Renal tubular function in glycerol-induced acute renal failure

Westenfelder, Christof; Arevalo, G.; Crawford, P.; Zerwer, Philip; Baranowski, R. L.; Birch, F.; Earnest, W. R.; Hamburger, R. K.; Coleman, Richard D.; Kurtzman, Neil A.

doi:10.1038/ki.1980.156

Cited by 45 publications

(18 citation statements)

References 19 publications

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“…The administration of hypertonic glycerol solution i.m. has been used to induce acute renal insufficiency through rhabdomyolysis in rats 4,15–17 . In this model, renal insufficiency is thought to be caused by myoglobinuria and the formation of myoglobin and acid haematin casts 3 .…”

Section: Discussionmentioning

confidence: 99%

“…has been used to induce acute renal insufficiency through rhabdomyolysis in rats. 4,[15][16][17] In this model, renal insufficiency is thought to be caused by myoglobinuria and the formation of myoglobin and acid haematin casts. 3 However, although 20% of all glycerol is metabolised by the kidneys, 18 the direct effect of glycerol on the kidney has not been investigated.…”

Section: Discussionmentioning

confidence: 99%

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Intraperitoneal Glycerol Induces Oxidative Stress in Rat Kidney

Rieger

Rech

Feksa

et al. 2008

Clin Exp Pharma Physio

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1. Glycerol has been used for the treatment of intracranial hypertension, cerebral oedema and glaucoma. Experimentally, intramuscular administration of hypertonic glycerol solution is used to produce acute renal failure. In this model, glycerol causes rhabdomyolysis and myoglobinuria, resulting in the development of renal injury. The pathogenesis is thought to involve vascular congestion, the formation of casts and oxidative stress. However, the effect of glycerol itself independent of rhabdomyolysis has not been investigated. Therefore, the aim of the present study was to investigate the effects of i.p. glycerol on some biochemical and oxidative stress parameters in the kidney of young rats. 2. Rats received 10 mL/kg, i.p., hypertonic glycerol solution (50% v/v) or saline (NaCl 0.85 g%) followed by 24 h water deprivation. Twenty-four hours after the administration of glycerol, rats were killed. Creatinine levels and the activity of creatine kinase (CK) and lactate dehydrogenase (LDH) were determined in the plasma. In addition, CK, pyruvate kinase and LDH activity and oxidative stress parameters (free radical formation, lipid peroxidation and protein carbonylation) were measured in renal tissue. 3. Glycerol did not alter plasma CK activity and increased plasma creatinine levels, suggesting renal insufficiency and the absence of rhabdomyolysis. Renal CK and pyruvate kinase activity was decreased, suggesting diminution of energy homeostasis in the kidney. Plasma and renal LDH activity was decreased, whereas the formation of free radicals, lipid peroxidation and protein carbonylation were increased, suggesting oxidative stress. 4. These results are similar to those described after the intramuscular administration of glycerol. Therefore, it is possible that glycerol may provoke renal lesions by mechanisms other than those induced by rhabdomyolysis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Intraperitoneal Glycerol Induces Oxidative Stress in Rat Kidney

Rieger

Rech

Feksa

et al. 2008

Clin Exp Pharma Physio

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“…In these early studies it was observed that the exposure of the kidney to a particular insult, uranyl nitrate, rendered the kidney resistant to subsequent challenges with the same nephrotoxin (9). Resistance to the same insult was thereafter noted with other, more clinically relevant insults including aminoglycoside antibiotics (12) and the glycerol model of acute renal failure (13,14), the latter representing a model of rhabdomyolysis. Resistance to renal injury was also recognized when the kidney was conditioned by dissimilar insults; for example, rats recovering from tubular injury induced by hypertonic glycerol were resistant to tubular damage induced by the tubular toxin, mercuric choride (15); rats treated with tubular toxins such as potassium dichromate (16) or mercuric chloride (17) exhibited reduced sensitivity to the nephrotoxic actions of gentamicin.…”

Section: Introductionmentioning

confidence: 99%

Glomerular inflammation induces resistance to tubular injury in the rat. A novel form of acquired, heme oxygenase-dependent resistance to renal injury.

Vogt¹,

Shanley²,

Croatt³

et al. 1996

J. Clin. Invest.

117

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Considerable attention is directed to a surprising biologic phenomenon wherein tissues exposed to one insult acquire resistance to another. We identify a novel example of acquired resistance to acute renal failure and a mechanism that contributes to such resistance. Nephrotoxic serum, administered to rats 24 h before the induction of glycerol-induced acute renal failure, reduces functional and structural injury that occurs in this model. Since heme oxygenase, the ratelimiting enzyme in heme degradation, protects against heme protein-induced renal injury, we questioned whether induction of heme oxygenase underlies the protection afforded by nephrotoxic serum. Kidney heme oxygenase (HO-1) mRNA was induced 6 h after nephrotoxic serum and renal tubules were identified as the site of expression of heme oxygenase protein.

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“…In contrast, Westenfelder et al 3, found depressed glucose reabsorption, PAH extraction, and bicarbonates reabsorption, but no decrease in ammonium excretion in their in vivo study concerning glycerol-induced ATN. What is the reason for discrepancy?…”

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confidence: 86%

Renal ammoniagenesis in kidney slices from rats undergoing glycerol-induced acute tubular necrosis

1982

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Summary. Compared to control, kidney slices from rats undergoing glycerol-induced ATN produce less ammonia from glutamate, but show no difference when glutamine is substrate. However, gluconeogenesis from glutamine, like glutamate, is decreased in acute tubular necrosis (ATN). We conclude that renal ammoniagenesis is influenced by ATN. Glycerolinduced ATN causes a relative increase in glutamine deamidation and a decrease in glutamate deamination.In an early in vitro study 2, we reported decreased ammonia production by kidney slices from rats undergoing glycerolinduced acute tubular necrosis (ATN). In contrast, Westenfelder et al. 3, found depressed glucose reabsorption, PAH extraction, and bicarbonates reabsorption, but no decrease in ammonium excretion in their in vivo study concerning glycerol-induced ATN. What is the reason for discrepancy? To determine this, we performed expanded in vitro studies on ammoniagenesis by renal slices from rats undergoing glycerol ATN. Differently, we now found no significant changes in ammoniagenesis, but decreased gluconeogenesis was still present. The obvious difference between this and our previous investigation 2 was that glutamate was the ammonia precursor earlier, while glutamine was used in the present study.Methods. Male Sprague-Dawley rats, weighing 250-350 g, were dehydrated for 24 h; 18 rats received a s.c. injection of 50% (V/V) glycerol-isotonic saline (1 ml/100 g b.wt) and 21 received an equal volume of isotonic saline. The rats were sacrificed 24 h later after blood was withdrawn from the lower aorta. Serum urea nitrogen was measured by standard procedures 4. In vitro methodology and measurements of ammonia and glucose were as previously described 2'5. Glutamine 0.6 mm was substrate. Statistics were assessed by Student's t-test using group analysis.

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Renal tubular function in glycerol-induced acute renal failure

Cited by 45 publications

References 19 publications

Intraperitoneal Glycerol Induces Oxidative Stress in Rat Kidney

Intraperitoneal Glycerol Induces Oxidative Stress in Rat Kidney

Glomerular inflammation induces resistance to tubular injury in the rat. A novel form of acquired, heme oxygenase-dependent resistance to renal injury.

Renal ammoniagenesis in kidney slices from rats undergoing glycerol-induced acute tubular necrosis

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