Nephrotoxicosis

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Sections available in full article Introduction, Presenting signs, Acute presentation, Special risks (e.g. anesthetic), Pathogenesis, Etiology, Predisposing factors, Pathophysiology, Timecourse (incubation, duration), Diagnosis, Presenting problems, Client history, Clinical signs, Diagnostic investigation, Confirmation of diagnosis, Differential diagnosis, Treatment, Initial symptomatic treatment, Standard treatment, Monitoring, Prevention, Prophylaxis, Sequelae, Prognosis, Expected response to treatment, Reasons for treatment failure,
Contributors

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 cause acute 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.

Diagnosis

Clinical signs

  • Anemia (due to hemolysis causing hyperhemoglobinemia).
  • Signs associated with hypercalcemia (neoplasia, hyperparathyroidism).

Diagnosis

Differential diagnosis

  • Causes of acute renal failure Pre-renal azotemia.

Sequelae

Prognosis

  • Guarded.

Expected response to treatment

  • Improving renal function.

Reasons for treatment failure

  • Treatment delayed and permanent damage occurs.

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