Extracorporeal Regional Complexing Haemodialysis Treatment of Acute Inorganic Mercury Intoxication

1990 ◽  
Vol 9 (3) ◽  
pp. 137-141 ◽  
Author(s):  
P.J. Kostyniak ◽  
H.B. Greizerstein ◽  
J. Goldstein ◽  
M. Lachaal ◽  
P. Reddy ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Suicide Attempt ◽  
Inorganic Mercury ◽  
Chelating Agent ◽  
White Female ◽  
Mercury Poisoning ◽  
Arterial Blood ◽  
Mercury Intoxication ◽  
Haemodialysis Treatment

A 70-year-old white female presented approximately 24 h after ingesting three 475 mg tablets (1.425 g) of mercuric chloride in a suicide attempt. Acute renal failure necessitated the initiation of haemodialysis approximately 4 d after the ingestion. Treatment with BAL (2,3-dimercaptopropanol) resulted in only small increases in mercury output into dialysate. A new procedure involving the extracorporeal infusion of the chelating agent dimercaptosuccinic acid (DMSA) into the arterial blood line during haemodialysis was initiated. This procedure of Extracorporeal Regional Complexing Haemodialysis (ERCH) had been effective in increasing methylmercury removal in patients poisoned by contaminated grain. The first DMSA-ERCH procedure was performed 6 d after poisoning. There was a dramatic increase in mercury output into the dialysate. During three treatment sessions of 80 min each, 1189 μg of mercury were removed from the patient. The dialysed mercury represented the only mercury output since the patient was anuric and not producing faeces. DMSA-ERCH appears to be much more effective than BAL and haemodialysis in the treatment of acute inorganic mercury poisoning. The long interval between poisoning and initiation of treatment probably contributed to the patients ultimate demise, 28 d after poisoning. Efficacy of the DMSA-ERCH procedure for inorganic mercury poisoning is likely to be improved as the interval between exposure and treatment is reduced.

scholarly journals Acute renal failure after massive ingestion of gliclazide in a suicide attempt

Renal Failure ◽  
1998 ◽  
Vol 20 (3) ◽  
pp. 533-537 ◽  
Author(s):  
A. Barracca ◽  
O. Ledda ◽  
B. Michittu ◽  
G. F. Pili ◽  
O. Manca ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Suicide Attempt

Metformin-Associated Nonketotic Metabolic Acidosis

1997 ◽  
Vol 31 (1) ◽  
pp. 53-55 ◽  
Author(s):  
Mark R Jurovich ◽  
John D Wooldridge ◽  
Rex W Force
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Early Recognition ◽  
Normal Serum ◽  
Anion Gap ◽  
Diabetic Patients ◽  
Strict Adherence ◽  
Arterial Blood

OBJECTIVE: To document a case of anion gap, nonketotic metabolic acidosis occurring in a patient with acute renal failure who was receiving metformin. CASE SUMMARY: A 67-year-old white man presented with a 9-day history of weakness, nausea, dizziness, and difficulty moving; he had also not eaten during the previous 2 days. The patient had numerous abnormalities on his serum chemistry panel and arterial blood gases, including a pH of 7.1 and an anion gap of 21 mEq/L. No ketones were detected in the urine. The patient was treated with intravenous fluids, sodium bicarbonate, insulin, and hemodialysis. All medications were discontinued. The acidosis resolved shortly after hemodialysis. The hospital course was complicated by the onset of atrial fibrillation occurring on day 2 that did not respond to chemical cardioversion. On day 6 the patient was discharged home with resolving acute renal failure and normal serum pH. CONCLUSIONS: The mortality rate of biguanide-induced lactic acidosis is approximately 50%; thus, early recognition and treatment are essential. Suspicion of lactic acidosis should be high when diabetic patients who are taking a biguanide present with acidosis. The majority of cases of metformin-induced lactic acidosis have occurred in patients with contraindications to the drug (i.e., renal dysfunction). Thus, it is important to maintain strict adherence to these contraindications and monitor patients for deteriorating renal function.

