Subcutaneous fat necrosis, hæmolysis without siderosis, and renal tubular atrophy following repeated glycerol injections

Campbell, J. A.

doi:10.1002/path.1700760216

Cited by 11 publications

(2 citation statements)

References 3 publications

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“…None have provided an adequate explanation. However, several growth factors have been shown to attenuate renal insults (25,26), including epidermal growth factor (27,28), insulin-like growth factor (29), and hepatocyte growth factor (30). Growth factors could be the major contributors to acquired resistance to repeated renal insults, and this mechanism would be very consistent with our findings.…”

Section: Discussionsupporting

confidence: 86%

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

et al. 1998

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Glycerol induced acute renal failure (ARF) is known to attenuate subsequent mercuric chloride nephrotoxicity. This protection was evaluated in rats. Glycerol induced varying degrees of renal insufficiency. After 14 days, when serum creatinine (SCr) creatinine clearance (CCr) and fractional excretion of sodium (FENa) had returned to baseline, injection of mercuric chloride caused significantly milder renal insufficiency in recovered rats than in controls (SCr 356 +/- 46 vs. 475 +/- 19 mumol/L; CCr 0.12 +/- 0.02 vs. 0.02 +/- 0.02 mL/min, p < .05; and mortality 0 vs. 45%, respectively, p < .01). A striking finding was that the degree of renal insufficiency induced by mercuric chloride correlated inversely with the degree of renal insufficiency previously induced by glycerol (r = -0.496, p < .05 for SCr and CCr), but there was no correlation with other measures of previous renal function such as urine volume, sodium excretion, or FENa. Glycerol induced ARF also attenuated the renal toxicity of mercuric chloride injected 4 days after glycerol, before full recovery of renal function. The decrements in renal function after the two insults were also inversely related (r = -0.76, p < .01). A third renal insult with a second mercuric chloride injection after three weeks was still attenuated. However, after the third insult, there was no longer an inverse or any statistical relationship with previous measurements of renal function. Histopathology revealed a good correlation between peak Scr after glycerol, and percentage of tubules undergoing re-generation 14 days later (r = 0.97, p < .01). There was an inverse correlation between Scr after mercuric chloride (administered 14 days after glycerol) and percentage of tubular regeneration seen two days later (r = -0.79, p < .05). The correlations of SCr and CCr with regeneration was greater than the correlations with tubular necrosis, suggesting that the regenerative process is involved in the protection from repeated renal insults. In conclusion, glycerol-induced ARF attenuates subsequent mercuric chloride renal insult. The attenuation correlates directly with the initial glycerol-induced damage, so that the more severe the initial renal insufficiency, the milder the renal insufficiency following subsequent mercuric chloride. This protection can be seen as early as 4 days and also 14 days after previous renal insult. The degree of renal tubular regeneration correlates well with the protection seen, and probably plays a role in acquired renal resistance to repeated insults.

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Section: Discussionsupporting

confidence: 86%

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

et al. 1998

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“…29 These studies include preconditioning by a prior ischemic insult, ureteral obstruction, nephrotoxic antiserum, gentamicin exposure, pretreatment with sodium arsenite, repeat exposure to uranium and/or single exposure after nephritis, repeat exposure to glycerol, and protection against mercuric chloride in animals with prior glycerol nephrotoxicity and vice versa. [41][42][43][44][45][46][47][48][49][50][51][52] Another limitation is that the STN model does not capture etiological or phenotypical features of kidney disease, but it does recapitulate the consequences of nephron reduction common to nearly all forms of kidney disease. Similar findings have been observed in different strains of rats and at different time points after STN.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Tubuloglomerular Feedback and HIF-1α Confer Resistance to Ischemia after Subtotal Nephrectomy

Singh

Blantz

Rosenberger

et al. 2012

Journal of the American Society of Nephrology

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Nephron loss in a diseased kidney invokes adaptations in the remaining nephrons. Whether and how these adaptations condition the response of the kidney to injury is not known. We examined the susceptibility of the kidney after subtotal (5/6th) nephrectomy (STN) to ischemic injury in rats. GFR in STN kidneys did not significantly change after ischemia reperfusion (IR), whereas GFR fell by 70% after IR in unilateral nephrectomy controls. In micropuncture experiments, single-nephron GFR responses mirrored the whole-kidney responses: in STN, single-nephron GFR decreased by 7% after IR compared with 28% in controls. Furthermore, we found that tubuloglomerular feedback, a mechanism that links proximal tubular injury to a fall in GFR, was inoperative in STN but was normal in controls. Restoration of normal feedback in STN attenuated the functional resistance to IR. In addition to the functional resilience, the morphology of the kidney was better preserved in STN. In STN kidneys, the S3 segment of the proximal tubule, normally injured after ischemia, constitutively expressed hypoxia-inducible factor-1a (HIF-1a), which is cytoprotective in ischemia. Inducing HIF before IR improved GFR in control animals, and inhibiting the HIF target hemeoxygenase-1 before IR reduced GFR in STN animals. Taken together, these data suggest that fewer functioning nephrons in a diseased kidney do not increase the susceptibility to injury, but rather, hemodynamic and molecular adaptations in the remnant nephrons precondition them against ischemic injury.

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Diphenylcarbodiimide, MethodI

Campbell

Monagle

2003

Organic Syntheses

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Subcutaneous fat necrosis, hæmolysis without siderosis, and renal tubular atrophy following repeated glycerol injections

Cited by 11 publications

References 3 publications

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Aberrant Tubuloglomerular Feedback and HIF-1α Confer Resistance to Ischemia after Subtotal Nephrectomy

Diphenylcarbodiimide, MethodI

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Subcutaneous fat necrosis, hæmolysis without siderosis, and renal tubular atrophy following repeated glycerol injections

Cited by 11 publications

References 3 publications

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl2-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl2-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Aberrant Tubuloglomerular Feedback and HIF-1α Confer Resistance to Ischemia after Subtotal Nephrectomy

Diphenylcarbodiimide, MethodI

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Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology