Kallikrein-like amidase activity in renal ischemia and reperfusion

We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9 percent NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 µg of Evans blue/g dry tissue in the basal condition and 1750 µg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.

Insuficiencia Renal Aguda (IRA) inducida por ifosfamida y contraste iodado

La toxicidad renal por ifosfamida puede ser potenciada por otras drogas. Se reporta un paciente varón de 57 años de edad con carcinoma indiferenciado de pulmón no a celulas pequeñas, estadio IIIB. Recibió cada 28 días ifosfamida 2,5 g/m2, días 1 y 15, dexametasona 8 mg, MESNA 4,8 g/ciclo y clorhidrato de granisetrón. Con orina y función renal normales, se realizó TAC de tórax con contraste y a las tres semanas recibió un cuarto ciclo. Un mes despues ingresó con IRA no oligúrica, urea 306 mg/dl, CrP 11 mg/dl, Kp 3 meq, Nap 130 mq/, Na urinario 30.5 meq/l, Hb 9,6 g/dl, GB 11.000, hipergamma con componente M gamma lento Kappa y Lambda, proteinuria 1.2 g/24 horas, tubular, Bence Jones negativa y microhematuria. Ecografía renal normal. La PAMO descartó plasmocitoma. La biopsia renal mostró nefritis túbulo - intersticial con necrosis y atrofia tubular, fibrosis instersticial y afectación glomerular con proliferación celular e inmunofluorescencia negativa. Realizó tratamiento medico con recuperación parcial de la función renal y proteinuria negativa a los seis meses. Se recomienda no utilizar contrastes iodados durante el tratamiento con ifosfamida y monitorear beta 2 microglobulina y función renal como indicadores de daño renal

Adenoacantoma del esofago superior: presentacion de un caso / Adenocanthoma of the upper esophagus: report of a case

We report 72 years old woman, with adenoacamthoma of the upper osophagus who was admitted in Hospital israelita "EZRAH" in April of 1991. We performed a review of the literature on this rare tumour, that is the reason of presenting this case