Idiopathic renal hematuria in a military working dog.

A 1.5-year-old male Belgian Malinosis Military Working Dog presented with a 1-month history of intermittent hematuria. Diagnostic ultrasound and contrast radiography demonstrated large blood clots in the urinary bladder and a filling defect in the right renal pelvis. At surgery, clotted blood was present in the right ureter and bladder. Following right nephrectomy, the dog returned to training. One month later, elevations in urea nitrogen and creatinine were noted. Hematuria recurred at 3 months and the dog was found dead in its kennel. Necropsy showed a blood-filled left renal pelvis and ureter.

The morphology of smoke inhalation injury in sheep.

Pulmonary injury resulting from inhalation of chemical and particulate products of incomplete combustion is one of the principal determinants of mortality following burn injury. In this study, the histopathology of inhalation injury was examined in sheep. Mild, moderate, or severe smoke injury was produced in anesthetized sheep by insufflation with various doses of ambient temperature smoke, generated by burning polyethylene, wood pulp, and nonwoven cellulose pads. A total of 64 sheep were exposed and evaluated at times ranging from 15 minutes to 4 weeks after exposure. Morphologic changes in the lungs were studied using light microscopy and both transmission and scanning electron microscopy. The primary, dose-responsive injury observed was acute cell membrane damage in the trachea and bronchi leading to edema, progressive necrotic tracheobronchitis with pseudomembrane formation, and airway obstruction. These inflammatory and occlusive effects were followed by congestion, alveolar space edema, atelectasis, and bronchopneumonia. Morphologic changes occurring in the alveolar epithelium following high smoke dosage included intracellular edema in type-I cells, changes in the membrane-bound vacuoles of type-II cells, and septal thickening caused by interstitial edema. No capillary endothelial changes were observed.

Smoke inhalation injury and the effect of carbon monoxide in the sheep model.

The role of carbon monoxide (CO) in causing the physiologic and anatomic changes characteristic of smoke inhalation injury was evaluated in 34 sheep. The smoke-exposed group received a dose of smoke known to produce mild inhalation injury. The CO group received a pure gas mixture that contained concentrations of oxygen, carbon dioxide, and CO similar to those in the smoke. Cardiopulmonary function was measured immediately after exposure, and 24 and 72 hours after exposure. The CO group showed a transient increase in cardiac output, but the smoke group showed no such response. The CO group maintained normal PaO2 levels during the 72-hour study period; the smoke group gradually developed hypoxemia. The lungs of the CO exposed animals had no discernible histologic changes; lungs of the smoke group showed progressive inflammatory changes. These results indicate that CO per se is not the primary etiologic agent of smoke inhalation injury.

A dose-responsive model of smoke inhalation injury. Severity-related alteration in cardiopulmonary function.

The dose responsiveness of selected physiologic indices was studied in a sheep model of smoke inhalation injury. In this model, graded severity of injury was achieved by changing the contact time with smoke (defined by "unit"), whereas other variables were kept constant. Blood gas and cardiopulmonary indices were measured in 70 sheep, including 12 controls, either 24 or 72 hours after exposure to 3, 6, 9, 12, 15, or 18 units of smoke. A 12-unit dose of smoke was fatal within 72 hours and an 18-unit dose was fatal within 24 hours. The best correlation between smoke dose and response was observed in arterial oxygen tension 24 hours after exposure. At 24 hours, most of the cardiopulmonary indices showed significant change only after a 12-unit exposure. Although the exact shape of the dose-response curve could not be defined, sigmoid or curved linear shape was suggested, reflecting the progressive deterioration.

Sequential postmortem changes of glomeruli. Their detection by scanning electron microscopy.

Postmortem changes were studied by scanning electron microscopy (SEM) in renal tissue from five species of animals. Specimens were collected at intervals up to 24 hours after death. Six distinct morphological alterations were identified in the renal glomerulus, including capillary loop constriction, changes in microvillus morphologic features, podocyte surface blebs, swelling or fusion of pedicels, podocytes erosion, and retraction or loss of pedicels. Glomerular size remained nearly constant in all five species. The results of these studies demonstrate that pathologic evaluation by SEM of tissue specimens from the kidney is acceptable up to 60 minutes post mortem.

