Nephrology Service and, Department of Medicine, University Hospital Arnau de, Vilanova, University of Lleida, Lleida, Spain
Sir,
Cocaine-induced acute renal failure has been reported in association with rhabdomyolysis [1,2]. However, only one case has been described in which acute renal failure developed in the absence of it [3].
We describe a case of acute renal failure which occurred after inhalation of cocaine without concomitant rhabdomyolysis.
A 31-year-old male, without a previous medical history, was admitted to the hospital because of acute renal failure in October 1998. He admitted having inhaled 5 g of cocaine 18 h before admission and denied the intake of any other nephrotoxic drug. Physical examination was normal except for a blood pressure of 150/100 mmHg. Blood analysis on admission disclosed a serum creatinine of 2 mg/dl, creatinin-phosphokinase (CPK) 107 U/l, and potassium 3.8 mmol/l, urinalysis showed a sodium of 30 mmol/l, trace of protein and 12 red blood cells per high-power field. His haemoglobin and coagulation tests were normal. Immunological studies showed normal levels of immunoglobulines, C3 and C4. HIV and HCV were negative. HBV anticore antibodies were positive (IgM negative), HbsAg negative. On ultrasound his kidneys were normal in size, with hyperechogenity of the right kidney. Diuresis was conserved throughout (1.52 l/day) and his body weight remained stable during the 10-day hospital stay.
After 10 days he had completely and spontaneously recovered from acute renal failure. His serum creatinine was 1.1 mg/dl on discharge. Hypertension resolved as renal function improved. On discharge his blood pressure was 120/70 mmHg without antihypertensive drugs.
The interest of this case is based on the fact that in this patient cocaine-induced acute renal failure occurred in the absence of rhabdomyolysis. The possibility that rhabdomyolysis developed before admission is extremely unlikely, because the half-life of serum creatinine kinase (CPK) is 17 h. It is even longer in the presence of renal failure. The patient was admitted 18 h after inhalation of cocaine, and CPK was determined on admission, and daily thereafter. Therefore, rhabdomyolysis can definitely be ruled out as the cause of acute renal failure.
In this case, cocaine was strongly suspected as the only cause of the acute renal failure and, in our opinion, the underlying mechanism was intense renal vasoconstriction. In the only similar case reported in the literature, acute renal failure lasted for 9 days. The authors attributed ARF to ischaemia induced by intense vasoconstriction [3].
The maximal concentration of cocaine is seen in the brain, lung, kidney and spleen. It is a well-known activator of the sympathetic and dopaminergic system. Cocaine has been implicated in the occurrence of myocardial infarction, hypertensive crisis, arrythmia, stroke and organ ischaemia including renal infarction [46].
Moreover, chronic cocaine use can cause exacerbation of pre-existing hypertension, narrowing of the lumen of renal vessels due to intimal fibrosis of the interlobar and intra-renal arteries [7,8].
Its chronic abuse can cause a vicious circle of vasoconstrictionhigh blood pressurerenal failure. We suggest that acute renal failure following cocaine abuse can supervene in the absence of concomitant rhabdomyolysis and that intense vasoconstriction is the most likely cause of the simultaneous hypertension.
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