Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was undertaken to evaluate the occurrence of renal failure following perinatal asphyxia in the newborns. Thirty newborns with severe birth asphyxia were included in the study along with 30 normal newborns who comprised the control group. Any neonate presenting with oliguria or blood urea more than 40 mg/dl or creatinine more than 1 mg/dl was subjected to a fluid and diuretic challenge. If oliguria or renal dysfunction persisted then the child was labelled as renal failure and these subjects were further investigated. It was observed that 43% of asphyxiated babies developed acute renal failure (ARF); 69.2% babies had oliguric renal failure. While no significant correlation could be seen between Apgar scores at 5 and 10 min and development of ARF, a significant relationship was seen between hypoxic-ischemic encephalopathy and ARF. Patients with oliguric ARF carried a poorer prognosis as compared to non-oliguric ARF.
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PMID:Acute renal failure in asphyxiated newborns. 205 7

The differentiation between cyclosporine nephrotoxicity (CyN) and acute rejection (AR) still remains a matter of intensive research. In a retrospective study over the last 2 years, we assessed the clinical and histopathological data of 43 episodes of renal dysfunction in 39 renal transplant recipients immunosuppressed with cyclosporine (CyA). Ten episodes (23.2%) were identified as AR and 10 (23.2%) as acute CyN; in six cases (13.9%), signs of both AR and CyN were found. Fever (80%), oliguria (50%), and edema (50%) were prominent features in AR, but not in CyN. Renal blood flow was higher in the nephrotoxicity group and for corresponding degree of renal dysfunction. Significant hyperuricemia (greater than 8 mg/dL) was a prominent finding in CyN (80%) and to a lesser extent in AR (20%). The helper to suppressor cell ratio in the peripheral blood remained stable or slightly decreased in all cases with CyN, but increased in 70% of the cases with AR. CyN was associated with significantly higher whole blood CyA levels (P less than 0.005) and there was a positive correlation between plasma creatinine and CyA levels during the nephrotoxicity episodes (P less than 0.02). Diffuse mononuclear cell infiltrate was observed in 90% of the biopsies with AR and only in 20% with CyN (P less than 0.005). Concerning the extent of the tubular lesions, no significant differences were observed between the two groups. In contrast, vascular lesions such as arterial endothelial proliferation (P less than 0.05), hyalinosis (P less than 0.05), and glomerular capillary thrombi (P less than 0.05) were more commonly seen in nephrotoxicity biopsies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differentiation between renal allograft rejection and cyclosporine toxicity: a clinicopathological study. 206 42

Three patients with internal leakage of urine are described. As a result of urine resorption into the blood a condition developed resembling acute renal failure. Internal loss of urine is divided into intraperitoneal and extraperitoneal leakage and usually gives rise to oliguria and microscopic haematuria. In the intraperitoneal type increasing abdominal complaints and ascites will develop whereas in the extraperitoneal type regional oedema will become present without, in the case of sterile urine, abdominal complaints of importance. Important clues as to the diagnosis are the concentrations in serum and urine of urea, creatinine and sodium, and the demonstration of the leak by means of imaging techniques. Treatment of choice is a drainage procedure, for instance by a bladder catheter. In acute renal failure this pseudo form should be distinguished from the real thing.
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PMID:Pseudo-renal failure associated with internal leakage of urine. 207 11

We have reviewed experience with aminoglycosides in cardiac surgical prophylaxis from 1984 to 1989. In the first two years, prospectively randomized trials (517 patients) allowed comparison of tobramycin (three-day course) with a non-toxic antibiotic, teicoplanin. A significant excess rise in serum creatinine was present at the end of the first postoperative week in patients given tobramycin (165 vs 149 patients, 95% CI 3-17 microM. P less than 0.01, which was most marked in ten oliguric patients with trough serum levels over 2 mg/l (95% CI 7-52 microM). However, no patient needed haemodialysis and only one case of possible ototoxicity was identified. During the next three years, of 912 patients given two to three days gentamicin, 29 patients were shown to have potentially toxic serum levels and oliguria. Three individual cases are described, including one of ototoxicity and one of nephrotoxicity neeeding haemodialysis. The hazards of aminoglycoside toxicity are probably small compared with the failure of other antibiotics to cover staphylococci that may later cause wound infection or endocarditis. However, surgeons should probably be advised to check the aminoglycoside level in all patients on the first post-operative day.
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PMID:Aminoglycoside toxicity following antibiotic prophylaxis in cardiac surgery. 207 53

Renal failure in sepsis often occurs without other organ failure such as cardiovascular or pulmonary dysfunction. An endotoxin-induced renal insufficiency model using rabbits, which does not complicate other organ failure, was developed. To selectively damage kidneys endotoxin (40 micrograms/kg/h, 3 h) was infused through a cannula placed into the abdominal aorta just distally to the take-off of the superior mesenteric artery after ligation of the aorta below the junction of renal arteries. The following manifestations of renal insufficiencies were observed with high reproducibility: oliguria, increase in plasma creatinine (from 1.1 to 1.6 mg/dl) and urine N-acetyl-beta-D-glucosaminidase (from 7.9 to 23.7 U/l), decrease in effective renal plasma flow (33%) and glomerular filtration rate (35%), and an apparent renal ischemic change in the histological examination. On the other hand, blood pressure, heart rate, respiration rate, body temperature and hematocrit were not significantly altered. The present model is useful for studying the effects of drugs on renal insufficiency in sepsis or endotoxemia and its pathogenesis. Most renal insufficiencies in clinical sepsis may be caused by endotoxin-induced renal ischemic change due to neither low blood pressure nor renal microthrombi.
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PMID:Renal insufficiency induced by locally administered endotoxin in rabbits. 208 49