Scanning electron microscopic observations on glomeruli: its use in thermally injured patients with renal impairment.

Previous scanning electron microscopic (SEM) studies have suggested that morphological changes occur in the glomeruli of animals with experimental acute renal failure (ARF). No SEM studies have been reported on human glomeruli in ARF. Sixteen thermally injured patients were studied by SEM and the observations were correlated with the light microscopic findings and clinical data. The group studied contained patients with normal renal function as well as patients with varying degrees of renal impairment, including ARF. The findings failed to demonstrate specific morphological alterations associated with ARF in the human.

Intrasinusoidal bodies in the livers of thermally injured patients.

Acidophilic intrasinusoidal liver bodies appearing at autopsy in cases in which thermal injury occurred were examined by light microscopy using several special stains and by scanning and transmission electron microscopy. Morphologically, these bodies were found to be membrane-bound protein material that were usually present in the hepatic sinuses but were also identified in hepatocytes, spaces of Disse, and Kupffer's cells. Correlation of clinical data with pathologic findings failed to determine a specific cause for the intrasinusoidal bodies.

An "abnormal" lymphoid proliferation simulating Hodgkin's disease in a burn patient.

A particularly exuberant and unusual lymphoid proliferation in the spleen of a burn patient is presented. Many Reed-Sternberg cell variants and occasional diagnostic Reed-Sternberg cells strongly suggested a diagnosis of Hodgkin's disease. The pattern of distribution and cytology of this lymphoid infiltrate, however, are incompatible with Hodgkin's disease or a non-Hodgkin lymphoma. Morphologic features in this case suggest that the Reed-Sternberg cell is a B lymphocyte. The most probable etiologies of this unusual lymphoid proliferation are reviewed.

An animal model for childhood convoluted T-cell lymphoma.

The light microscopic and ultrastructural characteristics of the AKR-J mouse lymphoma are described in detail. Clinical and histologic facets of convoluted T-cell lymphoma of childhood and AKR-J mouse lymphoma are reviewed. The remarkably close correlation between these two entities is demonstrated. The possibility that this mouse tumor should be utilized as a model for convoluted T-cell lymphoma of childhood is emphasized.

Diabetic glomerulosclerosis without glucose intolerance.

The pathophysiology of the microangiopathy of diabetes mellitus is poorly understood, and the relevance of carbohydrate intolerance remains uncertain. Four patients are presented with renal abnormalities suggestive of diffuse diabetic glomeruloscierosis. These patients have no evidence of carbohydrate intolerance by standard clinical technics. A familial incidence of diabetes mellitus and delayed insulin response to an oral glucose load support a classification of prediabetes or suspected diabetes mellitus for these patients. Early intercapillary nodule formation was seen in only two of the four patients. In the absence of this infrequent pathognomonic finding, an alternate approach to the diagnosis of diabetic glomerulosclerosis is suggested. Diffuse glomerular capillary basement membrane thickening, consistently present with diabetic glomerulosclerosis, is demonstrated by measurements utilizing the latex microsphere technic. The mean glomerular capillary basement membrane thickness of these patients was 4,403 A, compared with the control value of 3.098 A (P less than 0.001). Other pathologic findings suggestive of diabetic nephropathy include efferent arteriolosclerosis and linear immunofluorescence without electron dense deposits or inflammation. Skeletal muscle capillary basement membranes of all four patients also demonstrated significant thickening. The mean value for the patients was 1,510 A, as compared with a control value of 961 A (P less than 0.001). The importance of this muscle capillary basement membrane thickening to the diagnosis of diabetic microangiopathy is discussed. The pathologic alterations in the renal biopsy specimens and the demonstration of muscle capillary basement membrane thickening strongly suggest that diabetic glomerulosclerosis may occur in the absence of overt clinical carbohydrate intolerance.