analysis revealed that mRNAs for all the members were expressed ubiquitously. Transfection of cells with epitope-tagged ARFs revealed that ARFs 1-3 displayed a perinuclear Golgi localization, while ARFs 4-6 appeared to be widely dispersed throughout the cytoplasm. These results suggest that although all the ARF proteins play fundamental and critical roles in cellular function, they are involved in different vesicular transport processes.

ADP-Ribosylation Factor 1↗
PubMed1997

Acute renal failure: factors influencing nephrology referral and outcome.

We investigated the incidence, factors affecting referral and outcome of acute renal failure (ARF), in an unselected (predominantly Caucasian) population in the Grampian region of Scotland served by a single renal unit. Case-notes were examined for all patients with a serum creatinine > or = 300 mumol/l. ARF (311 patients) was defined as a temporary rise in serum creatinine > or = 300 mumol/l, or, if the patient died during the acute illness, clinical features indicating acute deterioration of previously normal renal function. Advanced ARF at presentation (51 of the 311 with ARF) was defined as a first recorded serum creatinine > or = 500 mumol/l. Patients were classified into low-, medium-, and high-risk groups according to presence of comorbidity and age. The annual incidence of ARF was 620/million population (pmp), that of advanced ARF 102 pmp. The age-related incidence of ARF ranged from 30 pmp in the age group (0-19 years) to 4266 pmp in the age group > 80 years. Overall, 22% were referred to a nephrologist (34% after excluding those with advanced cancer and age > 80 years). Referral of patients decreased from 100% in the age group 0-19 to 5% in those > 80 years. Referrals in the low-, medium- and high-risk groups were 75%, 30% and 14%, respectively. Patient survival at 2 years was 80%, 42% and 19% for low-, medium-, and high-risk groups, respectively (86%, 44% and 32% for referred patients). Referral and outcome in patients with ARF were significantly influenced by age and presence of comorbidity at presentation.

Acute Kidney Injury↗
PubMed1998

Improvement of postischemic acute renal failure with the novel orally active endothelin-A receptor antagonist LU 135252 in the rat.

The endothelin (ET) system may play an important role in the pathogenesis of acute renal failure (ARF). We hypothesize that the course of ARF in an ischemia-reperfusion model will be markedly attenuated by the orally active ET(A)-receptor antagonist LU 135252 (LU) because of an improvement of renal perfusion. ARF was induced in rats by clamping both renal arteries for 60 min. The study was divided into two parts. In part 1, Rats received LU orally (100 mg/kg/day) starting 1 h after induction of ARF for 14 days. Cr(s), Cl(cr) and FE(na) were measured on days 1, 6, 9, and 14 after ARF. Cr(s) was lower in the treatment group on days 1 [1.3 +/- 0.31 mg/dl (n = 9) vs. 2.7 +/- 0.46 mg/dl (n = 10); p < 0.05] and 6 [0.5 +/- 0.1 mg/dl (n = 9) vs. 1.0 +/- 0.2 mg/dl (n = 9); p < 0.05], and Cl(cr) was higher on day 1 [0.9 +/- 0.17 ml/min (n = 9) vs. 0.2 +/- 0.1 ml/min (n = 8); p < 0.05] and 6 [1.8 +/- 0.29 ml/min (n = 9) vs. 1.0 +/- 0.21 ml/min (n = 9); p < 0.05] compared with vehicle. Additionally, FE(na) was lower in treated rats on day 1 [1 +/- 0.4% (n = 9) vs. 8 +/- 3% (n = 8); p < 0.051 compared with vehicle. In part 2, ARF was induced as described. Treated animals received 10 mg/kg LU on days 0, 1, 3, 6, 9, and 14 after ARF as an i.v. bolus injection. RBF, cortex blood flow (CBF), and medulla blood flow (MBF) were measured after application of LU on the same days: LU induced an increase in RBF (day 1: 14 +/- 5.3%, n = 6, p = 0.04; day 3: 15 +/- 2.8%, n = 8; p = 0.0008; day 6: 21 +/- 5.8%, n = 6, p = 0.02; day 9: 13 +/- 4%, n = 6; p = 0.03) and CBF (day 1: 8 +/- 2.2%, n = 7, p = 0.03; day 3: 7 +/- 2.5%, n = 7; p = 0.05; day 6: 18 +/- 4.8%, n = 6, p = 0.04; day 9: 10 +/- 2.5%, n = 6; p = 0.008) up to the first 9 days. MBF did increase on days 1 (9 +/- 3.1%, n = 6; p = 0.04) and 6 (13 +/- 3.6%, n = 6; p = 0.03). Our data confirm the hypothesis that ET plays a major role in the genesis of ARF associated with ischemia-reperfusion.

