Lesions of the Kidney in Acute Renal Failure Following Shock

Brun, Claus; Munck, O.

doi:10.1016/s0140-6736(57)91069-3

Cited by 102 publications

(38 citation statements)

References 13 publications

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“…Several authors have commented on the imperfect correlation be tween the existence of acute renal failure in man and the histologic appearance of the kidney [5,6,21]. Histologic evidence of injury may be minimal in patients whose renal function impairment is severe.…”

Section: Discussionmentioning

confidence: 99%

Maintenance of Renal Function in Salt Loaded Rats Despite Severe Tubular Necrosis Induced by HgCl<sub>2</sub>

DiBona

McDonald

Flamenbaum

et al. 1971

Nephron

110

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Inulin and mannitol clearances, BUN concentrations and renal morphologic alterations were studied in rats 24 h after the injection of low doses of mercuric chloride. Water drinking rats given 4.7 mg/kg body weight of HgCl₂ developed renal failure and severe tubular necrosis. Their clearance of inulin was decreased to the same degree as their simultaneously determined mannitol clearance. Any significant change in tubular permeability should have resulted in a greater loss of mannitol than inulin, and it is suggested that tubular permeability to neither molecule was greatly increased. This is supported by the fact that rats drinking one percent saline in place of tap water for a month prior to receiving the same dose of HgCl₂ showed insignificant changes in inulin clearance and minimal elevations in BUN concentration. Nevertheless, histologic sections of their kidneys showed frank tubular necrosis that was equally severe as, but slightly less extensive than that observed in the water drinking rats whose inulin clearance was 6 % of normal. In view of these findings, it seems unlikely that alterationin tubular permeability per se are responsible for the development of acute renal failure in low dose mercury poisoning. The protective effect of salt loading does not depend on the prevention of tubular injury, and may well reflect inhibition of pre-glomerular vasoconstriction by suppression of the renin-angiotensin axis.

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Section: Discussionmentioning

confidence: 99%

Maintenance of Renal Function in Salt Loaded Rats Despite Severe Tubular Necrosis Induced by HgCl<sub>2</sub>

DiBona

McDonald

Flamenbaum

et al. 1971

Nephron

110

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“…In a controlled autopsy study, Finckh, Jeremey, and Whyte found instances of acute renal failure associated with minimal abnormalities of the tubules, although kidneys of some patients who did not have renal failure had relatively severe tubular lesions. Nor is there any necessary correlation between the degree of functional impairment and the histologic appearance of the kidney in renal biopsy specimens taken 2 to 66 days after the onset of anuria (19). The concept of a tubular basis for oliguria receives support from a widely quoted micropuncture study of Richards (20).…”

Section: Discussionmentioning

confidence: 99%

Renal Micropuncture Study of the Development of Anuria in the Rat with Mercury-induced Acute Renal Failure*

Flanigan¹,

Oken²

1965

J. Clin. Invest.

171

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Acute renal failure in man may result from such factors as trauma, transfusion accidents, sepsis, burns, and acute poisoning with carbon tetrachloride, ethylene glycol, or mercury. Regardless of the etiology and despite marked variability in the histologic appearance of the kidneys of individual cases, most patients with acute renal failure develop oliguria or anuria together with evidence of impaired tubular function. The cause of this decrease in urine volume, however, has not been well defined. Some theories commonly conjured to explain the oliguria of acute renal insufficiency stem largely from pathological findings rather than from functional studies in vivo. Of these findings, three have been stressed as possibly being responsible for oliguria: tubular obstruction by cellular debris (1-3), tubular compression by interstitial edema (4-7), and "passive backflow" of glomerular filtrate through holes in the wall of the tubule (6,8,9). We have attempted to determine the possible role of these factors in mercury-induced acute renal failure in the rat. perimentation. Their food and fluid intake and urine volume were measured; animals whose water intake was less than 10 ml during this period received supplementary fluids intraperitoneally in the form of 75 mM saline. Mercuric chloride, 12 mg per ml 140 mM NaCi, was injected intramuscularly at a dose of 12 mg per kg, control animals receiving a comparable volume of saline alone. Micropuncture experiments were performed at times ranging from 2 to 27 hours after mercury injection, and the fluid intake and output in the intervening period were recorded. Urine osmolalities, measured cryoscopically with a Fiske osmometer, were obtained routinely in early experiments to rule out hypovolemia due to a redistribution of body water and a resultant ADH effect as the sole cause of oliguria. Since urine osmolalities in mercury-treated animals were consistently less than 610 mOsm per kg, these measurements later were discontinued. MethodsAnimals were anesthetized with sodium pentobarbital, 35 mg per kg body weight, supplementary pentobarbital being added as necessary. They were placed supine and warmed from above with an infrared lamp to maintain body temperature at 400 C. The left kidney was exposed through an abdominal-flank incision and gently dissected from the perirenal fat. The renal capsule was left intact, but in dissecting the kidney from its bed collateral circulation through capsular vessels was virtually abolished. The kidney was placed in a Lucite holder as gently as possible, care being taken to avoid distortion of the renal vessels and ureter. The surface of the kidney was illuminated with a 25-w zirconium arc lamp and covered with warm mineral oil to prevent surface evaporation and facilitate visualization of the renal architecture. The blood pressure of each animal was monitored with either a tail microphone apparatus or direct aortic manometry. When the tail microphone was used, a 1-cm occluding cuff was placed at the base of the tail and the pickup positioned ...

