Measurement of Renal Red Cell and Plasma Transit Times in Acute Renal Failure

Shaldon, Stanley; Silva, H.; Lawson, Tanya; Walker, Josephine G.

doi:10.3181/00379727-112-28044

Cited by 18 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings correlate well with the ischaemic glomeruli noted by many observers when viewing light microscope sections of the kidney. The presence of intrarenal shunts as an important cause of the lesions (Trueta, Barclay, Daniel, Franklin, and Prichard, 1947) has been doubted by Shaldon, Silva, Lawson, and Walker (1963) labelled with 51Cr through the kidney. Their findings be activation of the renin angiotensin system which were more in keepingwith ared cell shunt occurringat is discussed below.…”

Section: Mechanism Of Production Of the Renal Lesionmentioning

confidence: 99%

A review of the pathology and pathogenesis of acute renal failure due to acute tubular necrosis

Dunnill¹

1974

J Clin Pathol

View full text Add to dashboard Cite

Section: Mechanism Of Production Of the Renal Lesionmentioning

confidence: 99%

A review of the pathology and pathogenesis of acute renal failure due to acute tubular necrosis

Dunnill¹

1974

J Clin Pathol

View full text Add to dashboard Cite

“…Anuria or oliguria in acute renal insufficiency has been attributed to various vascular mechanisms (2,4), tubular obstruction (15,16,22), or leakage o f the glomerular filtrate through the damaged tubular wall-'the kidney urinates into the kidney' (20,23).…”

Section: Introductionmentioning

confidence: 99%

Plasma Renin Activity in Acute Renal Insufficiency

Kokot¹,

Kuska²

1969

Nephron

View full text Add to dashboard Cite

Plasma renin activity (p.r.a.) was studied in 37 patients with acute renal insufficiency and in 20 healthy subjects. Significant increase of the p.r.a. in the oliguric phase of acute renal failure could be established. The p.r.a. decreased in the diuretic phase of this syndrome. No straight correlation between elevated p.r.a. on the one hand and the degree of hypertension and plasma sodium and potassium on the other hand could be found. The possible role of renin in the development of acute renal insufficiency is discussed and the importance of p.r.a. estimations in the differentiation of acute renal failure from exacerbated chronic renal disease is underlined.

show abstract

“…The oliguria of acute renal failure has been attributed to tubular obstruction (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12), "leakage" of the glomerular filtrate through rents in the tubular wall (13)(14)(15)(16)(17)(18)(19), and vascular mechanisms of various types (20)(21)(22)(23)(24)(25). In a previous paper, it was shown that the oliguria of mercury-induced acute renal failure in the rat reflects a primary decrease in glomerular filtration rate and cannot be attributed to tubular mechanisms (26).…”

mentioning

confidence: 99%

Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Oken¹,

Arce²,

Wilson³

1966

J. Clin. Invest.

217

126

View full text Add to dashboard Cite

The oliguria of acute renal failure has been attributed to tubular obstruction (1-12), "leakage" of the glomerular filtrate through rents in the tubular wall (13)(14)(15)(16)(17)(18)(19), and vascular mechanisms of various types (20)(21)(22)(23)(24)(25). In a previous paper, it was shown that the oliguria of mercury-induced acute renal failure in the rat reflects a primary decrease in glomerular filtration rate and cannot be attributed to tubular mechanisms (26). The applicability of these findings to most types of acute renal failure occurring in humans may be questioned, however, because of the very dissimilar etiologies and the known effect of large doses of mercury on the renal circulation (27). The present study concerns hours before glycerol injection. They lost an average of 8% of body weight in the period of dehydration, during which time their food intake was one-third less than that of nondehydrated animals. Blood samples were obtained by cardiac puncture from a number of glycerolinjected animals and dehydrated control rats that were exempted from micropuncture studies to determine the change in their blood urea nitrogen (BUN) occurring over a 48-hour period. BUN was measured on 0.2-ml samples by a modification of the urease method of Gentzkow (28). Urinary osmolalities were determined with an Advanced osmometer.Acute renal failure was induced by injecting 50%o glycerol in water into the muscle of both hind limbs at a total dose of 10 ml per kg of body weight. Within 2 hours after this injection, the urine was found to be burgundy red in color due to the presence of heme pigments.The animals were subjected to micropuncture experiments at times ranging from 30 minutes to 26 hours after glycerol injection. They were anesthetized with sodium pentobarbital given intraperitoneally at a dose of 40 to 50 mg per kg body weight. Their blood pressure was monitored as described earlier (26) either by a tail cuff microphone method or intra-arterial manometry. Although hypotension typically did not occur, animals whose mean arterial blood pressure was less than 85 mm Hg were excluded from micropuncture study. The left kidney was exposed through an abdominal incision and carefully dissected free of the perirenal fat. The renal hilus was disturbed as little as possible, and the renal capsule was left intact. The kidney was placed in a Lucite holder to minimize its displacement with respiration. Its surface was covered with warm mineral oil to prevent drying and to aid in visualization of the renal structures.Micropuncture methods were those described in an earlier paper (26). In short, proximal tubular hydrostatic pressure was measured by a modification of the manometric method of Wirz (29), using a water manometer to obtain maximal definition of the end point. The manometer was calibrated at zero pressure before each measurement. Glomerular filtration rate and fractional water absorption were determined at least 30 minutes after the injection of 40 ,uc of "C-labeled inulin 1 in 0.3 to 0.5 ml of 140 mM NaCl. Labele...

show abstract

Measurement of Renal Red Cell and Plasma Transit Times in Acute Renal Failure

Cited by 18 publications

References 0 publications

A review of the pathology and pathogenesis of acute renal failure due to acute tubular necrosis

A review of the pathology and pathogenesis of acute renal failure due to acute tubular necrosis

Plasma Renin Activity in Acute Renal Insufficiency

Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Contact Info

Product

Resources

About