Acute Kidney Injury↗
PubMed1998

Causes, management approaches, and outcome of acute renal failure in children.

Although acute renal failure (ARF) remains an uncommon problem in pediatrics, it is characterized by significant morbidity and mortality. This review addresses several broad topics related to ARF and summarizes the results of recent studies of particular significance. Following a brief discussion of the main causes of ARF in children, more detailed attention is paid to the problems of ARF caused by hemolytic-uremic syndrome and of ARF in neonates. Management of ARF is reviewed, including recent advances in dialysis modalities. Recent data on the outcome of ARF in children are summarized, and future approaches to the prevention and management of ARF are briefly examined.

Acute Kidney Injury↗
PubMed2004

Oxidative stress is increased in critically ill patients with acute renal failure.

Patients with acute renal failure (ARF) experience a high mortality rate. Dysregulated inflammation and altered metabolism may increase oxidative stress in ARF patients. Thirty-eight patients who met the Program to Improve Care in Acute Renal Disease (PICARD) Study inclusion criteria underwent plasma protein oxidation and plasma cytokine measurements. For comparison, similar measurements were also performed in 21 critically ill patients without ARF, 28 patients with ESRD, and 49 healthy subjects. Plasma protein thiol oxidation was measured by spectrophotometry. Plasma protein carbonyl content and cytokine concentrations were measured by ELISA. Plasma protein thiol oxidation and carbonyl content were markedly different in ARF patients compared with healthy subjects, ESRD patients, and critically ill patients (P < 0.001 in all cases). There were significant but less marked differences in plasma protein oxidation between ESRD patients and critically ill patients compared with healthy subjects. Plasma protein thiol oxidation in ARF patients improved with dialysis (P < 0.001); however, there was significant plasma oxidant reaccumulation during the interdialytic period (P < 0.001) not due to rebound equilibration of compartmentalized solutes. Plasma proinflammatory cytokine levels were significantly higher (P < 0.05) in ARF patients and critically ill patients than in healthy subjects. Plasma protein oxidation is markedly increased in ARF patients compared with healthy subjects, ESRD patients, and critically ill patients. Increased oxidative stress may be an important target for nutritional and pharmacologic therapy in ARF patients.

Acute Kidney Injury↗
PubMed2004

Enteral nutrition in patients with acute renal failure.

BACKGROUND: Systematic studies on safety and efficacy of enteral nutrition in patients with acute renal failure (ARF) are lacking. METHODS: We studied enteral nutrition-related complications and adequacy of nutrient administration during 2525 days of artificial nutrition in 247 consecutive patients fed exclusively by the enteral route: 65 had normal renal function, 68 had ARF not requiring renal replacement therapy, and 114 required renal replacement therapy. RESULTS: No difference was found in gastrointestinal or mechanical complications between ARF patients and patients with normal renal function, except for high gastric residual volumes, which occurred in 3.1% of patients with normal renal function, 7.3% of patients with ARF not requiring renal replacement therapy, 13.2% of patients with ARF on renal replacement therapy (P= 0.02 for trend), and for nasogastric tube obstruction: 0.0%, 5.9%, 14%, respectively (P < 0.001). Gastrointestinal complications were the most frequent cause of suboptimal delivery; the ratio of administered to prescribed daily volume was well above 90% in all the three groups. Definitive withdrawal of enteral nutrition due to complications was documented in 6.1%, 13.2%. and 14.9% of patients, respectively (P= 0.09 for trend). At regimen, mean delivered nonprotein calories were 19.8 kcal/kg (SD 4.6), 22.6 kcal/kg (8.4), 23.4 kcal/kg (6.5); protein intake was 0.92 g/kg (0.21), 0.87 g/kg (0.25), and 0.92 g/kg (0.21), the latter value being below that currently recommended for ARF patients on renal replacement therapy. Median fluid intake with enteral nutrition was 1440 mL (range 720 to 1960), 1200 (720 to 2400), and 960 (360 to 1920). CONCLUSION: Enteral nutrition is a safe and effective nutritional technique to deliver artificial nutrition in ARF patients. Parenteral amino acid supplementation may be required, especially in patients with ARF needing renal replacement therapy.

