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Pathogenesis of renal failure due to aminoglycosides and contrast media
Renal
failure
MephrotoxilBs
contrast media
Amlnoglycoaide antiblotks Drug nephrotoxlclty
lmmunoglobulin A deflclency Lung lavage
A brother and sister with classic, biopsy proved pulmonary alveolar proteinosis are described. Both had low serum and low normal secretory IgA levels. A tendency for familial occurrence is possible and it is recommended that patients with pulmonary alveolar proteinosis, and their families, be evaluated for immunologic deficiencies.
Webster JR, Batttfora Ii, Furey C, Harrison RA, Shapiro B: Pulmonary alveolar poteinosis in two siblings with decreased immunoglobulin A. Am J Med 1980;69: 786-789.
Alveolar protelnoels Lurp defense mechanlem
The etiology of acute renal failure has changed in recent years due to the recognition of drug nephrotoxicity as a more unwwon cause. In this communication recent information concerning the pathophystology of nephrotoxic acute renal failure produced by aminoglycoside antibiotics and amtrast m&a used fa roentgunogaphy is emphasiied. The aminoglycosidss are excreted primarily by glomerular filtration; however, net tubular reabsorption and renal paronchymal accumulation do occu. The pathogsnesis of nephrotoxicity, atthou@ probably linked to cortical accumulation, is complex since experimental animals recover from gentamicin-induced renal failure despite continued administration of the drug. Knowledge of the precise cellular mechanisms of injvy awaits further studiis. Histologic damage is usually limited to proximal tubular necrosis and. clinically. Ctrerenal failue is nonol)gwic. Although repats of contrast medh (used in roantgenography) produchg acute renal failure have increased. the pathcgenesis is unclear. Evidence supporting various theories is reviewed.
Bennett WM. Luft F, Porter CIA: Pathogsnesis of renal failure due to aminoglycosides and contrast media. Am J Med t 980; 69: 767-774.
Roentgenographlc
Anaerobic infection
Pulmonary tDyopnee
llWOIMOSiS
arlerectomy
Three cases of chronic persistent pulmonary embolism occurring despite anticoagulant therapy are presented with hemodynamic dataand follow-up of up to seven years. All patients had mikl to moderate espnea on exertion. All patients had norms1 resting pulmonary artery pressures; two patients demonstrated pulmonary hypertension with exercise. One patient underwent successful throMoe&arterectomy but had subsequent reocclusion secondary to in situ thrombosis. With all patients receiving long-term anticoagulant therapy, there was no clinical recurrence of embolization cr progression of symptoms. Patients with chronic persistent pulmonary embolism should be identified and should receive long-term follow-up. Therapy aimed at prevention of recurrent embolization is required. Pulmonary thromboendarterectomy is indicated for selected patients.
Shuck JW. Walder JS, Kam TH, Thomas HM: Chronic persistent pulmonary embolism Report of three cases. Am J Med 1980; 69: 790-794.
Pulmonary embolism Anticoegulatlon
Leptotrichia buccalis is a ubiquitous, obligately anaerobic, gram-negative rod classified in the family Bacteroidaceae. Unlike other members of this family L. buccalis has not previously been reported to be a cause of serious hfection. A case of cavkary pneumonia and septiiia caused by L. buccalis is repcrted. Leptotrichii have been shown to contain potent endotoxin. L. buccalis has the potential to be a virulent, pathogenic microorganism, especially in the compromised host.
Morgenstein AA, Citron CM. Crisek B, Finegotd SM: Serious infection with Leptotrichia buccalis. Report of a case and review of the literature. Am J Med 1960:69: 782785.
Leptotrlchia Bacteroidaceae Immunocompromlsed host
failure
MephrotoxilBs
contrast media
Amlnoglycoaide antiblotks Drug nephrotoxlclty
lmmunoglobulin A deflclency Lung lavage
A brother and sister with classic, biopsy proved pulmonary alveolar proteinosis are described. Both had low serum and low normal secretory IgA levels. A tendency for familial occurrence is possible and it is recommended that patients with pulmonary alveolar proteinosis, and their families, be evaluated for immunologic deficiencies.
Webster JR, Batttfora Ii, Furey C, Harrison RA, Shapiro B: Pulmonary alveolar poteinosis in two siblings with decreased immunoglobulin A. Am J Med 1980;69: 786-789.
Alveolar protelnoels Lurp defense mechanlem
The etiology of acute renal failure has changed in recent years due to the recognition of drug nephrotoxicity as a more unwwon cause. In this communication recent information concerning the pathophystology of nephrotoxic acute renal failure produced by aminoglycoside antibiotics and amtrast m&a used fa roentgunogaphy is emphasiied. The aminoglycosidss are excreted primarily by glomerular filtration; however, net tubular reabsorption and renal paronchymal accumulation do occu. The pathogsnesis of nephrotoxicity, atthou@ probably linked to cortical accumulation, is complex since experimental animals recover from gentamicin-induced renal failure despite continued administration of the drug. Knowledge of the precise cellular mechanisms of injvy awaits further studiis. Histologic damage is usually limited to proximal tubular necrosis and. clinically. Ctrerenal failue is nonol)gwic. Although repats of contrast medh (used in roantgenography) produchg acute renal failure have increased. the pathcgenesis is unclear. Evidence supporting various theories is reviewed.
Bennett WM. Luft F, Porter CIA: Pathogsnesis of renal failure due to aminoglycosides and contrast media. Am J Med t 980; 69: 767-774.
Roentgenographlc
Anaerobic infection
Pulmonary tDyopnee
llWOIMOSiS
arlerectomy
Three cases of chronic persistent pulmonary embolism occurring despite anticoagulant therapy are presented with hemodynamic dataand follow-up of up to seven years. All patients had mikl to moderate espnea on exertion. All patients had norms1 resting pulmonary artery pressures; two patients demonstrated pulmonary hypertension with exercise. One patient underwent successful throMoe&arterectomy but had subsequent reocclusion secondary to in situ thrombosis. With all patients receiving long-term anticoagulant therapy, there was no clinical recurrence of embolization cr progression of symptoms. Patients with chronic persistent pulmonary embolism should be identified and should receive long-term follow-up. Therapy aimed at prevention of recurrent embolization is required. Pulmonary thromboendarterectomy is indicated for selected patients.
Shuck JW. Walder JS, Kam TH, Thomas HM: Chronic persistent pulmonary embolism Report of three cases. Am J Med 1980; 69: 790-794.
Pulmonary embolism Anticoegulatlon
Leptotrichia buccalis is a ubiquitous, obligately anaerobic, gram-negative rod classified in the family Bacteroidaceae. Unlike other members of this family L. buccalis has not previously been reported to be a cause of serious hfection. A case of cavkary pneumonia and septiiia caused by L. buccalis is repcrted. Leptotrichii have been shown to contain potent endotoxin. L. buccalis has the potential to be a virulent, pathogenic microorganism, especially in the compromised host.
Morgenstein AA, Citron CM. Crisek B, Finegotd SM: Serious infection with Leptotrichia buccalis. Report of a case and review of the literature. Am J Med 1960:69: 782785.
Leptotrlchia Bacteroidaceae Immunocompromlsed host