Is rhabdomyolysis an additional factor in the pathogenesis of acute renal failure in leptospirosis?

Leptospirosis is an important cause of acute renal failure in our environment. Although several mechanisms are implicated, the role of rhabdomyolysis in the pathogenesis of acute renal failure in leptospirosis has not been analysed. Sixteen patients with the diagnosis of leptospiroses consecutively admitted to the hospital were prospectively studied. The disease was characterized by sudden onset in all patients and, at admission, jaundice, conjunctival suffusion and myalgias. Mild to moderate proteinuria with unremarkable urinary sediment was recorded in 37.5% of the patients and abnormal levels of urea creatinine were found in 87.5% and 74.0%, respectively. Increased levels of aminotranspherase were documented in all 12 and CPK in all 10 patients studied. Serum myoglobin levels greater than 120µg/l recorded in 56.2%. A correlation between myoglobin and renal failure or severity of disease, however, could not be established.

BIOPSY PROVEN ACUTE TUBULAR NECROSIS DUE TO RHABDOMYOLYSIS IN A DENGUE FEVER PATIENT: A CASE REPORT AND REVIEW OF LITERATURE

Renal histology results are very scarce in dengue-associated rhabdomyolysis patients developing acute kidney injury (AKI). We report a case of dengue fever-induced AKI associated to rhabdomyolysis with a renal biopsy showing acute tubular necrosis (ATN) and renal deposition of myoglobin. A 28-year-old patient who presented dengue fever (DF) complicated by severe AKI and rhabdomyolysis is described. The patient required hemodialysis for three weeks. A renal biopsy revealed ATN with positive staining for myoglobin in the renal tubuli. The patient was discharged with recovered renal function. In conclusion, this case report described a biopsy proven ATN associated to DF-induced rhabdomyolysis, in which renal deposition of myoglobin was demonstrated. We suggest that serum creatine phosphokinase should be monitored in DF patients to allow for an early diagnosis of rhabdomyolysis and the institution of renal protective measures.

Tetanus as a cause of acute renal failure: possible role of rhabdomyolysis

To study the frequency and examine the role of rhabdomyolysis in the acute renalfailure in tetanus 18 patients with the diagnosis of generalized tetanus consecutively admitted to the infectious disease hospital were evaluated. Ofthese 14 were male and 4female with mean age of 31.8± 2.0 years. Except for mild proteinuria recorded in 9 patients, the urinalysis were unremarkable. Serum creatinine higher than 1.4mg/dl was recorded in 39% of the patients, abnormal levels of CPK in 87,5% and serum myoglobin greater than 120µg/l in 39% of the patients. Oliguria was documented in one patient and none required diafysis therapy. No correlation wasfound between renal failure and myoglobin and/or CPK serum levels. Acute renalfailure in tetanus was not infrequent; usualfy it was non-oliguric, mild and transient and not related to the severity of the disease or to serum levels of myoglobin and/or CPK.

Afibrinogenemia following snake bite (Crotalus durissus terrificus)

This paper reports two cases of afibrinogenemia with normal platelet count following Crotalus durissus terrificus, snake bite Both patients presented high output acute renal failure and case two also had increased blood levels of CPK and LDH compatible with the diagnosis of rhabdomyolysis. Case one was given an unknown amount of antivenom and was treated with epsilonaminocaproic acid and a fresh whole blood transfusion and showed recovery of the coagulation disturbance 40 hours following these measures. Case two was given an adequate amount of crotalide antivenom and the coagulation tests performed 12 hours later showed a normal partial thromboplastin time and fibrinogen 86 mg/100ml. Case one presented no haemorrhagic disturbances. Case two presented persistent bleeding following venopuncture and after removal of impetigo crust in the legs. Acute renal failure was treated conservatively and both patients were discharged from the hospital with recovery of the renal function.