APACHE↗
PubMed2004

In vivo transfection of NF-kappaB decoy oligodeoxynucleotides attenuate renal ischemia/reperfusion injury in rats.

BACKGROUND: Ischemic acute renal failure (ARF) is a common and often fatal condition characterized by tubular epithelial cell necrosis and marked monocyte infiltration. Inflammatory mechanisms, including cell adhesion, cell infiltration, and cytokine production, are involved. These processes are thought to be directly or indirectly regulated by nuclear factor kappaB (NF-kappaB). Targeted of NF-kappaB might ameliorate ischemia/reperfusion (I/R) injury by inhibiting the production of genes that involved in ischemic ARF. The objective of the present study was to evaluate the effect of NF-kappaB decoy oligodeoxynucleotides (ODN) in experimental rat ischemic ARF. METHODS: Ischemic ARF was induced by left renal artery clamping for 60 minutes, while the right kidney was being removed in female Sprague-Dawley rats. The effect of cationic liposome-protamine-NF-kappaB decoy ODN was evaluated after infusion into the kidney via the renal artery before clamping. After 24 hours of reperfusion, we then assessed morphologic and functional parameters, NF-kappaB/DNA binding activity, monocyte/macrophage (M/MPhi) infiltration, and gene expression in I/R kidney. RESULTS: After 24 hours of reperfusion, compared with sham-operated animals, serum creatinine and blood urea nitrogen (BUN) levels in ischemic ARF animals were increased about 10-fold and fivefold respectively. (255.67 +/- 34.48 micromol/L vs. 25.33 +/- 2.23 micromol/L and 43.47 +/- 5.50 mmol/L vs. 8.45 +/- 0.43 mmol/L, P < 0.001), NF-kappaB/DNA binding activity was markedly elevated [median value was 1.75 vs. 0.15 relative density unit (RDU), P < 0.005]. NF-kappaB decoy ODN treatment reduced the elevation of serum creatinine level by 70% (79.17 +/- 8.64 micromol/L vs. 255.67 +/- 34.48 micromol/L, P < 0.01), BUN level by 40% (28.33 +/- 4.86 mmol/L vs. 43.47 +/- 5.50 mmol/L, P= NS), and almost abolished the NF-kappaB activation compared with levels observed in sham-operated rats (median value was 0.25 vs. 1.9 RDU, P < 0.005). Furthermore, NF-kappaB decoy ODN pretreatment prevented the occurrence of tubular necrosis and reduced the renal tubular damage scores markedly (1.85 +/- 0.06 vs. 3.63 +/- 0.06 scores, P < 0.01). In addition, M/MPhi infiltration was obviously suppressed (9.77 +/- 1.19 cells/hpf vs. 29.22 +/- 1.94 cells/hpf, P < 0.01), Moreover, results of reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry showed the up-regulation of monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) was greatly decreased, inducible nitric oxide synthase (iNOS) and endothelin-1 (ET-1) expression were also reduced, approaching levels observed in sham-operated animals. The data suggest that NF-kappaB decoy ODN treatment protects renal tissue from the effects of I/R injury and thus reduces the severity of ARF. CONCLUSION: These experiments demonstrated that NF-kappaB plays a critical role in renal I/R injury by reducing a series of inflammatory genes. NF-kappaB decoy ODN treatment reduces the renal dysfunction and damage associated with ischemic ARF. Therefore, in vivo transfection of NF-kappaB decoy ODN provides a new therapeutic strategy for ischemic ARF.

Acute Kidney Injury↗
PubMed2004

Plasma cytokine levels predict mortality in patients with acute renal failure.

