Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal impairment (ARI) secondary to immersion and near-drowning is rarely described and poorly understood. A retrospective case-control study was performed: (1) to determine the incidence of ARI associated with near-drowning or immersion and (2) to define the clinical syndrome and to assess clinical predictors of ARI. Of 30 patients presenting after immersion or near-drowning, 50% were identified with ARI, with a mean admission serum creatinine of 0.24 +/- 0.33 mmol/L (2.7 +/- 3.7 mg/dl). These patients were a heterogeneous group: Eight had mild reversible ARI, three had ARI related to shock and multisystem failure, two had rhabdomyolysis-related ARI, and two had severe isolated ARI. Two patients required supportive hemodialysis and two died. Patients with ARI experienced more marked acidosis than control patients, as measured by serum bicarbonate (P < 0.001), pH (P < 0.001), and base excess (P < 0.001). There was also a higher admission lymphocyte count in the ARI group (P = 0.056). Dipstick hematuria on admission was significantly more common in patients with ARI (P = 0.016), and patients with 2 to 3+ of admission dipstick proteinuria had a higher peak serum creatinine than patients with less proteinuria (P < 0.05). Admission predictors of ARI by univariate logistic regression analysis included reduced serum bicarbonate (P = 0.002), pH (P = 0.001), and base excess (P < 0.001). The best predictor of ARI on multivariate analysis was a negative base excess (P = 0.01). In summary, acute renal impairment commonly occurs after immersion and near-drowning and is a heterogeneous condition. Although mild reversible renal impairment (serum creatinine < 0.30 mmol/L) (3.4 mg/dl) is usual, severe acute renal failure requiring dialysis can occur. It is recommended that any patient who presents after near-drowning or immersion should be assessed for potential ARI by serial estimations of serum creatinine, particularly when there is an increase in the initial serum creatinine, marked metabolic acidosis, an abnormal urinalysis, or a significant lymphocytosis.
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PMID:Acute renal impairment after immersion and near-drowning. 1021 39

The objective of this paper is to document the prevalence of indicators of acute renal injury in a series of methanol-poisoned patients treated in an intensive care unit and to discuss the possible mechanisms. This is a retrospective analysis of the medical records of 25 consecutive patients admitted to the intensive care unit after severe intentional methanol poisoning. Acute renal impairment was defined as a serum creatinine concentration higher than 177 micro mol/L and/or a urinary output on admission and for the first 24 h below 0.5 ml/kg/h. Clinical pathological signs of acute renal injury were found in 15 patients. In comparison with the 10 other patients taken as control group, the patients who developed renal injury had a lower blood pH value on admission, a higher serum osmolality, and a higher peak formate concentration. Two factors contributing to renal injury could be identified: hemolysis and myoglobinuria. The role of osmotic changes (osmotic nephrosis) or of a direct cytotoxic effect of formic acid remains speculative. Analysis of proteinuria suggests that proximal tubular cells may be preferentially affected. Results of histopathological evaluation of the kidney on a limited sample size (n = 5) were inconclusive but suggestive of possible hydropic changes in the proximal tubule secondary to methanol toxicity. Acute renal injury may be associated with other signs of severity in methanol poisoning, but it is almost always reversible in survivors. Indicators of acute renal injury were identified. The pathophysiology of this acute renal injury is multifactorial and far more complex than shock-related tubular necrosis.
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PMID:Acute renal injury following methanol poisoning: analysis of a case series. 1537 Nov 71

Clofarabine is used as second-line therapy for acute myeloid leukemia. Acute renal impairment is reported with clofarabine; however, it is more likely to occur in patients with confounding factors that may underlie the adverse event. We describe a 65-year-old man treated with clofarabine for relapsed acute myeloid leukemia who experienced severe acute kidney injury and proteinuria temporally related to clofarabine administration. The morning after completion of clofarabine administration, his serum creatinine concentration increased to approximately 1.4-fold above his baseline value, and peaked at 2.8-3.6-fold over baseline within 72 hours. A 24-hour urine collection contained 4100 mg of protein. His serum creatinine concentration gradually returned to within 1.5 times his baseline value. Examination of the patient's clinical course, vital signs, and laboratory results did not yield any compelling evidence of alternative causes for acute kidney injury. The patient's comorbidities included a left ventricular ejection fraction of 35-40% and diabetes mellitus. His drug therapy with potential renal effects-lisinopril, furosemide, tobramycin, allopurinol, and valacyclovir-that preceded clofarabine administration was evaluated, and none was determined to be a major factor in the development of this adverse event. Bone marrow evaluations were negative for residual leukemia after clofarabine therapy. After approximately 11 weeks of hospitalization, the patient and his family made an informed decision to continue supportive care at home. Acute kidney injury in this patient was attributed to clofarabine administration due to the time course of events with respect to potential contributing factors. Use of the Naranjo adverse drug reaction probability scale indicated a probable relationship (score of 7) between the patient's development of renal effects and clofarabine therapy. To our knowledge, this is the first report of medically significant proteinuria associated with administration of clofarabine. Clinicians should be aware of the potential for acute kidney injury if their patients are administered clofarabine.
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PMID:Clofarabine-associated acute kidney injury and proteinuria. 2192 94