Primary renal non-Hodgkin’s lymphoma (NHL) with acute renal failure is a very rare condition, which frequently occurs in bilateral renal involvement. We report a 26-year-old male with primary bilateral renal NHL presenting with acute renal failure. A CT scan of the abdomen showed markedly enlarged kidneys with multinodularity and para-aortic lymphadenopathy. A percutaneous renal biopsy demonstrated ‘follicular center lymphoma, diffuse, small cell’. Thirteen cycles of systemic chemotherapy with cyclophosphamide-doxorubicin-vincristine-prednisolone (CHOP) and ifosfamide-methotrexate-etoposide-bleomycin (IMVP-Bleo) regimens were administered, which resulted in normalization of renal function with improvement of renal lymphoma. Since there was no further change of renal lesions after initial partial remission, a follow-up renal biopsy was performed 10 months after diagnosis, and no residual lymphoma was found.

To elucidate the possibility whether an elevation of intracellular Ca2+ concentration ([Ca2+]i) in rabbit coronary artery myocytes during ischemic cardioplegic period may serve as one of the mechanisms of the "no-reflow' phenomenon or not, the changes in [Ca2+]i were measured under ischemic cardioplegia conditions using a fluorescent Ca2+ indicator, fura 2/AM. When single cells were perfused with cardioplegic or ischemic cardioplegic solutions, [Ca2+]i was significantly increased and the degree of [Ca2+]i elevation was further augmented by the ischemic cardioplegic solution. Pretreatment of a sarcoplasmic reticulum emptying agent, 20 mM caffeine, had no effect on ischemic cardioplegia-induced [Ca2+]i changes, but application of a Ca2+ channel blocker, 5 x 10 (-1)M nifedipine, or an antagonist of Na+/Ca2+ exchange, 5 mM Ni2+, significantly inhibited the [Ca2+]i elevation, respectively. The magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate in the range of 0 and 25 mM. When Ni2+ was added to the reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with the controls. It is concluded that ischemic cardioplegia-induced [Ca2+]i elevation may serve as one of the mechanisms of the "no-reflow' phenomenon in rabbit coronary artery smooth muscle cells. We propose that Na+/Ca2+ exchange may serve as a key function in ischemic cardioplegia-induced [Ca2+]i elevation.

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