The Influence of Available Fluid on the Production of Experimental Hemoglobinuric Nephrosis in Rabbits

Lalich, Joseph J.

doi:10.1084/jem.87.2.157

Cited by 22 publications

(10 citation statements)

References 2 publications

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“…The present study indicates that a reproducible and significant renal functional lesion can be produced in the dehydrated rat by the intravenous injection of hemoglobin. In accord with the observations of others (8,9) hemoglobin injection in normally hydrated animals, not subjected to measures which produce renal ischemia, failed to produce significant renal failure. In the present study the combination of ether anesthesia and dehydration served to render the kidney susceptible to the deleterious effects of hemoglobinemia.…”

Section: Discussionsupporting

confidence: 80%

The Renal Lesion Associated With Hemoglobinemia

Jaenike

1966

The Journal of Experimental Medicine

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The precise mechanisms involved in the association of hemoglobinemia with acute renal failure remain unknown. The difficulties in studying this problem in patients are manifold, consequently the bulk of the investigation in this area has necessarily involved experimentally produced lesions in the laboratory animal. Largely as a result of such studies a variety of differing and conflicting hypotheses concerning the pathogenesis of this renal lesion have arisen. Perhaps the most favored of these are the suggestions that (a) tubular blockage by precipitated hemoglobin is the primary cause of excretory failure in the affected kidney, and (b) some undefined factor or factors produce a primary reduction in glomerular filtration rate, presumably as a consequence of renal ischemia. Carefully performed studies may be cited in support of either the first (1, 2) or second (3, 4) of these hypotheses. In addition, other explanations for the renal failure have been considered, particularly the role of abnormal back diffusion of tubular fluid through damaged tubular epithelial structures and the effect of renal edema in reducing renal blood flow and filtration rate. The establishment of an experimental model of a clinical renal disease in the laboratory animal affords the opportunity of making accurate functional measurements of the evolution of the lesion and of correlating structural alterations at each stage of the disorder with the corresponding functional data. This does not appear to have been accomplished with acute renal failure associated with hemoglobinemia. This lack of serial functional and morphological studies of a standard lesion may in part account for the conflicting views regarding the pathogenesis of this disorder. Consequently the present study was designed, with the ultimate objective of defining the mechanisms underlying the renal functional failure associated with this lesion.The present report describes a relatively simple method for the production of acute renal failure in the rat by the intravenous injection of hemoglobin. The lesion is reversible and relatively uniform in its functional and structural manifestations. Certain of the factors which influence its production and degree of severity have been examined. The functional evolution of the lesion, from its

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Section: Discussionsupporting

confidence: 80%

The Renal Lesion Associated With Hemoglobinemia

Jaenike

1966

The Journal of Experimental Medicine

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“…Heine proteinemia is common to both the experimental models of acute tubule necrosis. In many diverse clinical cases of acute tubule necrosis, heine proteinemia is also noted (12,13,15,21). Since it was established that hippurate transport could be used as an index of early tubule injury, the effects of various heme proteins on this transport system were investigated.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Renal Toxicity of Heme Proteins and Their Derivatives: A Role in the Genesis of Acute Tubule Necrosis

Braun

Weiss

Keller

et al. 1970

The Journal of Experimental Medicine

136

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This investigation studies the toxicity of heme proteins and/or their break-down products on renal function. Heme proteinemia precedes acute tubule necrosis at a frequency great enough to suggest a causal relationship between the two events. Physiological and metabolic functions of kidney slices are investigated in several models of acute tubule necrosis. Organic acid and organic base transport is depressed earliest. These alterations in tubule function cannot be explained by ischemia or obstruction alone. Heme proteinemia in rats or incubation of renal slices in medium containing heme proteins yields several interesting observations. Neither in vivo or in vitro do hemoglobin and methemoglobin alone produce a depressive effect on the transport systems studied. However, parallel to many clinical situations, when such secondary insults as hypoxia and elevated ammonia concentrations are included in the experimental design, transport functions are depressed. Ferrihemate, a molecule smaller than hemoglobin or methemoglobin, depresses transport function without secondary insults. From these studies it is concluded that heme proteins play a role in tubule dysfunction seen in acute tubule necrosis. A model is presented that collates these data with other factors known to play a part in the pathogenesis of this renal syndrome.

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“…Malgré l'émission massive d'urines très diluées au moment où l'on déclenche l'hémo globinurie par injection de glycérol, ces animaux développent une insuffisance rénale aiguë. La sévérité de l'insuffisance rénale est intermédiaire entre celle des Dehydration has been shown to be a potent predisposing factor in the development of acute renal failure (6,11,12). This effect has been attributed in the past to increased urine concentration and slowed flow through distal segments o f the kidney facilitating tubule ob struction with casts.…”

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The Role of the Concentration Mechanism in the Development of Acute Renal Failure: Micropuncture Studies Using Diabetes Insipidus Rats

Wilson

Thiel

Arce

et al. 1969

Nephron

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The role of the concentrating mechanism in the potentiation of acute renal failure by dehydration has been studied using rats with complete diabetes insipidus. These rats were shown to be continually dehydrated even when allowed free access to water. Despite massive volumes of highly dilute urine at the time that hemoglobinuria was induced by glycerol injection, these animals developed acute renal insufficiency whose severity was intermediate between that of non-dehydrated and severely dehydrated normal rats treated similarly. Micropuncture experiments showed the appearance of the kidney in vivo and the functional abnormalities of the three types of rats to be qualitatively identical. It appears that dehydration’s effect on hemoglobinuric acute renal failure is independent of the concentrating mechanism and correlates well with plasma volume depletion. It is suggested that factors other than ADH titre, high urine concentration and low flow rate are the prime determinants of the effect of dehydration on hemoglobinuric acute renal failure in the rat.

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The Influence of Available Fluid on the Production of Experimental Hemoglobinuric Nephrosis in Rabbits

Cited by 22 publications

References 2 publications

The Renal Lesion Associated With Hemoglobinemia

The Renal Lesion Associated With Hemoglobinemia

Evaluation of the Renal Toxicity of Heme Proteins and Their Derivatives: A Role in the Genesis of Acute Tubule Necrosis

The Role of the Concentration Mechanism in the Development of Acute Renal Failure: Micropuncture Studies Using Diabetes Insipidus Rats

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