1/152. anaphylaxis in labor secondary to prophylaxis against group B streptococcus. A case report. BACKGROUND: Two strategies have been recommended by the Centers for disease Control and Prevention and approved by the American College of obstetrics and gynecology to help prevent group B streptococcal disease in the newborn. Both involve using penicillin in labor. However, the potential for allergic and even anaphylactic reactions to penicillin exists. CASE: A patient was treated for risk factors for group B streptococcus in labor and suffered a serious anaphylactic reaction to penicillin; it resulted in an emergency cesarean section. Although the patient and infant were eventually discharged, the patient developed disseminated intravascular coagulation and suffered acute tubular necrosis that required dialysis. CONCLUSION: Prophylaxis against group B streptococcal sepsis is of proven benefit, but the possible harm to the mother and fetus from treatment with penicillin must be recognized. ( info) |
2/152. Spontaneous renal allograft rupture attributed to acute tubular necrosis. A renal allograft recipient receiving triple immunosuppressive therapy developed spontaneous allograft rupture 5 days after her second cadaveric renal transplantation. Renal biopsy showed interstitial edema with severe acute tubular necrosis (ATN). There was no evidence of acute rejection or renal vein thrombosis. The ruptured renal graft was salvaged by an aggressive fluid resuscitation therapy and surgical hemostasis. The renal function was satisfactory on discharge. We conclude that renal allograft rupture can be the result of interstitial edema solely attributed to ATN in the absence of graft rejection. The ruptured graft kidney is potentially salvageable for those patients whose hemodynamic status can be stabilized by appropriate supportive therapy. ( info) |
3/152. Thin basement membrane disease and acute renal failure secondary to gross hematuria and tubular necrosis. A patient with thin basement membrane disease (TBMD), macroscopic hematuria, and acute renal failure is described. A renal biopsy showed massive occlusion of renal tubules by red blood cells and casts. This was accompanied by tubular cell damage consistent with acute tubular necrosis. The patient was receiving warfarin because of a history of deep venous thrombosis at the time he developed the acute renal failure. The possible relationship of the warfarin therapy to the TBMD, intratubular hemorrhage, and acute renal failure are discussed. ( info) |
4/152. Case study of paired cadaver renal allografts from the same donor: influence of local DIC kidney and concomitant acute rejection on early graft outcome. We report the clinical course of 2 recipients whose renal allografts were obtained from the same cadaver donor after cardiac arrest. The recipients showed different outcomes after transplantation. Graft biopsy after reperfusion revealed disseminated intravascular coagulation (so-called DIC kidney) and severe acute tubular necrosis (ATN) in both recipients. While one graft showed primary nonfunction, the other graft became functional after a post-operative anuric period. Serial graft biopsies performed during the oligo-anuric period revealed recovery of ATN and no intra-glomerular fibrin thrombi, but development of acute rejection was detected in both recipients. The left kidney graft showed more severe local DIC kidney than the right kidney, as well as more severe acute rejection in the oligo-anuric period. Despite aggressive anti-rejection therapy, the left kidney graft showed primary nonfunction. Therefore, severe acute rejection leading to primary nonfunction might have been related to more severe ischemic injury and more extensive local DIC kidney in the left kidney. ( info) |
5/152. Acute tubular necrosis due to captopril. Angiotensin-converting enzyme (ACE) inhibitors are standard therapy for congestive cardiac failure. ACE inhibitors have been used worldwide and are usually safe and have relatively few side effects. hypotension can develop with the first dose of captopril and can lead to symptomatic renal hypoperfusion with subsequent acute renal failure (ARF). The case of a 65-year-old patient with congestive heart failure who developed acute renal failure following the first dose of captopril is described. He required hemodialysis for 8 weeks for the improvement of his renal function and urinary output. The renal biopsy confirmed the presence of acute tubular necrosis. The reversibility of captopril-induced ARF is confirmed and the patient made an uneventful recovery. An immunoallergic mechanism is not thought to have been responsible for this adverse effect. It is advised that caution should be exerted in giving ACE inhibitors to elderly patients with congestive heart failure, particularly if they are on diuretics. Routine biochemical monitoring is suggested before and during captopril therapy. ( info) |