BACKGROUND: Critically ill patients with acute renal failure (ARF) experience a high mortality rate. Animal and human studies suggest that proinflammatory cytokines lead to the development of a systemic inflammatory response syndrome (SIRS), which is temporally followed by a counter anti-inflammatory response syndrome (CARS). This process has not been specifically described in critically ill patients with ARF. METHODS: The Program to Improve Care in Acute Renal Disease (PICARD) is a prospective, multicenter cohort study designed to examine the natural history, practice patterns, and outcomes of treatment in critically ill patients with ARF. In a subset of 98 patients with ARF, we measured plasma proinflammatory cytokines [interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha)], the acute-phase reactant C-reactive protein (CRP), and the anti-inflammatory cytokine IL-10 at study enrollment and over the course of illness. RESULTS: When compared with healthy subjects and end-stage renal disease patients on maintenance hemodialysis, patients with ARF had significantly higher plasma levels of all measured cytokines. Additionally, the proinflammatory cytokines IL-6 and IL-8 were significantly higher in nonsurvivors versus survivors [median 234.7 (interdecile range 64.8 to 1775.9) pg/mL vs. 113.5 (46.1 to 419.3) pg/mL, P= 0.02 for IL-6; 35.5 (14.1 to 237.9) pg/mL vs. 21.2 (8.5 to 87.1) pg/mL, P= 0.03 for IL-8]. The anti-inflammatory cytokine IL-10 was also significantly higher in nonsurvivors [3.1 (0.5 to 41.9) pg/mL vs. 2.4 (0.5 to 16.9) pg/mL, P= 0.04]. For each natural log unit increase in the levels of IL-6, IL-8, and IL-10, the odds of death increased by 65%, 54%, and 34%, respectively, corresponding to increases in relative risk of approximately 30%, 25%, and 15%. The presence or absence of SIRS or sepsis was not a major determinant of plasma cytokine concentration in this group of patients. CONCLUSION: There is evidence of ongoing SIRS with concomitant CARS in critically ill patients with ARF, with higher levels of plasma IL-6, IL-8, and IL-10 in patients with ARF who die during hospitalization. Strategies to modulate inflammation must take into account the complex cytokine biology in patients with established ARF.

Acute Kidney Injury↗
PubMed2005

Administered mesenchymal stem cells enhance recovery from ischemia/reperfusion-induced acute renal failure in rats.

BACKGROUND: Adult stem cells are promising for the development of novel therapies in regenerative medicine. Acute renal failure (ARF) remains a frequent clinical complication, associated with an unacceptably high mortality rate, in large part due to the ineffectiveness of currently available therapies. The aim of this study was, therefore, to evaluate the therapeutic effectiveness of bone marrow-derived mesenchymal stem cells in a rat model of ischemia/reperfusion (I/R) ARF. METHODS: We used a common I/R model in rats to induce ARF by clamping both renal pedicles for 40 minutes. Mesenchymal stem cells were iron-dextran-labeled for in vivo tracking studies by magnetic resonance imaging (MRI) and kidneys were imaged for mesenchymal stem cells immediately after infusion and at day 3 after ARF. Renal injury was scored on day 3 and cells were additionally tracked by Prussian blue staining. RESULTS: We show in I/R-induced ARF in rats, modeling the most common form of clinical ARF, that infusion of mesenchymal stem cells enhances recovery of renal function. Mesenchymal stem cells were found to be located in the kidney cortex after injection, as demonstrated by MRI. Mesenchymal stem cells-treated animals had both significantly better renal function on days 2 and 3 and better injury scores at day 3 after ARF. Histologically, mesenchymal stem cells were predominantly located in glomerular capillaries, while tubules showed no iron labeling, indicating absent tubular transdifferentiation. CONCLUSION: We conclude that the highly renoprotective capacity of mesenchymal stem cells opens the possibility for a cell-based paradigm shift in the treatment of I/R ARF.

Acute Kidney Injury↗
PubMed2005

Identifying critically ill patients at high risk for developing acute renal failure: a pilot study.

BACKGROUND: Acute renal failure (ARF) occurs commonly in the intensive care unit (ICU), but predicting which patients will develop ARF is difficult. We set out to determine which risk factors would predict the development of ARF in critically ill patients who are admitted to the ICU without ARF. METHODS: From August 2002 to April 2003, we enrolled medical-surgical ICU admissions into a cohort using a sampling tool based on their risk factor (RF) profile. The risk factors we identified were separated into 3 categories: chronic major, chronic minor, and acute RFs. Combinations of these RFs were used to create a sampling tool and identify patients to enroll into our cohort. Patients with end-stage renal disease and ARF upon admission to the ICU were excluded. RESULTS: We enrolled 194 patients over a 14-month period. The mean age of the cohort was 64.6 +/- 14.7 years. The percentage of Caucasians, African Americans, and Hispanics was 40.7%, 50.5%, and 3.6%, respectively. In a univariate analysis of the entire cohort, increasing APACHE II quartile, increased A-a gradient, presence of systemic inflammatory response syndrome (SIRS), decreased levels of serum albumin, and presence of active cancer predicted ARF. In a multiple logistic regression analysis, decreased serum albumin (high levels of serum albumin were protective), increased A-a gradient, and cancer were associated with development of ARF (OR 2.17, 1.04, and 2.86, respectively). CONCLUSION: Decreased levels of serum albumin concentration, increased A-a gradient, and presence of active cancer predict which patients who are admitted to the ICU will develop ARF.

