Blood and Bone Marrow Studies in Renal Disease

Callen, Irwin R.; Limarzi, Louis R.

doi:10.1093/ajcp/20.1.3

Cited by 78 publications

(26 citation statements)

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“…A minor increase of RBC destruction or decrease in production causes a serious clinical problem in a patient al ready severely anemic while minor changes in either production and destruction would be difficult to measure. RBC survival was generally shortened in this group as would be expected in hypersplenism [9] and in chronic renal failure [1], Although the mechanism of anemia in uremia is commonly held to be due to a variety of factors, including a lack of erythro poietin [10], bone marrow depression [11], nutritional deficiencies [12] and increased RBC destruction [13,14], the spleen has just recently been im plicated in the anemia of renal failure [3,5], It was expected following splenectomy that RBC survival would increase since the anemia improved and there was no measurable increase in pro duction. However, the lack of uniform improvement in radiochromium RBC survival may have been due to technical factors such as an increase in hematocrit during the period of study, a change in chromium elution rate [15] or an error in the estimated blood loss during dialysis.…”

Section: Discussionmentioning

confidence: 93%

Hypersplenism in the Uremic Hemodialyzed Patient

Bischel¹,

Neiman²,

Berne³

et al. 1972

Nephron

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A hypersplenic syndrome developed in a group of 15 chronic hemodialysis patients. Splenectomy eliminated or reduced the need for routine transfusion requirements; granulocytopenia, lymphocytopenia and thrombocytopenia were corrected. Following renal transplantation azathioprine therapy was tolerated in the splenectomized group. One patient who refused splenectomy had persistent severe leukopenia. Spleens were normal to moderately increased in weight and contained an immunoreactive white pulp and a normal red pulp though increased hemosiderin was sometimes present. Serum ironsaturation decreased following removal of the spleen. Serum IgM levels fell after splenectomy but IgG and IgA were unchanged. Sources of chronic antigenic stimulation that may have produced the lymphoid hyperplasia included hepatitis antigen, bacterial and other viral antigens, and blood transfusions.The beneficial effect of splenectomy in these patients probably results from restoration of a delicate hematologic balance between hematopoiesis and destruction after removal of a major site of cellular sequestration and destruction and the hyperreactive immunoglobulin-producing lymphoidtissue.

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Section: Discussionmentioning

confidence: 93%

Hypersplenism in the Uremic Hemodialyzed Patient

Bischel¹,

Neiman²,

Berne³

et al. 1972

Nephron

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“…Patients with chronic renal failure almost always have mlarked anemia (1)(2)(3)(4)(5). Decreased production (3,5,6) and shortened survival of erythrocytes (7)(8)(9)(10)(11) have been implicated as the cause of this abnormality.…”

Section: Introductionmentioning

confidence: 99%

Effect of parathyroid hormone on erythropoiesis.

Meytes¹,

Bogin²,

Ma³

et al. 1981

J. Clin. Invest.

224

112

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A B S T R A C T Inhibitors of erythropoiesis have been found in the blood of uremic patients but their nature has not been identified. These patients have excess blood levels of parathyroid hormone (PTH) and it is possible that PTH inhibits erythropoiesis. The present study was undertaken to examine the effect of intact PTH molecules and some of its fragments on human peripheral blood and mouse bone marrow burst-forming units-erythroid (BFU-E), on mouse bone marrow erythroid colony-forming unit (CFU-E), and granulocyte macrophage progenitors (CFU-GM), and evaluate the interaction between PTH and erythropoietin (Ep) on human BFU-E. Intact PTH (1-84 bPTH) in concentrations (7.5-30 U/ml) comparable to those found in blood of uremic patients produced marked and significant (P < 0.01) inhibition of BFU-E and mouse marrow GFU-GM, but not of mouse marrow CFU-E. Inactivation of 1-84 bPTH abolished its action on erythropoiesis. Increasing the concentration of Ep in the media from 0.67 to 1.9 U/ml overcame the inhibitory effect of 1-84 bPTH on BFU-E. The N-terminal fragment of PTH (1-34 bPTH) and 53-84 hPTH had no effect on BFU-E.The results deomonstrate that (a) either the intact PTH molecule or a C-terminal fragment(s) bigger than 53-84 moiety exerts the inhibitory effect on erythropoiesis, and (b) adequate amounts of Ep can overcome this action of PTH. The data provide one possible pathway for the participation of excess PTH in the genesis of the anemia of uremia.

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“…Patients with chronic renal failure usually suffer from a hypoproliferative normochromic normocytic anemnia (1)(2)(3). In addition to hemolysis (4) and blood loss from various sources (5-7), two major factors have been implicated in the mechanism of the anemia of renal insufficiency which may be the cause of the hypoproliferative state of the bone marrow in patients with end-stage renal failure.…”

Section: Introductionmentioning

confidence: 99%

Identification of Spermine as an Inhibitor of Erythropoiesis in Patients with Chronic Renal Failure

Radtke¹,

Rege²,

Lamarche³

et al. 1981

J. Clin. Invest.

149

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A B S T R A C T Fetal mouse liver and normal human bone marrow cell cultures were used for studies on the inhibition of erythroid colony formation (CFU-E) by sera from anemic patients with end-stage renal failure and the polyamine spermine. Sera from each of eight predialysis uremic anemic patients with end-stage renal failure produced a significant (P < 0.001) inhibition of erythroid colony formation in the fetal mouse liver cell cultures when compared to sera from normal human volunteers. In vivo or in vitro dialysis of the uremic sera with a 3,500-dalton exclusion limit membrane removed the inhibitor from uremic sera. The uremic serum dialysate provided by the membrane fractionation was significantly inhibitory in the erythroid cell cultures. When this dialysate was applied to gel filtration chromatography (Bio-Gel P-2) the inhibitor was found to be in the same molecular weight range as [14C]spermine. The polyamine spermine produced a dose-related inhibition of erythroid colony formation (CFU-E) in fetal mouse liver and normal human bone marrow cultures. Thus, the following evidence is provided that the in vitro inhibitor of erythropoiesis found in chronic renal failure patients' sera is identical with the polyamine spermine: (a) the inhibitor and radiolabeled spermine appeared in identical Bio-Gel P-2 effluent fractions; (b) when spermine was added to normal human sera at concentrations reported in sera of uremic patients, and studied in both the fetal mouse liver cell culture and normal human bone marrow cultures, a dose-related inhibition of erythroid colony Heiz W. Radtke was a Postdoctoral Fellow in the Depart-

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Blood and Bone Marrow Studies in Renal Disease

Cited by 78 publications

References 0 publications

Hypersplenism in the Uremic Hemodialyzed Patient

Hypersplenism in the Uremic Hemodialyzed Patient

Effect of parathyroid hormone on erythropoiesis.

Identification of Spermine as an Inhibitor of Erythropoiesis in Patients with Chronic Renal Failure

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