Snakebites by Crotalus durissus ssp in children in Campinas, São Paulo, Brazil

From January, 1984 to March, 1999, 31 children under 15 y old (ages 1-14 y, median 8 y) were admitted after being bitten by rattlesnakes (Crotalus durissus ssp). One patient was classified as "dry-bite", 3 as mild envenoming, 9 as moderate envenoming and 18 as severe envenoming. Most patients had neuromuscular manifestations, such as palpebral ptosis (27/31), myalgia (23/31) and weakness (20/31). Laboratory tests suggesting rhabdomyolysis included an increase in total blood creatine kinase (CK, 28/29) and lactate dehydrogenase (LDH, 25/25) levels and myoglobinuria (14/15). The main local signs and symptoms were slight edema (20/31) and erythema (19/31). Before antivenom (AV) administration, blood coagulation disorders were observed in 20/25 children that received AV only at our hospital (incoagulable blood in 17/25). AV early reactions were observed in 20 of these 25 cases (9/9 patients not pretreated and 11/16 patients pretreated with hydrocortisone and histamine H1 and H2 antagonists). There were no significant differences in the frequency of patients with AV early reactions between the groups that were and were not pretreated (Fisher's exact test, p = 0.12). Patients admitted less than and more than 6 h after the bite showed the same risk of developing severe envenoming (Fisher's exact test, p = 1). No children of the first group (< 6 h) showed severe complications whereas 3/6 children admitted more than 6 h post-bite developed acute renal failure. Patients bitten in the legs had a higher risk of developing severe envenoming (Fisher's exact test, p = 0.04). There was a significant association between both total CK and LDH blood enzyme levels and severity (p < 0.001 for CK and p < 0.001 for LDH; Mann-Whitney U test). No deaths were recorded.

Acute renal failure after massive honeybee stings

Two clinical cases of patients who survived after numerous attacks of Africanized bees (600 and 1500 bee stings, respectively) are reported. Clinical manifestation was characterized by diffuse and widespread edema, a burning sensation in the skin, headache, weakness, dizziness, generalized paresthesia, somnolence and hypotension. Acute renal failure developed and was attributed to hypotension, intravascular hemolysis, myoglobinuria due to rhabdomyolysis and probably to direct toxic effect of the massive quantity of injected venom. They were treated with antihistaminic, corticosteroids and fluid infusion. One of them had severe acute renal failure and dialysis was required. No clinical complication was observed during hospital stay and complete renal function recovery was observed in both patients. In conclusion, acute renal failure after bee stings is probably due to pigment nephropathy associated with hypovolemia. Early recognition of this syndrome is crucial to the successful management of these patients.

Africanized honeybee stings: how to treat them

INTRODUCTION: In 1956, Africanized honeybees (AHB) migrated from Brazil to other regions of the Western Hemisphere, including South, Central, and North America, except for Canada. Despite being productive, they are highly aggressive and cause fatal accidents. This study aimed to evaluate patients at the Clinical Hospital of Botucatu Medical School (HC-FMB) and to propose treatment guidelines. METHODS: From 2005 to 2006, the clinical and laboratorial aspects of 11 patients (7 male and 4 female) and the anatomopathological aspects of one patient who had died in 2003 were analyzed. RESULTS: The age of the surviving patients varied from 5 to 87 years, with a mean of 42.5 years. The majority of accidents occurred in the afternoon, and the number of stings ranged from 20 to 500. The principal signs and symptoms were pain and local inflammatory signs, nausea, tachycardia, and vomiting. Biochemical findings presented increased levels of creatine phosphokinase, lactate dehydrogenase, and aspartate/alanine aminotransferase. An 11-year-old male patient died upon entering the attic of a two-storey building where he was attacked by a swarm, receiving more than 1,000 stings. He was sent to HC-FMB where he was treated, but he died 24h later. Observed at the autopsy were erythematous-purpuric skin lesions besides necrosis at the sting locations, rhabdomyolysis, focal myocardial necrosis, tubular hydropic degeneration and focal tubular acute necrosis of the kidneys, myoglobinuria, and centrolobular necrosis in the liver. CONCLUSIONS: Accidents caused by multiple AHB stings always constitute a medical emergency. As there is no specific antivenom, we have developed guidelines, including first aid, drugs, and the proper removal of stingers.