Pelger-Huët anomaly (PHA) is a benign inherited condition characterized by hyposegmentation of the neutrophil's nucleus and excessive chromatin clumping. An acquired neutrophil dysplasia similar to PHA has been described in hematological diseases and in some clinical conditions. It has been known as acquired or pseudo PHA. Although some hypotheses have been proposed to explain this phenomenon, the mechanism of nuclear change is still unclear. Only the laboratory and clinical data combined will yield a better understanding on the need for follow-up and management of patients in the appropriate cases. In addition, a possible cause of pseudo PHA must always be investigated to add insights to the full understanding of this abnormality. Whether this neutrophil phenomenon has clinical implications remains to be elucidated. It is clear that only a small number of patients under drugs (immunosuppressive and others) may present these neutrophil abnormalities. Most of them do not show this phenomenon and we are unable to explain the different responses in drug users. Whether these patients display a predisposition for developing bone marrow or other diseases in the future, it is a very intriguing matter and only a follow-up will solve this question.
Pelger-Huët anomaly is an inherited condition characterized by hyposegmentation of the neutrophil nucleus and excessive chromatin clumping. Acquired Pelger-Huët, also known as pseudo-Pelger-Huët, has been described in several clinical conditions including transplant recipients who received immunosuppressive drugs. The incidence of pseudo-Pelger-Huët in kidney transplant patients, characterized as neutrophil dysplasia, was observed in 9 of 170 patients (5.3%) at the São Francisco Hospital de Assis, Belo Horizonte, Brazil. Awareness of possible circulating neutrophil alterations in transplant patients is important for laboratory professionals who should report these findings of cell changes. It should be highlighted that the poor segmentation and the chromatin hypercondensation observed initially in pseudo-Pelger-Huët patients can be suggestive of early-stage neutrophils. Only a combination of laboratory and clinical data will facilitate a better understanding of this anomaly and its correct follow-up and management.
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Chronic kidney disease (CKD) can be defined as the progressive loss of renal function, characterized by decreased glomerular filtration rate (GFR). The etiology of CKD in childhood is mainly associated with congenital anomalies of the kidneys and urinary tract (CAKUT) and to glomerular diseases. The goal of this study was to investigate the hemostasis and oxidative stress in pediatric CKD of different etiologies. 54 CKD children and adolescents and 52 controls were enrolled in this study. The evaluation of hemostasis was carried out by determination of D-Dimer (D-Di) and plasminogen activator inhibitor (PAI-1) plasma levels, while oxidative stress by thiobarbituric acid reactive substances (TBARS) levels, protein carbonyl content, plasma antioxidant capacity (MTT) and ascorbate. The D-Di was increased in CAKUT stage 3 or 4 patients compared to those with glomerular disease. PAI-1 was increased in patients with glomerular disease compared to CAKUT. Carbonyl protein content was higher in the control group compared to glomerular disease stage 3 or 4 patients. Our findings showed that the reduction in GFR is associated with a state of hypercoagulability. The analysis of integrated networks showed an expansion of connections among hemostatic and oxidative stress markers in CKD children and adolescents comparing to controls.
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