Brain serotonin depletion induced by peripheral parachlorophenylalanine (pCPA) is frequently used to evaluate the role of the central serotoninergic system in the regulation of a number of physiological functions, including the secretion of renin by the kidney. We found that due to the treatments applied in the protocol used for the investigation of pCPA effect on renin and vasopressin secretion in rats (300 mg/kg i.p. 64 and 40 h before sacrifice) renal injury was induced as well. Typical changes indicating acute renal failure were observed--an initial polyuria, natriuresis and body mass loss, succeeded by oliguria, decreased glomerular filtration rate, and salt and creatinine retention. Morphological changes in the glomeruli included a thickening of the basal membranes, a confluence and a reduced number of podocyte pedicles. A slight to moderate granular degeneration was observed in epithelial cells of the proximal convoluted tubule, combined with mitochondrial changes--an increase in number, matrix disorganization, and myelin degeneration. In conclusion, the renal function changes after i.p. pCPA may be due not to brain serotonin depletion-alone, but also to nephrotoxic effect.
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PMID:Nephrotoxic effect of the specific brain serotonin depletor para-chlorophenylalanine. 215 5

In order to determine the frequency of acute renal failure (ARF) induced by drugs, to identify the agents responsible for it and to define its semiological characteristics, a prospective study was carried out between 1 October 1987 and 30 September 1988, in Sfax and southern Tunisia. Three Departments of Medicine and one Hemodialysis Center participated in this study. Twelve cases of drug-induced ARF were identified among the 73 cases of ARF reported, i.e., a frequency of 16%. Anti-inflammatory non-steroidal drugs (AINS) were implicated in 5 cases and antibiotics in 2. Symptoms of hypersensitivity were observed in 4 patients, 2/3 without oliguria. Renal insufficiency was usually marked: plasma creatinine was 523 +/- 425 mumol/l; proteinuria greater than 1 g/24 h was seen in 2 patients. Hypovolemia and/or hypotension (6 cases) and diabetes mellitus (4 patients) were found to favor ARF. Renal function returned to normal in 9 patients, whereas mild renal failure persisted in the remaining 3 patients. Drug-induced ARF occurs often. AINS are the most frequently incriminated agents and hypersensitivity symptoms without oliguria are the most common manifestations. Drug-induced ARF can be prevented by close monitoring of high-risk patients, i.e., those taking AINS.
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PMID:[Acute renal insufficiency caused by drugs or iodinated contrast media. Results of a prospective and multicenter study in south Tunisia]. 219 14

Uric acid, as the end-product of purine metabolism in humans, presents a clinical problem because of its relative insolubility, particularly in the acid environment of the distal nephron of the kidney. As a result, states of enhanced purine catabolism increase the urate load on the kidney, leading to intrarenal precipitation. Major causes of increased purine metabolism are malignancies with rapid cell turnover, such as leukemias and lymphomas, and the added acceleration of cell lysis that occurs with chemotherapy and radiation. Serum urate levels rise rapidly, and acute renal failure occurs as a consequence of tubular deposition of urate and uric acid. The keys to the diagnosis of acute uric acid nephropathy are the appropriate clinical setting of increased cell lysis, oliguria, marked hyperuricemia, and hyperuricosuria. A urinary uric acid-to-creatinine ratio greater than 1 helps to distinguish acute uric acid nephropathy from other catabolic forms of acute renal failure in which serum urate is elevated. Preventive treatment involves pharmacologic xanthine oxidase inhibition with allopurinol and alkaline diuresis. Occasionally, acute renal failure occurs despite allopurinol because of the tubular precipitation of the precursor metabolites, such as xanthine, which accumulate with xanthine oxidase inhibition. Dialysis therapy may be required both to correct azotemia and to reduce the body burden of urate. Hemodialysis is preferred because it can achieve greater clearance than other dialysis modes.
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PMID:Acute uric acid nephropathy. 219 58

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.
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PMID:Toxic acute renal failure and hepatitis after ingestion of raw carp bile. 224 75

Peritoneal dialysis was required in 20 (12.8%) of 156 neonates and infants for acute renal failure following open heart surgery using cardiopulmonary bypass. Cardiac diagnosis was TAPVD (7 cases), PA with IVS (2), ECD (2), coarctation of the aorta with VSD (2) and other cardiac malformations (7). The indication for dialysis was oliguria of less than 1.0 ml/kg over 4 hours resistant to volume repletion, inotropic agent and diuretics. Peritoneal dialysis was performed using dialysis catheter and glucose containing dialysis solutions. The mean predialysis BUN and serum creatinine were 30.4 mg/dl and 2.7 mg/dl respectively. The highest serum creatinine during dialysis was 4.5 mg/dl, and all but one patient had BUN level of under 100 mg/dl. Dialysis with glucose containing solution could allow sufficient fluid removal as a result, fluid overload was restored. Plasma protein and electrolytes balance were corrected within 48 hours. Two neonates and 4 infants survived. Thirteen patients died on dialysis: nine of those deaths were related to low cardiac output, 2 death were attributable to respiratory insufficiency, and 2 cases died due to sepsis. One infant died of an unexplained cardiac arrhythmia after renal failure had been improved. It is concluded that peritoneal dialysis is beneficial in neonates and infants who become oliguria following open heart surgery.
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PMID:[Peritoneal dialysis in neonates and infants after open heart surgery]. 224 28


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