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The effects of primary tumors on the host systemic environment and resulting contributions of the host to tumor growth are poorly understood. Here, we find that human breast carcinomas instigate the growth of otherwise-indolent tumor cells, micrometastases, and human tumor surgical specimens located at distant anatomical sites. This systemic instigation is accompanied by incorporation of bone-marrow cells (BMCs) into the stroma of the distant, once-indolent tumors. We find that BMCs of hosts bearing instigating tumors are functionally activated prior to their mobilization; hence, when coinjected with indolent cells, these activated BMCs mimic the systemic effects imparted by instigating tumors. Secretion of osteopontin by instigating tumors is necessary for BMC activation and the subsequent outgrowth of the distant otherwise-indolent tumors. These results reveal that outgrowth of indolent tumors can be governed on a systemic level by endocrine factors released by certain instigating tumors, and hold important experimental and therapeutic implications.

The presence of FEG suggests underlying IBD. Although FEG is particularly common in children with Crohn's disease, it does not reliably differentiate between Crohn's disease and ulcerative colitis.

The effect of hemorrhagic reduction in systemic blood pressure (SBP) to 90 mm Hg for four hours on autoregulation of renal blood flow (RBF), renal function, and renal histology was examined in control rats, one week norepinephrine-induced acute renal failure (NE-ARF) rats with intact renal nerves, and one week NE-ARF rats with prior renal denervation. The results showed that in control rats, hemorrhagic SBP reduction to 90 mm Hg had no effect on autoregulation of RBF (autoregulatory index = 0.09 +/- 0.02), creatinine clearance, or renal histology. However, in one week NE-ARF rats with intact renal nerves, hemorrhagic reduction in SBP to 90 mm Hg was associated with marked impairment of autoregulation of RBF (autoregulatory index = 3.49 +/- 0.25), further reduction in creatinine clearance from 0.59 +/- 0.08 ml/min to 0.36 +/- 0.14 ml/min, and histologic evidence of recurrent ischemic injury. Renal denervation prior to SBP reduction improved autoregulation of RBF (autoregulatory index = 0.30 +/- 0.09), prevented the further reduction in creatinine clearance, and significantly ameliorated the deleterious effect on renal histology seen in innervated NE-ARF rats. These results suggest the potential importance of the loss of autoregulation of RBF on the course of NE-ARF, and further support the pathogenetic role of renal nerves in the loss of autoregulation.

The responsiveness of the renal vascular system was investigated in uninephrectomized Sprague-Dawley rats in which acute renal failure had been induced by norepinephrine. The animals were studied at 1' and 3 wk after norepinephrine infusion. Uninephrectomized littermates served as controls. Compared with controls, there was an absence of renal blood flow autoregulation in 1-wk acute renal failure that returned in part by 3 wk. In 1-wk rats there was a marked increase, rather than decrease, in renovascular resistance as renal perfusion pressure was decreased. The renal vasculature was significantly less responsive in 1-wk rats than in control or 3-wk animals when acetylcholine, angiotensin II, or norepinephrine was infused into the renal artery at minimal vasoactive doses (all P less than 0.01). Paradoxically, renal vasoconstriction in response to renal nerve stimulation was greater in 1-wk than in 3-wk and control rats (P less than 0.01) and was not inhibited by renal artery infusion of phenoxybenzamine. Renal denervation significantly improved renal blood flow autoregulation in 1-wk animals (P less than 0.001) and completely abolished the increase in renovascular resistance as renal perfusion pressure was lowered. No effects of renal denervation on renal blood flow autoregulation were seen in control and 3-wk rats. It is concluded that renovascular responses to neurohumoral stimuli are aberrant in acute renal failure. The loss of renal blood flow autoregulation is related to an increased renovascular resistance that is due to increased activity of non-alpha-adrenergic mechanisms of the autonomic nervous system.

Eosinophiluria is considered a useful marker of drug-induced acute interstitial nephritis. However, recognition of eosinophiluria by Wright's staining is technically difficult, and the spectrum of disorders causing eosinophiluria is not completely defined. We have adapted Hansel's stain for the examination of urinary sediment. Whereas there was a variable uptake of Wright's stain by eosinophils in the urine, such eosinophils were readily recognized with Hansel's stain by the presence of bright red granules. The prevalence of eosinophiluria in acute interstitial nephritis was 10 of 11 patients, in acute tubular necrosis none of 30, in acute pyelonephritis none of 10, in acute cystitis 1 of 15, in postinfectious glomerulonephritis 1 of 6, in rapidly progressive glomerulonephritis 4 of 10, and in acute prostatitis 6 of 10. Eosinophiluria in acute interstitial nephritis was demonstrated by Hansel's stain in 10 of 11 patients but by Wright's stain in only 2 of 11 patients. We conclude that Hansel's stain substantially improves the recognition of eosinophiluria as compared with Wright's stain. Eosinophiluria is useful in distinguishing acute interstitial nephritis from acute tubular necrosis. The clinical spectrum of eosinophiluria also includes rapidly progressive glomerulonephritis, acute prostatitis, and occasionally, acute cystitis or postinfectious glomerulonephritis.

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