APACHE↗
PubMed2005

Acute renal failure after Crotalus durissus snakebite: a prospective survey on 100 patients.

BACKGROUND: Acute renal failure (ARF) is the main cause of death after the South American crotalid snakebite. The aim of this study was to assess the prevalence, risk factors, and characteristics of Crotalus durissus venom-induced ARF. METHODS: One hundred cases of Crotalus durissus bite were studied from hospitalization to discharge or death. Creatinine clearance (GFR) <60 mL/min/1.73 m(2) in the first 72 hours after snakebite was defined as ARF. Data are expressed as median (range of variation) or%, and were analyzed by univariate analysis and logistic regression. RESULTS: Twenty-nine patients developed ARF. Of those, 24% required dialysis and 10% died. ARF patients had smaller body surface [1.55 (0.6-2.3) vs. 1.7 (0.6-2.1) m(2), P= 0.0097], received antivenom (AV) later [12 (2-48) vs. 2 (1-14) hours, P < 0.0001], received more AV [190 (90-536) vs. 158 (75-500) mg/m(2), P < 0.0001], presented lower diuresis at admission [62 (0-182) mL/hr vs. 100 (25-325) mL/hr, P= 0.0004], and showed a striking creatine kinase (CK) increase [50,250 (69-424,120) vs. 1108 (88-133,170) U/L, P < 0.0001]. Age <12 years (OR 5.6, P= 0.026), time for AV >2 hours (OR 11.1, P= 0.032), CK at admission >2000 U/L (OR 12.7, P= 0.0009) were identified as independent risk factors for ARF, whereas diuresis at admission >90 mL/hr (OR 0.20, P= 0.014) was an independent protector factor. CONCLUSION: C. durissus venom-induced ARF had high prevalence (29%). Delay for AV treatment, CK at admission >2000 U/L, and age <12 years were independent risk factors for ARF development. Diuresis at admission >90 mL/hr was a protective factor.

Acute Kidney Injury↗
PubMedDate not supplied

A retrospective case-control of acute renal failure in 99 dogs.

The objective of this study was to evaluate retrospectively demographic and clinicopathologic factors that may be associated with the diagnosis and outcome of acute renal failure (ARF) in dogs presented to a large referral hospital. Medical records of dogs presented to the hospital were searched for a diagnosis of ARF. The diagnosis of ARF was based on clinical signs, renal imaging findings, and clinicopathologic data and, in most cases, was confirmed by histopathology, prior serum creatinine concentrations, response to therapy, and known recent nephrotoxin exposure or ischemic event. Demographics, selected clinicopathologic findings, and concurrent disorders that may have been associated with development of ARF were extracted from these records. A reference population was derived from 481 dogs presenting to the same hospital. Demographic data also were collected from these medical records. The demographic factors associated with a diagnosis of ARF and the factors associated with outcome of ARF were assessed by reviewing a series of multiple logistic regression models. Conclusions from this study were as follows: (1) Intact male dogs and nonsporting dogs were more likely to develop ARF and be admitted to the teaching hospital. (2) Dogs with severe azotemia (serum creatinine concentration > 10 mg/dL), hypocalcemia (< 8.6 mg/ dL), and proteinuria were less likely to survive ARF and be discharged from the hospital. (3) Dogs that survived in the hospital for more than 5 days were more likely to recover and be discharged from the hospital.

Acute Kidney Injury↗
PubMed2003

Effects of acute renal failure on the pharmacokinetics of chlorzoxazone in rats.

The purpose of this study is to report the changes of CYP2E1, CYP1A2, CYP2B1/2, CYP2C11, CYP3A23, and CYP3A2 expression and pharmacokinetics and tissue distribution of chlorzoxazone (CZX) and 6-hydroxychlorzoxazone (OH-CZX) in rats with acute renal failure induced by uranyl nitrate (U-ARF), and the role of CYP3A23 and CYP3A2 in the formation of OH-CZX in rats with U-ARF. In rats with U-ARF, CYP2C11 decreased to 20% of control, whereas CYP2E1 and CYP3A23 increased 2.3 and 4 times, respectively, compared with control. But expression of CYP1A2 and CYP2B1/2 was not changed by U-ARF. After i.v. administration of CZX at a dose of 20 mg/kg to rats with U-ARF, the areas under the plasma concentration-time curve from time 0 to time infinity (AUCs) of CZX and OH-CZX were significantly smaller and greater, respectively, than those in control rats. In rats with U-ARF, CZX was below the detection limit at 120 min in all rat tissues studied, whereas it was detected in all tissues of control rats at both 30 and 120 min. However, in control rats, OH-CZX was below the detection limit at both 30 and 120 min in all rat tissues except kidney, whereas it was detected in all tissues of rats with U-ARF at both 30 and 120 min. Based on results from supporting experiments with DDT and 2,2-bis(4-chlorophenyl)1,1-dichloroethylene treatment of rats, the contribution of CYP3A23 and CYP3A2 to the enhanced formation of OH-CZX in rats with U-ARF is likely to be negligible.

