1. Posttransplant erythrocytosis
Demetrios V. Vlahakos, Katerina P. Marathias, Basil Agroyannis, Nicolaos E. Madias 
Kidney International 
Volume 63, Issue 4, Pages (April 2003)
DOI: /j x
Copyright © 2003 International Society of Nephrology Terms and Conditions

2. Figure 1
Percentage of male subjects in the general renal transplant population (A) in the United States in and in patients with posttransplant erythrocytosis (PTE) (B) in American studies reported in the mid-1990s13,15,16,18,19,23,36.
Kidney International  , DOI: ( /j x)
Copyright © 2003 International Society of Nephrology Terms and Conditions

3. Figure 2
Relationship of mean plasma erythropoietin levels and hematocrit determinations in published series on posttransplant erythrocytosis (PTE) Table 1. The dashed lines represent the 95% confidence limits for nonuremic individuals1. The erythropoietin/hematocrit relationship in untreated patients with PTE (closed circles within the oval perigram) is shifted to the right due to inappropriately sustained erythropoietin secretion despite erythrocytosis (a form of “tertiary hypererythopoietinemia”). After treatment with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II AT1 receptor antagonist, the erythropoietin/hematocrit relationship returns within the normal limits (open circles).
Kidney International  , DOI: ( /j x)
Copyright © 2003 International Society of Nephrology Terms and Conditions

4. Figure 3
A proposed schema for the multiple pathogenetic pathways involved in the development of posttransplant erythrocytosis (PTE). Solid arrows depict positive feedback loops; dashed arrow depicts inhibitory action.
Kidney International  , DOI: ( /j x)
Copyright © 2003 International Society of Nephrology Terms and Conditions