The kidney has a remarkable capacity to regenerate after injury, as it is not a terminally differentiated organ. This regenerative potential is somehow incomplete, however, and as the insult continues, progressive and irreversible scarring results in chronic renal disease. Dialysis and organ transplantation are nonspecific and incomplete methods of renal replacement therapy. Stem cells may provide a more efficacious method for both prevention and amelioration of renal disease of many etiologies. Although many reports have claimed the existence of renal-specific stem or progenitor cells isolated and characterized by various methods, the results have been diverse and debatable. The bone marrow stem cells seem to play a minor role in renal regeneration after acute ischemia in mice through transdifferentiation and cell fusion, but their immediate paracrine effects result in considerable improvements in renal function. Therefore, as in stem cell therapy for the heart, bone marrow-derived stem cells show promise in regeneration of the kidney. Although more research is needed in the basic science of renal regeneration, clinical research in animals has demonstrated the versatility of stem cell therapy. The first phase of clinical trials of bone marrow mesenchymal cells in protection against acute kidney injury may begin shortly. This will enable further exploration of stem cell therapy in renal patients with multiple comorbidities.

A 57-year-old black female presented with a 1-month of right-sided congestive heart failure and clinical evidence of pulmonic and tricuspid valvular stenosis and insufficiency. The echocardiographic examination and ventriculography demonstrated a large right atrial tumor interfering with the function of both right-sided valves. The patient underwent successful surgical resection of the tumor. Histologically, the tumor had cellular areas typical of myxoma, as well as glandular areas, a feature which has been described very rarely in this lesion. Electron microscopy of the glandular zones, which has never been reported previously, shown cells having essential homology with the usual myxoma elements. The atypical histopathology of this lesion supports the theory that atrial myxomas are true neoplasms, and are not derived from unusually organized mural thrombi.

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The efficacy and safety of amlodipine (2.5 mg, 5 mg, or 10 mg) once daily was compared with atenolol (50 mg to 100 mg) once daily in patients with mild-to-moderate essential hypertension in a randomized, double-blind, parallel, placebo-controlled study. One hundred and twenty-five patients were randomly allocated at the end of a 4-week run-in placebo period to 8 weeks' double-blind treatment with amlodipine (n = 41), atenolol (n = 43), or placebo (n = 41). The mean changes from baseline in blood pressure 24 h postdose for amlodipine (mean daily dose 8.8 mg) were -12.8/-10.1 mm Hg for supine and -11.5/-9.8 mm Hg for standing blood pressure (P < .001). For atenolol (mean daily dose 83.7 mg) the changes were -11.3/-11.7 mm Hg for supine and -13.3/-12.3 mm Hg for standing blood pressure (P < .001). There were no statistically significant differences between treatments. The responder rates for amlodipine, atenolol, and placebo were 61.1%, 64.9%, and 11.1%, respectively. Determinations taken over the 24-h period at the final visit revealed that amlodipine and atenolol maintained the group mean supine blood pressure at or below 140/90 mm Hg throughout the period of observation; the corresponding time-effect curve for the placebo group was clearly in the hypertensive range. Heart rate was significantly lowered by atenolol only. Both amlodipine and atenolol were well-tolerated. Only one patient was withdrawn because of the development of peripheral edema, arthralgia, and fatigue after treatment with amlodipine. This study demonstrates that once-daily administration of amlodipine or atenolol to mild-to-moderate hypertensive patients was well-tolerated and provided adequate blood pressure control throughout the 24-h dosing interval.