Cocaine-induced acute renal failure, hemolysis, and thrombocytopenia mimicking thrombotic thrombocytopenic purpura

Volcy, Judith; Nzerue, Chike; Oderinde, Adesoji; Hewan-Iowe, Karlene

doi:10.1016/s0272-6386(00)70321-0

Cited by 59 publications

(39 citation statements)

References 17 publications

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“…1 Acute renal failure related to cocaine use most commonly occurs in the setting of rhabdomyolysis, although multiple other patterns of renal injury, including most notably malignant hypertension with thrombotic microangiopathy and renal cortical necrosis, have been reported. [2][3][4][5] Rhabdomyolysis has been reported in 24% of cocaine users and approximately 20-33% of patients with cocaine-induced rhabdomyolysis develop myoglobinuric acute renal failure. 6,7 The pathogenesis of cocaine-induced rhabdomyolysis likely involves vasoconstriction, increased muscle activity, hyperpyrexia, and endothelial injury.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 The pathogenesis of cocaine-induced rhabdomyolysis likely involves vasoconstriction, increased muscle activity, hyperpyrexia, and endothelial injury. 2,4,8,9 Cocaine-induced renal vasoconstriction has been implicated as a cause of acute renal failure even in cases without evidence of rhabdomyolysis. 10,11 Chronic administration of cocaine is associated with tubular injury and necrosis and appears to be able to stimulate mesangial cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

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Acute bilateral renal infarction secondary to cocaine-induced vasospasm

Madhrira

Mohan

Markowitz

et al. 2009

Kidney International

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A 47-year-old African-American male with a history of hypertension for 1 year and cocaine use presented to the emergency department with acute onset of bilateral flank pain, nausea, vomiting, and diarrhea. Physical examination was unremarkable. Laboratory evaluation revealed a white blood count of 15.1 K/ml (normal 4.5-11.5 K/ml) and a serum creatinine of 2.4 mg/100 ml. A non-contrast CT scan of the abdomen was unremarkable. The patient was treated with morphine (for pain) and i.v. fluids, felt better, and was discharged for out-patient follow-up.The patient saw his primary care physician 2 days later (day 3) and reported persistence of the bilateral flank pain. The patient also reported a transient inability to urinate for 36 h before the visit. An abdominal ultrasound and blood chemistry were obtained. On day 5, he was referred by his physician to the emergency department for a serum creatinine of 9.2 mg/100 ml from day 3. At the time of admission, the patient reported using 5-6 g/day of ibuprofen for the previous 4 days and admitted to sniffing cocaine a few hours before the initial onset of flank pain.On physical examination, the patient was a well-built African-American male with a temperature of 99.2 1F, pulse rate of 60/min, blood pressure of 150/85 mm Hg and weight of 85 kg (BMI 27.7 kg/m 2 ). There was no orthostasis, pallor, or skin rash. The heart and lung examinations were unremarkable. The abdomen was soft, with no suprapubic dullness. There was no costovertebral angle tenderness or pitting edema. The extremity pulses were symmetric and equal.Laboratory results are presented in Table 1. Serologic tests for hepatitis B and C viruses, human immunodeficiency virus, antinuclear antibody, and rheumatoid factor were negative. Serum complements, including C3, C4, and CH50, were within the normal range. Hemoglobin electrophoresis, chest X-ray, electrocardiogram, and echocardiogram were unremarkable. Renal ultrasound revealed normal-sized kidneys with mildly increased echogenecity and no hydronephrosis. A 99m Tc-MAG3 (mercaptoacetyltriglycine) radionuclide renogram showed multiple wedge-shaped photopenic areas in both kidneys (Figure 1a). Owing to the absence of a clear explanation for the patient's acute renal failure, renal biopsy was performed 12 days after the onset of symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acute bilateral renal infarction secondary to cocaine-induced vasospasm

Madhrira

Mohan

Markowitz

et al. 2009

Kidney International

View full text Add to dashboard Cite

show abstract

“…He had no previous history of atherosclerosis. This patient suffered cocaine-induced rhabdomyolysis with acute renal failure (14). Renal biopsy findings were inconsistent with thrombotic microangiography and glomerular ischemia.…”

Section: Discussionmentioning

confidence: 81%

“…Renal biopsy findings were inconsistent with thrombotic microangiography and glomerular ischemia. The patient demonstrated renal endothelial injury and vasoconstriction (14). In 1998, perioperative angiography detected occlusive gastrointestinal arterial lesions.…”

Section: Discussionmentioning

confidence: 97%

Crack cocaine causing fatal vasoconstriction of the aorta

Williams

Wasserberger

2006

The Journal of Emergency Medicine

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“…These clinical features were the basis for our suspicion of alendronate, cocaine, and trimethoprim-sulfamethoxazole, although tests drug-dependent antibodies were negative for each of these three patients (including tests for quinine-dependent antibodies in the patient whose acute TMA followed cocaine exposure). There have been reports of TMA associated with cocaine [36] and trimethoprim-sulfamethoxazole [37], but there has e179 Table II Drugs that have been associated with thrombotic microangiopathy (TMA) in the Oklahoma TTP-HUS Registry, 1989-2009.…”

Section: Discussionmentioning

confidence: 99%