Prognostic Factors in Neonatal Acute Renal Failure

PEDIATRICS ◽  
1984 ◽  
Vol 74 (2) ◽  
pp. 265-272
Author(s):  
Robert L. Chevalier ◽  
Fern Campbell ◽  
A. Norman A. G. Brenbridge
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Perinatal Asphyxia ◽  
Urine Flow ◽  
Peak Serum ◽  
Serum Creatinine Concentration ◽  
Creatinine Concentration ◽  
Renal Anomalies ◽  
Renal Uptake

Sixteen infants, 2 to 35 days of age, had acute renal failure, a diagnosis based on serum creatinine concentrations > 1.5 mg/dL for at least 24 hours. Eight infants were oliguric (urine flow < 1.0 mL/kg/h) whereas the remainder were nonoliguric. To determine clinical parameters useful in prognosis, urine flow rate, duration of anuria, peak serum creatinine, urea (BUN) concentration, and nuclide uptake by scintigraphy were correlated with recovery. Nine infants had acute renal failure secondary to perinatal asphyxia, three had acute renal failure as a result of congenital cardiovascular disease, and four had major renal anomalies. Four oliguric patients died: three of renal failure and one of heart failure. All nonoliguric infants survived with mean follow-up serum creatinine concentration of 0.8 ± 0.5 (SD) mg/dL whereas that of oliguric survivors was 0.6 ± 0.3 mg/dL. Peak serum creatinine concentration did not differ between those patients who were dying and those recovering. All infants who were dying remained anuric at least four days and revealed no renal uptake of nuclide. Eleven survivors were anuric three days or less, and renal perfusion was detectable by scintigraphy in each case. However, the remaining survivor (with bilateral renal vein thrombosis) recovered after 15 days of anuria despite nonvisualization of kidneys by scintigraphy. In neonates with ischemic acute renal failure, lack of oliguria and the presence of identifiable renal uptake of nuclide suggest a favorable prognosis.

Protective Effect of Prostaglandin [PGE2] in Glycerol-Induced Acute Renal Failure in Rats

1978 ◽  
Vol 55 (5) ◽  
pp. 505-507 ◽  
Author(s):  
R. Werb ◽  
W. F. Clark ◽  
R. M. Lindsay ◽  
E. O. P. Jones ◽  
D. I. Turnbull ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Prostaglandin E2 ◽  
Serum Creatinine Concentration ◽  
Sprague Dawley ◽  
Glomerular Permeability ◽  
Creatinine Concentration ◽  
Significant Difference ◽  
Group B

1. Acute renal failure was induced in female Sprague—Dawley rats by the subcutaneous injection of glycerol. 2. Four groups of rats were studied; all animals received a glycerol challenge. Group A (control) were sham-operated only, group B received an infusion of sodium chloride solution (150 mmol/l; saline) for 24 h, group C received an infusion containing prostaglandin E2 (PGE2, 1.7 μmol/l) in saline and group D a solution containing PGE2 (3.4 μmol/l) in saline. 3. All rats were killed 48 h after glycerol challenge. The degree of renal impairment was assessed by serum creatinine concentration, which did not differ in sham-operated animals and the group receiving saline alone. The group of rats receiving the lower dose of PGE2 has a significantly lower mean serum creatinine concentration than the saline-infused control rats (P < 0.0025). Creatinine concentration was further lowered by the higher dose of PGE2 but there was not a significant difference in the number of rats showing severe tubular necrosis histologically. 4. The study demonstrates that intravenous infusion of prostaglandin E2 has a protective influence on glycerol-induced renal failure in the rat; the protection afforded may be due to the vasodilator effect of PGE2 and/or an effect on glomerular permeability.

