Myeloid sarcoma presenting with acute renal failure and bilateral ureteral obstruction: a case report and review of the literature.

Myeloid sarcoma (MS) is a very rare disease that either presents with acute myeloid leukemia or as relapse of acute myeloid leukemia. The common sites include the small intestine, skin, bone, and lymph nodes. We present an unusual case of MS presenting with acute renal failure (ARF) and bilateral ureteral obstruction. Ultrasonography showed bilateral hydronephrosis and a large pelvic mass displacing the uterus. Pelvic mass biopsy showed fibroadipose tissue with diffuse neoplastic cell infiltration and immunostaining was positive for leukocyte common antigen (LCA) and myeloperoxidase consistent with myeloid sarcoma. Bone marrow biopsy revealed 63% myeloblasts. The patient died the 17th day of induction therapy. We came across only four MS cases in English literature that presented with ARF. To our knowledge, this case is the first description of myeloid sarcoma presenting with ARF and bilateral ureteral obstruction not originating from urogenital system. Physicians should consider possible hematological malignancies in patients with similar presentation.

A rare case of postinfectious glomerulonephritis caused by pneumococcus in an adult patient.

Postinfectious glomerulonephritis (PIGN) is commonly seen as a complication of infection with nephritogenic strains of group A streptococci, mostly with Streptococcus pyogenes. Pneumococcal pneumonia leading to glomerulonephritis has been reported in the pediatric literature, but only one adult case has been previously reported. We are presenting a case of postinfectious glomerulonephritis caused by pneumococcal pneumonia in an adult. In the present case, other possible etiologies of nephritic syndrome were ruled out with negative antineutrophilic cytoplasmic antibody (ANCA), anti-glomerular basement membrane antibody (Anti-GBM), antistreptolysin O (ASO), antinuclear antibody (ANA), HIV and viral hepatitis profile. The low CH50 indicated a complement-mediated injury. Renal biopsy was done showing immune complex-mediated crescentic glomerulonephritis consistent with postinfectious etiology. The patient received pulse dose steroids for 5 days followed by oral steroids. His urinary output improved along with normalization of his renal function, therefore dialysis was discontinued. We are presenting this case to alert clinicians to the possibility of postinfectious glomerulonephritis following pneumococcal pneumonia and to report the successful use of steroid therapy in such a situation.

Impact of myocardial structure and function postinfarction on diastolic strain measurements: implications for assessment of myocardial viability.

We sought to assess the role of regional diastolic function by Doppler echocardiography in predicting myocardial viability. Sixteen dogs underwent left anterior descending coronary artery (n = 8) or circumflex (n = 8) occlusion. All animals were imaged at baseline and 1-8 wk postinfarction (post-MI). In 10 dogs, invasive hemodynamic monitoring with a conductance catheter placed in the left ventricle (LV) was performed at the above time points. Dobutamine was infused at 1-8 wk post-MI to determine LV contractile reserve. Histomorphological analysis was performed to determine the presence of viable myocardium and changes in interstitial matrix. Post-MI, diastolic strain rate measurements (in radial and longitudinal planes) decreased significantly in the distribution of the diseased artery (P < 0.01) and on multiple regression analysis were determined by time constant of LV relaxation, end-diastolic pressure, regional stiffness, and the ratio of cellular infiltration to collagen deposition in the interstitial matrix. Among several indexes, diastolic strain rate during dobutamine infusion readily identified segments with >20% transmural infarction and related best to the extent of interstitial fibrosis (r = -0.86, P < 0.01). In an animal model of healing canine infarcts, diastolic strain rate by Doppler echocardiography appears to be a promising novel index of myocardial viability.

Vascular mural cells in healing canine myocardial infarcts.

Angiogenesis is a critical process in healing of myocardial infarcts, leading to the formation of highly vascular granulation tissue. However, effective cardiac repair depends on mechanisms that inhibit the angiogenic process after a mature scar is formed, preventing inappropriate expansion of the fibrotic process. Using a canine model of reperfused myocardial infarction, we demonstrated that maturation of the infarct leads to the formation of neovessels, with a thick muscular coat, that demonstrate distinct morphological characteristics. Many of these "neoarterioles" lack a defined internal elastic lamina and demonstrate irregular deposits of extracellular matrix in the media. Vascular mural cells in healing infarcts undergo phenotypic changes, showing minimal expression of desmin during the proliferative phase (1 hr occlusion/7 days reperfusion) but in the mature scar (8 weeks reperfusion) acquire a phenotype similar to that of vascular smooth muscle cells in control areas. Non-muscle myosin heavy chains A and B are induced in infarct endothelial cells and myofibroblasts, respectively, but are not expressed in neovascular mural cells. Recruitment of a muscular coat and formation of neoarterioles in mature scars may inhibit endothelial cell proliferation and vascular sprouting, stabilizing the infarct vasculature.