Acute Kidney Injury↗
PubMed1998

Pharmacokinetics of a new carbapenem, DA-1131, after intravenous administration to rats with uranyl nitrate-induced acute renal failure.

Because the physiological changes that occur in patients with acute renal failure could alter the pharmacokinetics of the drugs used to treat the disease, the pharmacokinetics of DA-1131, a new carbapenem antibiotic, were investigated after 1-min intravenous administration of the drug (50 mg/kg of body weight) to control rats and rats with uranyl nitrate-induced acute renal failure (U-ARF rats). The impaired kidney function was observed in U-ARF rats on the basis of physiological parameters observed by microscopy of the kidney and obtained by chemical analysis of the plasma. After a 1-min intravenous infusion of DA-1131, the concentrations in plasma and the total area under the plasma concentration-time curve from time zero to time infinity increased significantly in U-ARF rats compared with those in control rats (13,000 versus 4,400 microg x min/ml). This was due to the significantly slower total body clearance (CL) of DA-1131 (3.84 versus 11.4 ml/min/kg) from U-ARF rats than from control rats. The significantly slower CL of DA-1131 from U-ARF rats was due to both significantly slower renal clearance (0.000635 versus 4.95 ml/min/kg because of a significant decrease in the 8-h urinary excretion of unchanged DA-1131 [1.54 versus 43.8% of the intravenous dose] due to impaired kidney function, as proved by the significant decrease in creatinine clearance [0.0159 versus 4.29 ml/min/kg]) and significantly slower nonrenal clearance (3.80 versus 6.34 ml/min/kg because of a significant decrease in the metabolism of DA-1131 in the kidney) in U-ARF rats. The amounts of DA-1131 recovered from all tissues studied (except the kidneys) were significantly higher for U-ARF rats than for control rats; however, the ratios of the amount in tissue to the concentration in plasma (except those for the kidney, small intestine, and spleen) were not significantly different between the two groups of rats, indicating that the affinity of DA-1131 for rat tissues was not changed considerably in U-ARF rats.

Acute Kidney Injury↗
PubMed2001

Bax loss impairs Myc-induced apoptosis and circumvents the selection of p53 mutations during Myc-mediated lymphomagenesis.

The ARF and p53 tumor suppressors mediate Myc-induced apoptosis and suppress lymphoma development in E mu-myc transgenic mice. Here we report that the proapoptotic Bcl-2 family member Bax also mediates apoptosis triggered by Myc and inhibits Myc-induced lymphomagenesis. Bax-deficient primary pre-B cells are resistant to the apoptotic effects of Myc, and Bax loss accelerates lymphoma development in E mu-myc transgenics in a dose-dependent fashion. Eighty percent of lymphomas arising in wild-type E mu-myc transgenics have alterations in the ARF-Mdm2-p53 tumor suppressor pathway characterized by deletions in ARF, mutations or deletions of p53, and overexpression of Mdm2. The absence of Bax did not alter the frequency of biallelic deletion of ARF in lymphomas arising in E mu-myc transgenic mice or the rate of tumorigenesis in ARF-null mice. Furthermore, Mdm2 was overexpressed at the same frequency in lymphomas irrespective of Bax status, suggesting that Bax resides in a pathway separate from ARF and Mdm2. Strikingly, lymphomas from Bax-null E mu-myc transgenics lacked p53 alterations, whereas 27% of the tumors in Bax(+/-) E mu-myc transgenic mice contained p53 mutations or deletions. Thus, the loss of Bax eliminates the selection of p53 mutations and deletions, but not ARF deletions or Mdm2 overexpression, during Myc-induced tumorigenesis, formally demonstrating that Myc-induced apoptotic signals through ARF/Mdm2 and p53 must bifurcate: p53 signals through Bax, whereas this is not necessarily the case for ARF and Mdm2.

Animals↗