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“…We have used the term "acute renal failure" to describe the similar consequences of glycerol injection in the rabbit. We do not imply that acute tubular necrosis is the pathological counterpart of ARF since either condition frequently occurs without the other (19)(20)(21).…”

Section: Terminologymentioning

confidence: 95%

Renin and Acute Circulatory Renal Failure in the Rabbit

Brown

Gavras

et al. 1972

Circulation Research

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Plasma renin concentration (PRC) was measured in 25 rabbits before and 6, 24, or 72 hours after subcutaneous injection of glycerol. Renal failure and tubular necrosis developed in most animals and PRC rose sixfold to a maximum at 24 hours. Small insignificant changes of PRC were present at 6 and 72 hours. None of these changes was observed in a control group of nine animals killed 24 hours after an injection of saline. The amount of renin extractable from single superficial glomeruli and from renal cortical tissue was reduced after injection of glycerol. In a second study of 11 anesthetized rabbits, renal venous PRC increased on average from 151 to 1810 units/liter following a 4-hour period of renal artery occlusion. Arterial PRC did not change significantly during this time, but the kidneys showed histological changes of acute tubular necrosis. These experiments are compatible with the suggestion that renin is involved in the pathogenesis of acute circulatory renal failure. KEY WORDSglomerular renin glycerol-induced renal failure acute tubular necrosis angiotensin renal artery occlusion• Vasoconstriction within the kidney, particularly in the outer layers of the cortex, is held to be important in the pathogenesis of acute renal failure (ARF) (1, 2). Renin is stored mainly in the outer layers of the renal cortex (3, 4) and, like the plasma or blood levels of renin, renin activity and angiotensin are often increased during the early stages of ARF in man (5-10) and may, by their vasoconstrictor effect, play some part in producing the condition (9, 11). However, analysis of results in man is compromised by lack of information on changes in renin in the early stages of ARF (9). In the first group of experiments reported here, therefore, plasma renin concentration was measured in rabbits before and during the development of ARF produced by glycerol.From the MRC Blood Pressure Unit and the Department of Pathology, Western Infirmary, Glasgow, W.I., Scotland.Received April 2, 1971. Accepted for publication September 27, 1971.The second question investigated was the extent to which levels of renin in peripheral plasma reflect those within the kidney under conditions, such as in ARF, in which renal blood flow is reduced. It is known, for example, that renal venous plasma renin concentration is inversely related to renal blood flow (12). In a second series of rabbits, therefore, the renal artery was occluded for a period sufficient to produce ischemic changes within the kidney, and renin was measured in samples of arterial and renal venous plasma taken before, during, and after the occlusion.A brief account of some of these results has been given recently (13). Methods A. ACUTE RENAL FAILURE PRODUCED BY GLYCEROLForty-nine rabbits were given the acidifying diet described by Lalich (14) to increase susceptibility to ARF (15), which in preliminary experiments had proved difficult to produce. Within 3 weeks, urine pH had decreased from 6.9 or more to 5.5 or less in all animals. Drinking water was then withheld, and aft...

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Lesions of the Kidney in Acute Renal Failure Following Shock

Cited by 102 publications

References 13 publications

Maintenance of Renal Function in Salt Loaded Rats Despite Severe Tubular Necrosis Induced by HgCl<sub>2</sub>

Maintenance of Renal Function in Salt Loaded Rats Despite Severe Tubular Necrosis Induced by HgCl<sub>2</sub>

Renal Micropuncture Study of the Development of Anuria in the Rat with Mercury-induced Acute Renal Failure*

Renin and Acute Circulatory Renal Failure in the Rabbit

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