Delayed onset of acute renal failure after significant paracetamol overdose: A case series

2009 ◽  
Vol 29 (1) ◽  
pp. 63-68 ◽  
Author(s):  
WS Waring ◽  
H. Jamie ◽  
GE Leggett
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Alanine Aminotransferase ◽  
Paracetamol Overdose ◽  
Peak Serum ◽  
Wilcoxon Test ◽  
Aminotransferase Activity ◽  
Baseline Serum ◽  
Alanine Aminotransferase Activity

Acute renal failure is a recognized manifestation of paracetamol toxicity, but comparatively little data is available concerning its onset and duration. The present study sought to characterize the time course of rising serum creatinine concentrations in paracetamol nephrotoxicity. Renal failure was defined by serum creatinine concentration ≥150 μmol/L (1.69 mg/dL) or ≥50% increase from baseline. Serum creatinine concentrations and alanine aminotransferase activity were considered with respect to the interval after paracetamol ingestion. There were 2068 patients with paracetamol overdose between March 2005 and October 2007, and paracetamol nephrotoxicity occurred in 8 (0.4%). All had significant hepatotoxicity, and peak serum alanine aminotransferase activity occurred at 2.5 days (2.2 to 2.9 days) after ingestion. Peak serum creatinine concentrations did not occur until 5.5 days (4.4 to 5.9 days) after ingestion (p = .031 by Wilcoxon test). Serum creatinine concentrations slowly restored to normal, and renal replacement was not required. In this patient series, rising serum creatinine concentrations only became detectable after more than 48 hours after paracetamol ingestion. Therefore, renal failure might easily be missed if patients are discharged home before this. Further work is required to establish the prevalence of paracetamol-induced nephrotoxicity, and its clinical significance.

Theophylline-induced protection in myoglobinuric acute renal failure: further characterization

1987 ◽  
Vol 65 (1) ◽  
pp. 42-45 ◽  
Author(s):  
A. K. Bidani ◽  
P. C. Churchill ◽  
W. Packer
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Biological Fluids ◽  
Peak Serum ◽  
Tubuloglomerular Feedback ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Adenosine Receptor Antagonist ◽  
Myoglobinuric Acute Renal Failure

We have reported previously that aminophylline has an ameliorating effect on the course and severity of glycerol-induced myoglobinuric acute renal failure in rats. Since aminophylline dissociates into theophylline in biological fluids and since theophylline is an adenosine receptor antagonist, we attributed the ameliorating effects to antagonism of the hemodynamic effects of endogenous adenosine. However, theophylline blocks tubuloglomerular feedback and produces natriuresis, and either of these effects might have accounted for the beneficial effects in acute renal failure. Therefore, this study was designed to further characterize the effects of theophylline in glycerol-induced acute renal failure in rats. Aminophylline had dose-dependent beneficial effects, as judged by the peak serum creatinine during the 3 days following induction of acute renal failure, by the number of animals with peak serum creatinine >1 mg/dL, and by the mortality rate. Both furosemide and theophylline block tubuloglomerular feedback and produce natriuresis, but aminophylline had protective effects, whereas furosemide actually increased mortality, compared with aminophylline, following induction of myoglobinuric acute renal failure. Therefore, aminophylline's protective effects are independent of tubuloglomerular feedback and natriuresis. These results offer further support for the hypothesis that adenosine-induced hemodynamic changes play a pathogenic role in glycerol-induced acute renal failure in rats.

Use of free and transthyretin-bound retinol-binding protein in serum as tests of vitamin A status in humans: effect of high creatinine concentrations in serum

1990 ◽  
Vol 36 (4) ◽  
pp. 674-676 ◽  
Author(s):  
B J Burri ◽  
D D Bankson ◽  
T R Neidlinger
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Vitamin A ◽  
Serum Creatinine ◽  
Binding Protein ◽  
High Serum ◽  
Retinol Binding Protein ◽  
Creatinine Concentration ◽  
Vitamin A Status ◽  
Chromatographic Peaks

Abstract We measured immunologically active (apo + holo) retinol-binding protein (RBP), vitamin A-carrying (holo) free RBP, and transthyretin-bound (TTR) holo-RBP in serum from 34 retrospective cases of fluctuating acute renal failure. All subjects had high serum creatinine concentrations caused by renal failure. Apo + holo, holo-TTR-RBP, and (especially) holo-free RBP all correlated poorly but significantly with serum creatinine concentration. Therefore, the use of any form of RBP to measure vitamin A status may be of limited value in subjects with high creatinine concentrations in serum. However, molecular-exclusion HPLC may be able to distinguish increases in RBP concentration associated with renal failure from those caused by altered vitamin A status, because renal failure causes abnormalities in the number and retention times of chromatographic peaks as well as their areas.

scholarly journals Long-Term Effects of Arterial Stenting on Kidney Functionfor Patients with Ostial Atherosclerotic Renal Artery Stenosis and Renal Insufficiency

