Kidney and drugs

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Introduction :

  • Drug nephropathy are responsible 20% acute renal failure (IRA).
  • More than a quarter of the patients should undergo renal replacement more d & rsquo; one in ten guards renal sequelae.

Nephropathy tubulointerstitial chronic and acute direct drug toxicity :

  1. They manifest as renal organic with urinary urea / urea blood < 5, decreased urine concentration of power, natriurèse conservée > 20mmol/l.
  2. Proteinuria t are zero or minimal, the blood pressure is normal, no sodium and water retention unless such impairment of renal function is important and / vents excessive intakes.
  3. Urine output may be normal or decreased (oliguria, anuria egg) rarely raised. L & rsquo; s general condition is preserved. There is no fever, or rash, ni hyperleucocytose ni hyperéosinophilie.

The main classes of drugs are responsible :

A- antibacterial :

1- aminoglycosides it is the most prescribed antibiotics nephrotoxic. The margin between the therapeutic and toxic dose is very étroite.Parmi them gentamicin seems most toxic and & rsquo; amikacin least toxic.

Aminoglycosides s & rsquo; eliminated by the kidneys and s & rsquo; accumulate in the lysosomes of cells of the proximal tubule where their presence will remain detectable for several weeks after the & rsquo; stopping treatment.

Aminoglycoside toxicity depends on multiple factors including the injected dose and the duration of treatment.

A pre-existing renal insufficiency even modest, recent treatment by the same or another aminoglycoside, prolonged treatment over 10 days require to regularly monitor kidney function and serum levels of & rsquo; antibiotic.

2- colimycine Eliminated only by the kidney. It is nephrotoxic from therapeutic doses. It is also neurotoxic. A good sign of overdose is the & rsquo; perioral paresthesia existence. Its parenteral administration should be reserved for absolute indications are exceptional.

3- Vancomycin Éiminée exclusively renally. It should regularly monitor kidney function in d & rsquo; prolonged treatment.

4- sulfonamides Filtered speaks glomerulus and reabsorbed and secreted party talks tube. Sparingly soluble their high dose administration results in a risk of massive precipitation in the renal tubule and in the urinary tract with micro or macroscopic hematuria, renal colic and sometimes trace anuria.

B- L&rsquo;amphothérécine B :

A pus of antifungal used especially in the art and frequent cryptococos aspergillosis in particular immunocompromised patients with AIDS. She has a very long half-life and an almost obligatory renal toxicity.

C- iodinated contrast agents :

Toxic under specific conditions :

  1. Diabetes mellitus with renal insufficiency.
  2. Multiple myeloma with Bence Jones proteinuria.
  3. Application of high doses.
  4. repeated administrations within 5 days & rsquo; interval.
  5. pre-existing renal insufficiency caused some ilo.
  6. d & rsquo situations renal hypoperfusion.
  7. obstructive jaundice.
  8. Honeymoon.
  • It must be prevented when & rsquo; there are risk factors:
  1. Maintaining & rsquo; normal blood volume or slightly increased (500 to 1000ml saline before and after the & rsquo; review) ;
  2. Maintaining & rsquo; an abundant diuresis and compensated for and the 2 days after the & rsquo; review,
  3. A urine alkalinization (pH > 6) with sodium bicarbonate ;
  4. The correction of & rsquo; preexisting hyperuricemia ;
  5. Limiting doses of contrast agents ;
  6. The use of iso-osmolar products.
  • Curative treatment is based on the same principles. L & rsquo; renal replacement is rarely required.

D- Anticancer and immunomodulatory :

New drugs and new treatment modalities allow survival prolonged in patients with various types of cancer.

L & rsquo; improving the oncologic prognosis balance by including kidney complications related to the toxicity of certain products or certain associations. This toxicity is substantially tubular.

L & rsquo; IRA can be prevented :

By limiting the dose if serum creatinine is greater than 120pmol / l and stopping the processing if it is greater than 160pmol / l; and speaks maintaining & rsquo; an abundant diuresis.

Common risk factors in renal interstitial acute partoxicité direct drugs :

  1. L & rsquo; pre-existing renal insufficiency.
  2. Diabetic nephropathy with renal insufficiency.
  3. L & rsquo; renal hypoperfusion whatever its cause : digestive losses, fever.
  4. Strict diet without salt, diuretics, effective hypovolemia by heart failure.
  5. decompensated cirrhosis, nephritic syndrome.
  6. Shock states.
  7. L & rsquo; association or succession in time of several nephrotoxic.
  8. Prolonged treatment.
  9. The high doses.
  10. The cholestatic jaundice.

Les néphropathies tubulo-interstitielles chroniques

Analgesics and anti-inflammatory drugs :

Sides intermittent treatment with a given product n & rsquo; not cause severe irreversible kidney damage, the analgesic associations and & rsquo; surunmode chronic aspirin administered on years are responsible for serious chronic interstitial nephropathy.

The renal tubulo-interstitielles dites immuno-allergic :

It s & rsquo; watch 10 days 3 weeks after & rsquo; & rsquo introduction, a drug used in a conventional dose or sooner s & rsquo; s it & rsquo; d & rsquo acts; reintroduction.

The diagnosis is easy if the table combines clinical and biological d & rsquo; hypersensitivity :

(fever,rash cutané, eosinophilia, increased IgEsériques), and if urinary symptoms is rich (renal failure without proteinuria or proteinuria with minimal, gross hematuria, eosinophiluria).

Conclusion

1- Think about it if renal sufficiency ins.
2- In renal insufficient
a- Dose titration
b- Ask for expert advice
3- Use caution in the elderly.

Cours du Pr Y. Kitouni – Faculty of Constantine