Foscarnet-Induced Acute Renal Failure and Effectiveness of Haemodialysis

Deray, Gilbert; Hoang, P. Le; Soubrié, C; Morer, I.; Cacoub, Patrice; Baumelou, A; Roussélie, F; Jacobs, C

doi:10.1016/s0140-6736(87)90794-x

Cited by 18 publications

(4 citation statements)

References 2 publications

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“…In these observations the diagnosis of acute toxic tubulopathy was supported by low proteinuria, normal urinary sediment, absence of urinary tract obstruction, absence of acute variation of arterial blood pressure and favorable evolution within 2-4 weeks. In 1 patient we found that foscarnet is signif icantly cleared through hemodialysis [18]. This evolu tionary profile is confirmed in our present retrospective analysis.…”

Section: Discussionsupporting

confidence: 85%

“…Hemodialysis clearance of foscarnet with a dialyzer Fitted with a cuprophane membrane was found to be 80 ml/min. Moreover, 24 h after stopping dialysis the plasma foscarnet concentration was only marginally higher than the postdialysis value, which suggests only moderate replenishment from the intracellular compart ment [18]. 1 month later the patient's serum creatinine was 107 pmol/1.…”

Section: Renal Functionmentioning

confidence: 88%

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Foscarnet Nephrotoxicity: Mechanism, Incidence and Prevention

Deray

Martinez²,

Katlama³

et al. 1989

Am J Nephrol

210

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Foscarnet is a pyrophosphate analogue that has been successfully used in severe cytomegalovirus (CMV) infections. Little is known of the incidence and mechanisms of foscarnet-induced nephrotoxicity as most data comes from recipients of renal allografts or from patients with severe underlying disease or with other nephrotoxic drugs. We have retrospectively analyzed the evolution of renal function after 56 courses of foscarnet. In addition, we have prospectively studied the protective effects of hydration on foscarnet nephrotoxicity (2.5 liters of saline/day during the night before the foscarnet therapy and throughout the course of treatment). Foscarnet-induced acute renal failure was defined as a rise in serum creatinine of at least 25% from the basal value. An increase in serum creatinine occurred in 37 cases out of the 56 courses of foscarnet (66%). The mean serum creatinine prior to foscarnet was 80.5 ± 3.3 μmol/l and the mean increase was 190 ± 28.3 μmol/l (range 80–1,000). Peak serum creatinine was higher than 200 and 300 μmol/l in 16 and 13 patients, respectively. Kidney obtained at autopsy from a 30-year-old male with AIDS, CMV pneumonitis and acute renal failure secondary to foscarnet administration showed an extensive tubular necrosis. In the group which was prospectively hydrated only 1 patient had an acute renal failure. The mean serum creatinine at the peak (96 ± 4 μmol/l) and at the end of the treatment (83 ± 4 μmol/l) was significantly lower (p < 0.05) than in non hydrated patients. In conclusion, foscarnet is a highly nephrotoxic drug which induces acute tubular necrosis. Prehydration with 2.5 liters of isotonic saline throughout the course of foscarnet therapy almost completely abolishes its nephrotoxicity.

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Section: Discussionsupporting

confidence: 85%

Section: Renal Functionmentioning

confidence: 88%

Foscarnet Nephrotoxicity: Mechanism, Incidence and Prevention

Deray

Martinez²,

Katlama³

et al. 1989

Am J Nephrol

210

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“…1 Biopsy-or autopsy-based reports on foscarnet nephrotoxicity described two main patterns of lesions: tubular lesions with acute tubular necrosis with or without crystal deposition, [2][3][4] and glomerular crystal deposits. [5][6][7] Case report A 42-year-old man underwent bilateral lung transplantation in July 2007 for usual interstitial pneumonia.…”

Section: Introductionmentioning

confidence: 99%

Crystal precipitation and granulomatous inflammation in multiple organs after foscarnet therapy in a lung transplant recipient

Tischler

Schuurmans

Boehler

et al. 2012

The Journal of Heart and Lung Transplantation

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“…Favorable results have also been reported in AIDS patients with CMV pneumonitis [7]. In contrast, however, several centers have noted a high incidence of renal insufficiency during foscarnet treatment of various viral infections in nontransplanted patients [3,5,8,9].…”

mentioning

confidence: 99%

Tubulointerstitial nephritis caused by the antiviral agent foscarnet

et al. 1989

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The antiviral agent foscarnet has long been used in our unit to treat cytomegalovirus (CMV) infections in renal transplant patients. The clinical effect has been convincing and, apart from changes in serum calcium levels, very few side effects have been noted. We have, however, observed a nephrotoxic reaction in a series of patients with initially good renal function who therefore received high doses of foscarnet. Transplant biopsies performed in five of those patients revealed degenerative changes in the tubular epithelial cells as well as tubular calcium deposits and an infiltration of the interstitium by mixed mononuclear and polymorphonuclear leucocytes. Renal insufficiency was accompanied by high fever. After withdrawal of the drug, the temperature rapidly normalized, whereas serum creatinine continued to rise for about 3 days and then fell back towards previous levels. We conclude that transplant biopsies are of great value in distinguishing between a foscarnet nephrotoxic effect and CMV nephritis, various forms of rejection, and other causes of impaired renal function.

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Foscarnet-Induced Acute Renal Failure and Effectiveness of Haemodialysis

Cited by 18 publications

References 2 publications

Foscarnet Nephrotoxicity: Mechanism, Incidence and Prevention

Foscarnet Nephrotoxicity: Mechanism, Incidence and Prevention

Crystal precipitation and granulomatous inflammation in multiple organs after foscarnet therapy in a lung transplant recipient

Tubulointerstitial nephritis caused by the antiviral agent foscarnet

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