Success with plasmapheresis treatment for recurrent focal segmental glomerulosclerosis in pediatric renal transplant recipients.

FSGS recurs in approximately 30% of transplanted kidneys and may lead to graft loss. We retrospectively examined the efficacy of early and intensive PP without additional IS in pediatric kidney transplant patients with recurrent FSGS at our center. Seven of 24 patients (29%) had nephrotic proteinuria and histologic evidence of FSGS recurrence within 1-5 days post-transplantation. PP was initiated early after transplantation and initially performed daily until sustained decline in proteinuria. PP frequency was then individually tapered according to proteinuria. Recurrent FSGS in all seven patients responded to a four- to 32-wk course of PP. Two of seven patients had a second recurrence of FSGS, and both recurrences remitted after an additional 3-6 wk of PP. Median observation period was 4.5 yr (0.8-16.3 yr). Complete remission of recurrent FSGS has been sustained in all seven patients, and all patients have stable graft function with recent plasma creatinine <1.5 mg/dL in six of seven patients. Most recent urine protein/creatinine is 0.13-0.61 mg/mg in six of seven patients. One patient has heavy proteinuria secondary to chronic allograft nephropathy 16 yr post-transplant. Intensive and prolonged PP, when initiated early in the post-operative period, is effective in treating recurrent FSGS and preventing graft loss without the use of additional immunosuppressants.

Pediatric Pulmonary Embolism: Diagnostic and Management Challenges.

A rare case of massive pulmonary embolism is presented in an oligosymptomatic teenager with predisposing factors. Computed tomography pulmonary angiography supported by three-dimensional reconstruction was diagnostic. The embolus qualified as massive by conventional anatomical guidelines, but as low risk by more recent functional criteria. Functional assessment has complemented morphologic assessment for risk stratification in adult patients. Such evidence is scarce in pediatrics. The patient underwent surgical embolectomy, followed by prophylactic anticoagulation, without further events. Diagnostic and management challenges are discussed.

Lead contamination of chicken eggs and tissues from a small farm flock.

Twenty mixed-breed adult laying hens from a small farm flock in Iowa were clinically normal but had been exposed to chips of lead-based paint in their environment. These chickens were brought to the Iowa State University Veterinary Diagnostic Laboratory, Ames, Iowa, where the concentration of lead in blood, eggs (yolk, albumen, and shell), and tissues (liver, kidney, muscle, and ovary) from 5 selected chickens was determined over a period of 9 days. Blood lead levels ranged from less than 50 to 760 ppb. Lead contamination of the yolks varied from less than 20 to 400 ppb, and shells were found to contain up to 450 ppb lead. Albumen contained no detectable amount. Lead content of the egg yolks strongly correlated with blood lead levels. Deposition of lead in the shells did not correlate well with blood lead levels. Mean tissue lead accumulation was highest in kidneys (1,360 ppb), with livers ranking second (500 ppb) and ovarian tissue third (320 ppb). Muscle contained the lowest level of lead (280 ppb). Lead contamination of egg yolks and edible chicken tissues represents a potential public health hazard, especially to children repeatedly consuming eggs from contaminated family-owned flocks.

Thermoregulatory response of dairy cows fed ergotized barley during summer heat stress.

Claviceps purpurea infects the seed heads of cereal grains and grasses and produces ergopeptine alkaloids that cause hyperthermia and agalactia in cattle during periods of heat stress. A field experiment was undertaken to examine the effects of ergopeptine alkaloids found in barley on thermal status of dairy cattle during periods of heat stress. Production end points were also measured to identify the effect of the change in thermal status. Contaminated barley screenings containing known levels of ergopeptine alkaloids were fed to lactating Holstein cattle (10 microg total ergopeptine alkaloids/kg BW/day) for 10 days during summer heat stress. Air temperature increased 14.4 C during the first 8 days of treatment and then declined the same during the last 2 days. Extreme daily values for rectal temperature and respiration rate, using averages of all animals, showed maximum increases of 2.3 C and 56.8 breaths/minute, respectively, during this period. Group afternoon milk production decreased 2 kg/day during the heat stress period, with no measurable change in feed intake. A greater level of hyperthermia occurred in cattle consuming the diet with ergopeptine alkaloids, with only marginal symptoms of ergot toxicosis reflected in feed intake and milk production. Therefore, the ergopeptine alkaloid dose used in this study represents a level for minimal induction of the ergot toxicity response.

