Renal Failure Caused by Chemicals, Foods, Plants, Animal Venoms, and Misuse of Drugs

Jg, Abuelo

doi:10.1001/archinte.1990.00390150019004

Cited by 46 publications

(12 citation statements)

References 113 publications

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“…These can be broadly divided into three categories; food poisons, biting poisons and sting poisons (envenomation), as indicated in Table 3. Renal injury has been reported following envenomation by snakes, spiders, caterpillars and scorpions [1,2,4,8,77,78,79]. Acute kidney injuries (AKI) induced by natural venoms included acute tubular necrosis caused by impairment of renal hemodynamics, intravascular hemolysis, rhabdomyolysis, disseminated intravascular coagulation (DIC) and direct toxin-mediated effects, including thrombotic microangiopathy similar to that observed in HUS.…”

Section: Acute Kidney Injuries Induced By Natural Venomsmentioning

confidence: 99%

Exploiting the Nephrotoxic Effects of Venom from the Sea Anemone, Phyllodiscus semoni, to Create a Hemolytic Uremic Syndrome Model in the Rat

2012

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In the natural world, there are many creatures with venoms that have interesting and varied activities. Although the sea anemone, a member of the phylum Coelenterata , has venom that it uses to capture and immobilise small fishes and shrimp and for protection from predators, most sea anemones are harmless to man. However, a few species are highly toxic; some have venoms containing neurotoxins, recently suggested as potential immune-modulators for therapeutic application in immune diseases. Phyllodiscus semoni is a highly toxic sea anemone; the venom has multiple effects, including lethality, hemolysis and renal injuries. We previously reported that venom extracted from Phyllodiscus semoni induced acute glomerular endothelial injuries in rats resembling hemolytic uremic syndrome (HUS), accompanied with complement dysregulation in glomeruli and suggested that the model might be useful for analyses of pathology and development of therapeutic approaches in HUS. In this mini-review, we describe in detail the venom-induced acute renal injuries in rat and summarize how the venom of Phyllodiscus semoni could have potential as a tool for analyses of complement activation and therapeutic interventions in HUS.

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Section: Acute Kidney Injuries Induced By Natural Venomsmentioning

confidence: 99%

Exploiting the Nephrotoxic Effects of Venom from the Sea Anemone, Phyllodiscus semoni, to Create a Hemolytic Uremic Syndrome Model in the Rat

2012

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“…Cellular binding, uptake and/or intratubular drug accumulation; for example, aminoglycosides are internalised into proximal tubule cells via brush border receptor mediated binding to an anionic phospholipid, and stored in cytosegresomes which are transformed into myeloid bodies. The mechanisms of aminogylcoside nephrotoxicity leading to tubular necrosis still remain speculative [1][2][3]. 2.…”

Section: Renal Cell Injury Following Administration Of Nephrotoxic Drugsmentioning

confidence: 99%

“…Chronic cisplatin administration to rats caused diffuse injury in the proximal segment and an overall reduction in Na+-dependent phosphate and glucose transport by brush border vesicles [21]. Toxic cell damage due to some cephalosporins apparently follows, after they have entered renal epithelial cells, from occupation of basal-lateral organic acid transport $35 systems and subcellular binding to mitochondria, hence leading to marked energy deficiency [1][2][3]22]. 3.…”

Section: Renal Cell Injury Following Administration Of Nephrotoxic Drugsmentioning

confidence: 99%

“…Toxic cell damage due to some cephalosporins apparently follows, after they have entered renal epithelial cells, from occupation of basal-lateral organic acid transport $35 systems and subcellular binding to mitochondria, hence leading to marked energy deficiency [1][2][3]22]. 3. Loss of barrier function of the tubular plasma membrane: rise in cytosolic free calcium with consecutive mitochondrial damage (Ca + + overload), activation of phospholipases (phospholipase A2) which is involved in breakdown of lipids, pertubation of the cytoskeleton, especially of the microtubule network (apical web, apicobasal bundles), and destabilisation of cell-cell contact.…”

Section: Renal Cell Injury Following Administration Of Nephrotoxic Drugsmentioning

confidence: 99%

“…Most of the clinically important drugs with nephrotoxic potential, such as cis-platin, aminoglycosides, cyclosporin A, amphotericin B and X-ray contrast media are excreted by the kidney, either by glomerular ultrafiltration or by tubular secretion [1][2][3]. The intraluminal concentrations of filtered drugs may exceed that in the serum more than 50-fold; in addition, drugs and xenobiotics frequently Fig.…”

mentioning

confidence: 99%

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Shedding and repair of renal cell membranes following drug-induced nephrotoxicity in humans

Scherberich

Wolf²,

Schoeppe³

1993

Eur J Clin Pharmacol

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Nephrotoxic drugs may account for approximately at least 20% of clinically observed cases of acute renal failure in whom tubular lethal or sublethal damage is a predominant finding. Acute toxic tubular cell injury is characterized by loss of cellular polarization, intrinsic energy deficiency, calcium overload, release of toxic proteases and free oxygen radicals, derangement of the cytoskeleton, and vacuolar transformation of brush border microvilli. These events may finally lead to irreversible cell death. Shedding of membrane enzymes and cytoskeletal components in urine (kidney tissue proteinuria) may serve as a noninvasive early marker for assessing tubular cell injury. Successful recovery of renal function depends on early repair of lethally or sublethally damaged nephrons, in which intrinsic nephrogenic adaptive and proliferative responses cooperate in concert with auto/para/-juxtacrine growth promoting factors and cytokines. Exogenously administered growth factors may enhance renal cell recovery, as shown in animal models. Increased expression of immediate early genes in tubular cells after renal injury reflects the ongoing mitogenic activity necessary for reepithelialization and remodeling (new, polarized, differentiated cells). Further progress in understanding the molecular mechanisms of renal tubular injury will probably influence the diagnostic modalities and therapeutic approaches to acute drug induced renal failure.

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Acute Renal Failure After an Overdose of Ciprofloxacin

George¹

1991

Arch Intern Med

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Renal Failure Caused by Chemicals, Foods, Plants, Animal Venoms, and Misuse of Drugs

Cited by 46 publications

References 113 publications

Exploiting the Nephrotoxic Effects of Venom from the Sea Anemone, Phyllodiscus semoni, to Create a Hemolytic Uremic Syndrome Model in the Rat

Exploiting the Nephrotoxic Effects of Venom from the Sea Anemone, Phyllodiscus semoni, to Create a Hemolytic Uremic Syndrome Model in the Rat

Shedding and repair of renal cell membranes following drug-induced nephrotoxicity in humans

Acute Renal Failure After an Overdose of Ciprofloxacin

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