2001 ◽  
Vol 12 (7) ◽  
pp. 1475-1481
Author(s):  
JAAP J. BEUTLER ◽  
JACOBINE M. A. VAN AMPTING ◽  
PETER J. G. VAN DE VEN ◽  
HEIN A. KOOMANS ◽  
FREDERIK J. A. BEEK ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Serum Creatinine ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Stent Placement ◽  
Serum Creatinine Concentration ◽  
Atherosclerotic Renal Artery Stenosis ◽  
Creatinine Concentration

Abstract. It is uncertain whether renal artery stent placement in patients with atherosclerotic renovascular renal failure can prevent further deterioration of renal function. Therefore, the effects of renal artery stent placement, followed by patency surveillance, were prospectively studied in 63 patients with ostial atherosclerotic renal artery stenosis and renal dysfunction (i.e., serum creatinine concentrations of >120 μmol/L (median serum creatinine concentration, 171 μmol/L; serum creatinine concentration range, 121 to 650 μmol/L). Pre-stent renal (dys) function was stable for 28 patients and declining for 35 patients (defined as a serum creatinine concentration increase of ≥20% in 12 mo). The median follow-up period was 23 mo (interquartile range, 13 to 29 mo). Angioplasty to treat restenosis was performed in 12 cases. Five patients reached end-stage renal failure within 6 mo, and this was related to stent placement in two cases. Two other patients died or were lost to follow-up monitoring within 6 mo, with stable renal function. For the remaining 56 patients, the treatment had no effect on serum creatinine levels if function had previously been stable; if function had been declining, median serum creatinine concentrations improved in the first 1 yr [from 182 μmol/L (135 to 270 μmol/L) to 154 μmol/L (127 to 225 μmol/L); P < 0.05] and remained stable during further follow-up monitoring. In conclusion, stent placement, followed by patency surveillance, to treat ostial atherosclerotic renal artery stenosis can stabilize declining renal function. For patients with stable renal dysfunction, the usefulness is less clear. The possible advantages must be weighed against the risk of renal failure advancement with stent placement.

Acute Kidney Injury - Part II: Special Situations

2019 ◽  
Author(s):  
Paul W Sanders ◽  
Anupam Agarwal
Keyword(s):  
Multiple Myeloma ◽  
Acute Kidney Injury ◽  
Renal Failure ◽  
Serum Creatinine ◽  
Hepatorenal Syndrome ◽  
Kidney Injury ◽  
Serum Creatinine Concentration ◽  
Creatinine Concentration ◽  
Waste Products ◽  
Abrupt Decrease

Acute renal failure (ARF) has been defined as a syndrome in which an abrupt decrease in renal function produces retention of nitrogenous waste products. Translating this abstract description into a clinically useful, accurate, and widely accepted definition has been challenging, in large part because of the focus on serum creatinine concentration, which is easily obtained but has the inherent limitation of poor detection of rapid or subtle, but clinically important, changes in the glomerular filtration rate (GFR). In recent years, therefore, the term acute kidney injury (AKI) has replaced ARF because AKI denotes the entire clinical spectrum from mild increases in serum creatinine to overt renal failure. AKI is defined by the Risk-Injury-Failure-Loss-ESRD (RIFLE) criteria, based on serum creatinine concentration and urine flow rate. The Acute Kidney Injury Network (AKIN) subsequently modified the definition further and divided AKI into three stages. This part of the AKI review specifically discusses special situations: rhabdomyolysis, aristolochic acid nephropathy, acute urate nephropathy, acute phosphate nephropathy, AKI in multiple myeloma, ehytlene glycol poisoning, contrast-induced nephropathy, AKI in sepsis, hepatorenal syndrome, and AKI in pregnancy. This review contains 10 tables, and 47 references. Keywords:Acute kidney injury, dialysis, contrast, rhabdomyolysis, nephropathy, urinalysis, multiple myeloma, ethylene glycol, sepsis, hepatorenal syndrome

Acute Kidney Injury - Part I

2019 ◽  
Author(s):  
Paul W Sanders ◽  
Anupam Agarwal
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Acute Kidney Injury Network ◽  
Serum Creatinine Concentration ◽  
Cardiac Conduction ◽  
Creatinine Concentration ◽  
Waste Products ◽  
Abrupt Decrease

