ISSN 2398-2969      

Nephrotoxicosis

icanis
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Introduction

  • The renal cortex is particularly susceptible to toxins because it receives 90% of the renal blood flow and the tubular renal cells are exposed to high concentration of toxins due to renal excretion of toxins and reabsorption of water and other solutes.
  • Early recognition is important to limit renal damage.
  • Cause: different toxins cause renal damage at different sites, but ultimately causeacute renal failure Pre-renal azotemia.
  • Signs: usually present with renal failure.
  • Diagnosis: laboratory tests, histopathology.
  • Treatment: emesis, gastric lavage, intravenous fluids, specific management of underlying condition if appropriate.
  • Prognosis: guarded.

Pathogenesis

Etiology


Ingestion of nephrotoxins
  • Antifreeze(ethylene glycol Ethylene glycol poisoning ).
  • Heavy metals, eg lead, mercury, cadmium, chromium, arsenic, thallium.
Iatrogenic Endogenous nephrotoxins

Predisposing factors

General
  • Dehydration.
  • Decreased renal perfusion.
  • Pre-existing renal disease.

Pathophysiology

  • Different nephrotoxins act at different levels within the kidney:
    • Aminoglycosides→ decreased available surface in the glomeruli for ultrafiltration and increased glomerular permeability for negative proteins.
    • Azathioprine→ renal mesangial cell proliferation.
    • NSAIDs→ decreased renal prostaglandin synthesis → decreased renal blood flow.
    • The renal cortex is particularly susceptible to toxins, because it receives 90% of the renal blood flow and the tubular renal cells are exposed to high concentration of toxins (glomerular filtration, proximal tubular excretion, re-absorption of water and other solutes).

Timecourse

  • Ethylene glycol poisoning → signs of acute renal failure 12-72 hours post-ingestion.
  • Gentamycin accumulates and acute renal failure can develop after five days (sooner if overdosed).

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

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