Micropuncture Studies of the Basis for Protection of Renin Depleted Rats from Glycerol Induced Acute Renal Failure

Thiel, G; McDonald, Franklin D.; Oken, D.E.

doi:10.1159/000179809

Cited by 94 publications

(47 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The kidneys of these animals showed essentially the same changes found earlier in rats whose fluid deficit had not been systematically restored (e.g., 5,[16][17][18]. Two populations of nephrons existed side by side, one fluid-filled and the other totally collapsed.…”

Section: Discussionsupporting

confidence: 73%

“…Renal failure thus reflected both the number of totally nonfunctioning nephrons and the degree to which filtration was impaired in the remainder. The finding of one superficial nephron that is filtering briskly surrounded by others that form virtually no filtrate, noted previously in this form of ARF (5,(16)(17)(18)(19), suggests a local basis for filtration failure.…”

Section: Discussionsupporting

confidence: 62%

“…In our hands, these agents have provided only minor and inconsistent protection (37). A new and extremely potent adenosine receptor blocker, BW A 1433U, did appear to totally protect glomerular filtration in initial experiments (37) (38), but biologically effective active or passive immunization against renin (39) and angiotensin (40), and treatment with angiotensin-converting enzyme (unpublished data) have all been of no discernible value. This form of renal failure is not mitigated in Brattleboro rats with complete central diabetes insipidus (41), making the antidiuretic hor-.…”

Section: Discussionmentioning

confidence: 99%

“…As in the human syndrome, this ARF model yields near total renal failure (5,(16)(17)(18) from which the rats recover spontaneously after some 5-7 d (19). The pathogenetic features and natural history of this model have been well characterized in previous studies (e.g., 5,[16][17][18][19], but the mechanisms immediately responsible for the apparent filtration deficit thus far have not been examined. The present report describes the glomerular dynamic abnormalities responsible for failed filtration in this murine ARF model.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Glomerular hemodynamics in established glycerol-induced acute renal failure in the rat.

Wolfert

Oken²

1989

J. Clin. Invest.

View full text Add to dashboard Cite

The glomerular dynamic correlates of failed filtration were studied in volume replete rats with established glycerol-induced acute renal failure (ARF). Over one-half of all nephrons formed virtually no filtrate, while the single nephron glomerular filtration rate (SNGFR) of fluid-filled nephrons, measured at the glomerulotubular junction to preclude the possibility of covert tubular leakage, averaged one-sixth of control (P < 0.001). Even that low mean value was elevated by a few nephrons with a near normal SNGFR. Renal failure thus reflected both total filtration failure in the majority of nephrons and massively reduced filtration in most of the remainder. Glomerular capillary pressure (Pg) averaged some 14 mmHg below control (P < 0.001), whereas the arterial colloid osmotic and Bowman's space pressures were not significantly altered. Renocortical and whole kidney blood flow were also unchanged. Marked internephron functional heterogeneity precluded estimates of the ultrafiltration coefficient. However, the fall in SNGFR correlated well with the markedly depressed Pg and afferent net filtration pressure (APnetA, P < 0.001), which in turn were caused by increased preglomerular resistance and a reciprocal fall in efferent arteriolar resistance. This complex change in intrarenal resistances was largely, if not entirely, responsible for failed filtration in this ARF model.

show abstract

Section: Discussionsupporting

confidence: 73%

Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Glomerular hemodynamics in established glycerol-induced acute renal failure in the rat.

Wolfert

Oken²

1989

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Enhanced responses to vasoconstrictor stimuli and decreased vasodilatory responses were also observed (25). These hypotheses were strengthened by the observations that volume depletion worsened, whereas high salt intake and a hyper-or euvolemic state ameliorated the severity and mortal-ity rate in AKI (26,27). Importantly, the hemodynamic basis of AKI was also demonstrated in human studies in various settings (28 -30,24,31).…”

Section: Pathogenesis Of Akimentioning

confidence: 97%

Chronic Kidney Disease

Singh

Rifkin

Blantz

2010

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Epidemiologic evidence suggests that chronic kidney disease (CKD) is a risk factor for acute kidney injury (AKI) due to the prevalence of CKD in patients who have episodes of AKI. However, the high burden of comorbidities such as age, diabetes, peripheral vascular, cardiovascular, and liver disease accompanying CKD, and the difficulties of defining AKI in the setting of CKD make these observations difficult to interpret. These comorbidities not only could alter the course of AKI but also may be the driving force behind the epidemiologic association between CKD and AKI because of systemic changes and/or increased exposure to potential nephrotoxic risks. Here, we contend that studies suggesting that CKD is a risk factor for AKI may suffer from residual confounding and reflect an overall susceptibility to illness rather than biologic susceptibility of the kidney parenchyma to injury. In support of our argument, we discuss the clinical evidence from epidemiologic studies, and the knowledge obtained from animal models on the pathophysiology of AKI and CKD, demonstrating a preconditioning influence of the previously impaired kidneys against subsequent injury. We conclude that, under careful analysis, factors apart from the inherent pathophysiology of the diseased kidney may be responsible for the increased frequency of AKI in CKD patients, and the impact of CKD on the risk and severity of AKI needs further investigation. Moreover, certain elements in the pathophysiology of a previously injured kidney may, surprisingly, bear out to be protective against AKI.

show abstract

Pathophysiology of Acute Renal Failure

Flamenbaum¹

1973

Arch Intern Med

109

View full text Add to dashboard Cite

Despite the availability of modern techniques, mortality continues to be high in acute renal failure (ARF) (Fig 1, top).The acute renal failure resulting from glycerol-induced myohemoglo¬ binuria and methemoglobin adminis¬ tration have been most extensively investigated, primarily because of some similarities to human acute re¬ nal failure. Micropuncture of super¬ ficial renal cortical tubules has been used in many recent studies, since oli-

show abstract

Micropuncture Studies of the Basis for Protection of Renin Depleted Rats from Glycerol Induced Acute Renal Failure

Cited by 94 publications

References 7 publications

Glomerular hemodynamics in established glycerol-induced acute renal failure in the rat.

Glomerular hemodynamics in established glycerol-induced acute renal failure in the rat.

Chronic Kidney Disease

Pathophysiology of Acute Renal Failure

Contact Info

Product

Resources

About