6/152. Acute tubular necrosis induced by high level of cyclosporine A in a lung transplant. We report a case of acute accidental cyclosporine A intoxication in a lung transplant patient. The intoxication led to renal failure due to acute tubular necrosis, which was partially reversible. A review of the literature on the renal consequences of cyclosporine A intoxication is given. ( info) |
7/152. peritonitis as a risk factor of acute renal failure in nephrotic children. Idiopathic acute renal failure (IARF) is an uncommon but severe complication in children with relapsing nephrotic syndrome and may require long-term dialytic support until recovery of renal function takes place. Due to limited understanding of the pathophysiology of IARF, specific guidelines for its prevention and therapy have not been developed. Among triggering factors, peritonitis was present in half of all pediatric patients with this complication described in the English literature over the past 15 years. We report an additional nephrotic child who developed IARF following spontaneous bacterial peritonitis. The renal biopsy showed tubular epithelial changes consistent with acute tubular necrosis. A discussion of related literature and possible pathogenesis of this association is presented. ( info) |
8/152. A simple objective parameter for perfusion study of renal transplant. We proposed a simple parameter, the kidney-to-aorta ratio (KAR), for evaluation of renal transplant perfusion. KAR was calculated from the peak counts of the kidney and the aorta. The calculated values were compared with the visual interpretation of the radionuclide first-pass flow study, percent renal uptake (%RU), and tubular extraction rate (TER) by Bubeck's one point sampling method in 37 studies. KAR correlated well with the visual interpretation of the flow study and the other quantitative parameters. Representative cases, which showed the usefulness of KAR for the objective assessment of the perfusion status of renal transplants, were presented. In conclusion, KAR is a simple and practically useful parameter for objective evaluation and follow-up of renal transplant perfusion. ( info) |
9/152. Incidental recognition of left subclavian vein obstruction on renal scintigraphy. In a renal transplant recipient with persistently poor graft function, the flow phase of a renal scan incidentally revealed multiple venous collaterals with focally increased vascular activity near the left lobe of the liver (quadrate lobe). This was initially assumed to represent superior vena cava (SVC) obstruction. A renal biopsy was contemplated to exclude acute rejection because of a nondiagnostic flow phase (loss of a bolus effect). However, because the possibility of venous obstruction at the level of the subclavian and/or brachiocephalic veins (without involving the SVC) also existed, another renal scan was performed, with injection of radiotracer into the contralateral arm. This showed a patent SVC and reasonably preserved renal perfusion consistent with acute tubular necrosis. Subsequently, left subclavian vein obstruction was identified. The graft function improved with conservative management for acute tubular necrosis. These findings illustrate the danger of considering only SVC obstruction when collateral flow patterns and focal hot spots in the liver are present. ( info) |
| BACKGROUND: tumor necrosis factor-alpha (TNF-alpha) may have an important role in the clinical exacerbation of sarcoidosis. OBJECTIVE: To treat sarcoidosis with infliximab, a chimeric human-murine anti-human TNF-alpha monoclonal antibody. DESIGN: Case report. SETTING: U.S. academic medical center. PATIENT: A 72-year-old woman with sarcoidosis presenting with severe protein-losing enteropathy, hypoalbuminemia, and proximal myopathy who had not responded adequately to corticosteroid therapy and whose clinical course was further complicated by acute tubular necrosis and renal failure requiring long-term hemodialysis. INTERVENTION: Intravenous infusion of infliximab, 5 mg/kg of ideal body weight; infusion was repeated at 2 and 6 weeks. MEASUREMENTS: Clinical response of enteropathic and myopathic symptoms and serum albumin level. RESULTS: Enteropathic and myopathic symptoms resolved after infliximab therapy, and the serum albumin level also improved. However, the clinical course was complicated by the development of a hypercoagulable state associated with circulating anticardiolipin antibodies, which prompted discontinuation of infliximab therapy. CONCLUSIONS: Infliximab therapy was successful in a patient with sarcoidosis. tumor necrosis factor-alpha may be an important mediator of clinical disease in sarcoidosis and could be an attractive target for therapeutic intervention. However, infliximab may cause adverse effects associated with cytokine cascade manipulation. ( info) |