Erythropoietin enhances recovery from cisplatin-induced acute renal failure

1994 ◽  
Vol 266 (3) ◽  
pp. F360-F366 ◽  
Author(s):  
N. D. Vaziri ◽  
X. J. Zhou ◽  
S. Y. Liao
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Functional Recovery ◽  
Deficiency Anemia ◽  
Control Group ◽  
Cortical Tissue ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Significant Difference ◽  
Epo Deficiency

Acute renal failure (ARF) is associated with erythropoietin (EPO) deficiency anemia. The present study was designed to determine whether the course of ARF can be altered by preventing EPO deficiency and the associated anemia. Sprague-Dawley rats were injected with a single dose of cisplatin (CP), 7 mg/kg intraperitoneally, and randomized into recombinant EPO-treated (EPO), placebo-treated (control), recombinant EPO-treated pair-fed (EPO-PF), and EPO-treated anemic (EPO-anemic) groups. They were then treated with daily injections of recombinant EPO, 100 U/kg, or placebo for 9 days. Animals in the EPO-anemic group received daily phlebotomies gauged to maintain hematocrits equal to those in the control group. Rats in the EPO-PF group were pair fed with the controls. The control and EPO-anemic groups showed a fall, whereas the EPO and EPO-PF groups showed a rise in hematocrit on day 9. Although blood volume on day 9 was significantly greater in the EPO group than in either the EPO-anemic group or the control group, it was comparable in the latter groups. An equally severe reduction in creatinine clearance (CCr) was found in all groups on day 4. However, measurements of CCr and inulin clearance on day 9 revealed a significantly greater functional recovery in the EPO, EPO-PF, and EPO-anemic groups than in the controls. The enhanced functional recovery with EPO administration was accompanied by an increased tubular regeneration and [3H]thymidine incorporation in the cortical tissue. No significant difference was found in either cortical tissue iron content or arterial blood pressure in the study groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemolysis and Methemoglobinemia Secondary to Rasburicase Administration

2005 ◽  
Vol 39 (11) ◽  
pp. 1932-1935 ◽  
Author(s):  
Linda A Browning ◽  
James A Kruse
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Hemolytic Anemia ◽  
G6pd Deficiency ◽  
Tumor Lysis Syndrome ◽  
Simultaneous Occurrence ◽  
Arterial Blood Gas ◽  
Chemotherapy Administration ◽  
Arterial Blood ◽  
Patients At Risk

OBJECTIVE To report a case of hemolytic anemia and methemoglobinemia developing after rasburicase administration to a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. CASE SUMMARY A 50-year-old African American man was hospitalized with new onset seizure, diabetic ketoacidosis, respiratory failure, and acute renal failure. Serum uric acid concentrations were elevated, and the patient was treated with one dose of intravenous rasburicase 22.5 mg for acute renal failure secondary to hyperuricemia. Routine arterial blood gas analyses performed after rasburicase was administered revealed elevated methemoglobin concentrations, which peaked at 14.7%. Hemolytic anemia developed as evidenced by a fall in blood hemoglobin from 14.8 to 5.3 g/dL. The patient made a full recovery following aggressive fluid therapy, blood transfusions, and respiratory support. G6PD deficiency was subsequently confirmed. The Naranjo probability scale indicated that rasburicase was a probable cause of hemolytic anemia and methemoglobinemia. DISCUSSION Rasburicase is contraindicated in patients with G6PD deficiency as it may cause hemolytic anemia and methemoglobinemia. As of September 26, 2005, simultaneous occurrence of hemolytic anemia and methemoglobinemia has not been reported in patients receiving rasburicase. CONCLUSIONS As of September 26, 2005, screening for G6PD deficiency should be performed whenever possible prior to chemotherapy administration in patients at risk of developing tumor lysis syndrome.

scholarly journals Two consecutive episodes of acute renal failure following mercury poisoning

1997 ◽  
Vol 12 (2) ◽  
pp. 328-330 ◽  
Author(s):  
A. Fraco ◽  
A. Antolin ◽  
M. Trigueros ◽  
C. Munoz ◽  
J. Navas ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mercury Poisoning

The effect of dipyridamole on the initiation phase of postischemic acute renal failure in rats

1987 ◽  
Vol 65 (7) ◽  
pp. 1491-1495 ◽  
Author(s):  
Jen-Jar Lin ◽  
Paul C. Churchill ◽  
Anil K. Bidani
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Plasma Flow ◽  
Left Kidney ◽  
Artery Occlusion ◽  
Control Group ◽  
Left Renal Artery ◽  
Initiation Phase ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood

Several previous observations support the hypothesis that increased adenosine production and release mediate, at least in part, the reductions in renal blood flow and glomerular filtration rate in ischemic acute renal failure (ARF). If this hypothesis is correct, dipyridamole should potentiate these changes, since it blocks cellular adenosine uptake, thereby increasing the concentration and potentiating the effects of extracellular adenosine. Moreover, theophylline should block the effects of dipyridamole, since it is an adenosine receptor antagonist. These predictions were tested in three groups of anesthetized rats. All rats were subjected to 30 min of left renal artery occlusion; 30 min after relieving the occlusion, a 45-min clearance period was begun. The control group was given saline i.v.; the two experimental groups received either dipyridamole (24 μg∙min−1∙kg−1) or dipyridamole plus theophylline i.v. (111 μmol/kg as a prime, 1.1 μmol∙min−1∙kg−1 as an infusion). In the control group, the previously ischemic left kidneys exhibited decreased clearances of para-aminohippurate and inulin (CPAH and CIn), filtration fraction (FF), and urine/plasma inulin concentration (U/PIn), and increased urine flow (V), Na excretion (UNaV), and fractional Na excretion (FENa) in comparison with the contralateral right kidney. Dipyridamole pretreatment did not affect the right kidney, but it intensified the reductions in left kidney CPAH, CIn, and FF. Theophylline blocked all these effects of dipyridamole on the left kidney, and increased renal plasma flow (CPAH/PAH extraction), despite a decrease in systemic arterial blood pressure. These results are further support for the hypothesis that adenosine mediates, at least in part, the hemodynamic changes in postischemic ARF in rats.

Endotoxemic acute renal failure in awake rats

1986 ◽  
Vol 250 (6) ◽  
pp. F1098-F1106 ◽  
Author(s):  
D. Kikeri ◽  
J. P. Pennell ◽  
K. H. Hwang ◽  
A. I. Jacob ◽  
A. V. Richman ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Systemic Hemodynamics ◽  
Sprague Dawley ◽  
Ultrastructural Studies ◽  
Arterial Blood ◽  
Peritubular Capillaries

The sequence of changes in renal function in endotoxemic acute renal failure (ARF) and the role of hypotension and systemic hemodynamics were evaluated in awake female Sprague-Dawley rats given an intravenous bolus of Escherichia coli endotoxin (20-40 mg/kg). After endotoxin ARF was abrupt in onset as glomerular filtration rate (GFR) fell promptly and progressively by 53% within 3.5 h, whereas renal blood flow decreased by 42% and renal vascular resistance nearly doubled. Systemic hemodynamics remained stable, including mean arterial blood pressure, cardiac output, and total peripheral resistance. Early endotoxemic ARF was associated with oliguria and sodium retention, a finding consistent with intact tubular function. Three and one-half hours after endotoxin, however, fractional water and sodium excretion were significantly increased. Ultrastructural studies then demonstrated sequestration of phagocytic leukocytes and intracellular edema in the peritubular capillaries with normal glomeruli. The decrease in GFR was spontaneously reversible within 7-9 days. Extracellular fluid volume expansion with saline either before or 24 h after administration of endotoxin failed to prevent the decrease in GFR or to normalize renal function. The data suggest that endotoxin has direct renal effects. The endothelial cells may be the primary target of endotoxin in the kidney.

Angiotensin Blood Levels during the Evolution of Acute Renal Failure

1970 ◽  
Vol 38 (2) ◽  
pp. 225-231 ◽  
Author(s):  
E. Ochoa ◽  
S. Finkielman ◽  
A. Agrest
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Systolic Blood Pressure ◽  
Negative Correlation ◽  
Correlation Coefficients ◽  
Blood Levels ◽  
Urinary Volume ◽  
Plasma Urea ◽  
Arterial Blood

1. Angiotensin blood levels (ABL) have been measured in thirteen white patients with diagnoses of acute renal failure of different aetiologies during several stages of the disease and with no evidence of other conditions that could stimulate renin release by the kidney. 2. Mean ABL on admission was 770 SEM 62 ng/l. When daily urinary volume was higher than 1500 ml, these values were significantly lower: 114 SEM 49·6 ng/l. 3. A negative correlation between ABL and systolic blood pressure was obtained (r = −0·35, P = 0·01). The partial correlation coefficients between ABL and systolic blood pressure showed the same results. 4. A negative correlation between the logarithm of ABL and daily urinary volume was obtained. The partial linear correlation coefficients between ABL and urine volume confirmed this relationship. 5. There was no correlation between the ABL and the aetiology of the anuria, its final course, the duration of the disease, the arterial blood pressure and the plasma urea, sodium or potassium levels. 6. It is suggested that the decrease in the ABL has some connection with the re-establishment of the diuresis, possibly through an increase of glomerular filtration rate and in sodium excretion affecting the macula densa cells.

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