Acute renal failure (ARF) has been defined as a syndrome in which an abrupt decrease in renal function produces retention of nitrogenous waste products. Translating this abstract description into a clinically useful, accurate, and widely accepted definition has been challenging, in large part because of the focus on serum creatinine concentration, which is easily obtained but has the inherent limitation of poor detection of rapid or subtle, but clinically important, changes in the glomerular filtration rate (GFR). In recent years, therefore, the term acute kidney injury (AKI) has replaced ARF because AKI denotes the entire clinical spectrum from mild increases in serum creatinine to overt renal failure. AKI is defined by the Risk-Injury-Failure-Loss-ESRD (RIFLE) criteria, based on serum creatinine concentration and urine flow rate. The Acute Kidney Injury Network (AKIN) subsequently modified the definition further and divided AKI into three stages. This chapter includes discussions of the etiology and diagnosis of AKI in hospitalized patients and community-acquired AKI. The specific causes, management, and complications of AKI are also discussed. Figures illustrate the pathophysiologic classification of AKI and the effect of hyperkalemia on cardiac conduction—electrocardiogram (ECG) changes. A worksheet for following patients with AKI is provided.  This review contains 3 figures, 20 tables, and 46 references. Keywords:Acute kidney injury, dialysis, contrast, rhabdomyolysis, nephropathy, urinalysis, multiple myeloma, ethylene glycol, sepsis, hepatorenal syndrome

Acute Kidney Injury - Part I

2019 ◽  
Author(s):  
Paul W Sanders ◽  
Anupam Agarwal
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Acute Kidney Injury Network ◽  
Serum Creatinine Concentration ◽  
Cardiac Conduction ◽  
Creatinine Concentration ◽  
Waste Products ◽  
Abrupt Decrease

Acute renal failure (ARF) has been defined as a syndrome in which an abrupt decrease in renal function produces retention of nitrogenous waste products. Translating this abstract description into a clinically useful, accurate, and widely accepted definition has been challenging, in large part because of the focus on serum creatinine concentration, which is easily obtained but has the inherent limitation of poor detection of rapid or subtle, but clinically important, changes in the glomerular filtration rate (GFR). In recent years, therefore, the term acute kidney injury (AKI) has replaced ARF because AKI denotes the entire clinical spectrum from mild increases in serum creatinine to overt renal failure. AKI is defined by the Risk-Injury-Failure-Loss-ESRD (RIFLE) criteria, based on serum creatinine concentration and urine flow rate. The Acute Kidney Injury Network (AKIN) subsequently modified the definition further and divided AKI into three stages. This chapter includes discussions of the etiology and diagnosis of AKI in hospitalized patients and community-acquired AKI. The specific causes, management, and complications of AKI are also discussed. Figures illustrate the pathophysiologic classification of AKI and the effect of hyperkalemia on cardiac conduction—electrocardiogram (ECG) changes. A worksheet for following patients with AKI is provided.  This review contains 3 figures, 21 tables, and 46 references. Keywords:Acute kidney injury, dialysis, contrast, rhabdomyolysis, nephropathy, urinalysis, multiple myeloma, ethylene glycol, sepsis, hepatorenal syndrome

Definitions, Classification, and Screening of Acute Kidney Injury

2017 ◽  
Author(s):  
Andrew Davenport
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Glomerular Filtration Rate ◽  
Serum Creatinine ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Kidney Injury ◽  
Creatinine Concentration

Acute kidney injury (AKI; previously acute renal failure) is defined as an acute and sustained deterioration in kidney function. As AKI is a descriptive term, an attempt should be made to establish a diagnosis in patients with AKI. There are numerous causes of AKI, and all or part of the kidney may be affected. This review discusses the definitions of AKI, measurement of renal function, incidence of AKI, baseline serum creatinine, grading and severity of AKI, and screening for AKI. Figures show renal reserve and renal tubule. Tables list consensus definitions of AKI, effect of patient demographics on serum creatinine concentration, endogenous compounds that can interfere with colorimetric modified Jaffe-based reactions for determining serum creatinine concentration, risk factors for developing AKI in adult patients proposed by the Renal Angina Index, and risk factors for developing acute contrast-induced kidney injury in adult patients. Key Words: Acute kidney injury; Acute renal failure; Glomerular filtration rate; Serum creatinine; Kidney function; Estimated glomerular filtration rate; Biomarkers of AKI

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