Nephrotoxicity of Paraquat in Man

Nd, Vaziri; Rl, Ness; Rd, Fairshter; Wr, Smith; Sm, Rosen

doi:10.1001/archinte.1979.03630390032014

Cited by 58 publications

(9 citation statements)

References 18 publications

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“…Paraquat is toxic to renal proximal tubular cells and can induce acute tubular necrosis, resulting in elevated BUN and creatinine . Ninety percent of absorbed paraquat is excreted unchanged in urine within 12–24 h after ingestion; thus, additional elimination can be relatively modest .…”

Section: Discussionmentioning

confidence: 99%

Hemolytic uremic syndrome associated with paraquat intoxication

Jang¹,

Bae²,

Hwang³

et al. 2013

J of Clinical Apheresis

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We report a case of a 66-year-old patient with paraquat intoxication resulting in the requirement for hemoperfusion, hemodialysis, and plasma exchange. His initial serum paraquat level was 0.24 µg/mL (0.0-0.1 µg/mL). Activated charcoal (50 g) was administered orally, and high-dose N-acetylcysteine (150 mg/kg) was administered intravenously. In addition, immediate 4 h hemoperfusion was also performed for three consecutive days after admission. Hemodialysis was started on the 4th day after admission because of uremia. On the 9th day after admission, laboratory findings demonstrated hemolytic uremic syndrome (HUS): microangiopathic hemolytic anemia (MAHA), thrombocytopenia, elevated reticulocyte count, and lactate dehydrogenase (LDH). Plasma exchange was performed three times consecutively. Anemia and thrombocytopenia were improved, and LDH was normalized after plasma exchange. Urine output increased to 2240 mL/day on the 18th day after admission, and hemodialysis was discontinued. He is currently being observed at our follow-up clinic without renal impairment or pulmonary dysfunction for 1.5 years since discharge. We should suspect paraquat-associated HUS when thrombocytopenia and anemia are maintained for a long time after paraquat intoxication.

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Section: Discussionmentioning

confidence: 99%

Hemolytic uremic syndrome associated with paraquat intoxication

Jang¹,

Bae²,

Hwang³

et al. 2013

J of Clinical Apheresis

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“…The classic syndrome can also be acquired because of heavy metal exposure, ( 8 ) multiple myeloma, ( 9 ) and immunologic disorders such as light‐chain nephropathy ( 9 ) or interstitial nephritis. Acquired Fanconi's syndrome has also been associated with the use of a number of medications including aminoglycosides, ( 10 ) valproate, ( 11 ) methyl‐3‐chromone, ( 12 ) paraquat, ( 13 ) l ‐lysine, ( 14 ) and outdated tetracycline. ( 15,16 ) There have been several cases recently reported of Fanconi's syndrome in HIV + patients treated with antinucleoside antiretrovirals.…”

Section: Introductionmentioning

confidence: 99%

Fanconi's Syndrome in HIV+ Adults: Report of Three Cases and Literature Review

Earle

Seneviratne

Shaker

et al. 2004

Journal of Bone and Mineral Research

125

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We diagnosed Fanconi's syndrome (phosphate depletion and dysfunction of the renal tubules) in three HIV؉ patients. This was temporally related to their HIV treatment. Physicians caring for patients with HIV should recognize the association of this rare syndrome with antiretroviral medications and monitor their patients carefully.Introduction: Fanconi's syndrome is caused by increased excretion of phosphate, glucose, amino acids, and other intermediary metabolites, and can result in osteomalacia. Materials and Methods:We diagnosed this syndrome in three HIV ϩ patients. Results: The first was a 43-year-old woman referred for multiple painful stress fractures. She demonstrated hypophosphatemia, metabolic acidosis, phosphaturia, glucosuria, and generalized aminoaciduria. These abnormalities resolved with oral phosphate replacement and discontinuation of the antiretroviral medication tenofovir. The second patient was a 39-year-old man with hypophosphatemia and bone pain. His symptoms improved with discontinuation of adefovir and supplementation of phosphate, potassium, and calcitriol. The third patient was a 48-year-old man who presented with symptomatic tetany caused by hypocalcemia (total serum calcium of 6.5 mg/dl [8.5-10.5 mg/dl]). Nine months before presentation, he had been treated with cidofovir for retinitis caused by cytomegalovirus. With calcium, phosphate, potassium, and calcitriol therapy, his laboratory abnormalities improved substantially, although he continues to require daily electrolyte replacement. Conclusions: Each patient demonstrated generalized renal tubular dysfunction temporally related to treatment with antiretroviral drugs. The mechanism responsible for these abnormalities is not known; however, physicians caring for patients with HIV disease should recognize the association of Fanconi's syndrome with antiretroviral medications and monitor susceptible patients to prevent potential skeletal and neuromuscular complications.

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“…Acute renal failure usually is associated with mild pro- teinuria, glucosuria, and increased fractional excretion of sodium or phosphorus, compatible with proximal tubular dysfunction. 7 Paraquat-induced liver dysfunction mainly consists of cholestasis attributed to extensive injuries of small-and medium-sized bile ducts in centrilobular areas. 8 The biochemical mechanisms underlying paraquatinduced tissue injury are not fully understood.…”

Section: Analytical Datamentioning

confidence: 99%