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

• Antifreeze(ethylene glycol Ethylene glycol poisoning ).
• Heavy metals, eg lead, mercury, cadmium, chromium, arsenic, thallium.

• Antibiotics, eg aminoglycosides Digoxin , polymixins, cephalosporins Cefalexin , sulfonamides , tetracyclines Tetracycline.
• NSAIDs, eg aspirin Acetyl salicylic acid , ibuprofen Ibuprofen toxicity , phenylbutazone Phenylbutazone.
• Chemotherapeutic agents, eg azathioprine Azathioprine , cisplatin Cisplatin , methotrexate Methotrexate , doxorubicin Doxorubicin , adriamycin.
• Intravenous radiographic contrast agents.
• Potentiators of nephrotoxins, eg dehydration, diuretics, general anesthesia.

• Calcium Hyperadrenocorticism , myoglobin, hemoglobin.

Predisposing factors

• 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

Treatment

Prevention

Outcomes