Tremorgenic mycotoxin intoxication with penitrem A and roquefortine in two dogs.

In this report, we describe the natural intoxication of 2 dogs that consumed moldy dairy products found in the household garbage and the procedures used to identify and quantify the tremorgenic mycotoxins, roquefortine and penitrem A, in the remaining portions of ingested materials. Following the ingestion of mycotoxins, the dogs of our report developed muscle tremors or seizures that resembled clinical signs of strychnine poisoning. Roquefortine was the predominant mycotoxin in a moldy cream cheese wrapper that was found among scattered garbage consumed by the first dog. Penitrem A was the only mycotoxin detected in discarded moldy macaroni and cheese that was consumed by the second dog. Treatment of dogs with tremorgenic mycotoxin intoxication involves supportive care. Close monitoring is important because the development of aspiration pneumonia is common and has been reported as the cause of death. Clinical signs of intoxication gradually resolve within 24 to 48 hours.

Non-steroidal anti-inflammatory drugs-associated acute interstitial nephritis with granular tubular basement membrane deposits.

Acute tubulo-interstitial nephritis (ATIN) is an important cause of acute renal failure resulting from a variety of insults, including immune complex-mediated tubulo-interstitial injury, but drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) are a far more frequent cause. Overall, as an entity, ATIN remains under-diagnosed, as symptoms resolve spontaneously if the medication is stopped. We report on a 14-year-old boy who developed acute renal failure 2 weeks after aortic valve surgery. He was put on aspirin following surgery and took ibuprofen for fever for nearly a week prior to presentation. He then presented to the emergency department feeling quite ill and was found to have a blood urea nitrogen (BUN) concentration of of 147 mg/dl, creatinine of 15.3 mg/dl and serum potassium of 8.7 mEq/l. Dialysis was immediately initiated. A kidney biopsy showed inflammatory infiltrate consistent with ATIN. However, in the tubular basement membrane (TBM), very intense granular deposits of polyclonal IgG and C3 were noted. He needed dialysis for 2 weeks and was treated successfully with steroids for 6 months. His renal recovery and disappearance of proteinuria took a year. In conclusion, this is a first report of NSAIDs-associated ATIN, showing deposits of granular immune complex present only in the TBM and not in the glomeruli.

Overingestion of methionine tablets by a dog.

Methionine tablets are used as urinary acidifiers for pets and to decrease damage from dog urine to lawns. A 39-kg Labrador Retriever ingested approximately 350 tablets containing 150 mg methionine/tablet and was presented after repeated episodes of vomiting. The only abnormality was posterior ataxia suggestive of spinal cord injury. The animal was treated with i.v. fluids, steroids and gastrointestinal protectants. Approximately 4.5 h after entering the clinic the dog had a single seizure episode lasting 2-3 min which was treated with phenobarbital. Serum ammonia at that time was normal (0.19 mg/dL). The animal did not show further CNS abnormalities and awoke apparently normal. A musty odor to the breath was noticed through the course of the day, possibly due to volatile mercaptans produced from methionine metabolism. The animal made an uneventful recovery and was discharged the next day.

Acute poisoning of cattle by fertilizer-contaminated water.

Three cases of accidental acute fertilizer poisoning in cattle resulted in substantial death loss. Water hauled in tanks previously contaminated with a nitrogen-based fertilizer was the source in all cases. In 2 cases, analysis of the water measured urea at 1,640 and 2,300 ppm and ammonia-nitrogen at 640 and 750 ppm, respectively. Confirmation of urea toxicosis was made by measurement of toxic levels of ammonia-nitrogen in the rumen contents (>800 ppm) and blood (>8.0 ppm). In Case 3, no urea was detected in the water but ammonia-nitrogen was measured at 1,670 ppm and nitrate at 1.1%. Toxic levels of nitrate were measured in ocular fluid from 2 animals (60 ppm). Rumen contents contained toxic levels of ammonia-nitrogen (300 ppm) and a pH of 8.7. Interpretation of ammonia levels in rumen contents should take into account the source of ammonia as well as the pH since urea is more toxic than some ammonium salts. When the source is unknown, analysis of blood and/or serum ammonia-nitrogen instead of rumen content is recommended. The rapid progression of signs to death with ammonium nitrate poisoning may explain the lower levels of nitrate attained in ocular fluid than observed with pure nitrate intoxications.