Iron Status of Cats with Chronic Kidney Disease

Background

Iron deficiency is a proposed mechanism for the anemia that occurs in cats with chronic kidney disease (CKD). Minimal research investigating the iron status of these cats has been performed.

Objective

To compare indicators of iron status in cats with CKD versus healthy cats and cats with nonrenal illness (NRI). To compare indicators of iron status in anemic versus nonanemic cats with CKD.

Animals

Thiry‐nine client or employee owned healthy cats, 40 cats with CKD and 34 cats with NRI included.

Methods

Exclusion criteria included prior iron or erythropoiesis stimulating agent administration, blood transfusion, or concurrent CKD and NRI. Complete blood counts, serum chemistries, serum iron concentrations, total iron binding capacity (TIBC), and ferritin concentrations were measured and percent transferrin saturation (TSAT) calculated on all cats. Data were analyzed using nonparametric statistical testing.

Results

No statistically significant differences were detected among groups for iron concentration (P = .50), ferritin concentration (P = .47), or TSAT (P = .19). TIBC was significantly lower in CKD (median 262 μg/dL; IQR 233–302; range 165–488) versus healthy cats (median 316 μg/dL; IQR 272–345, range 196–464); (P = .0030). When comparing anemic (hemoglobin <9.5 g/dL) versus nonanemic cats with CKD, TSAT was significantly lower (P = .033) in anemic (median 20.2%; IQR 17.8–34.5; range 17.6–35.9) compared to nonanemic (median 29.0%; IQR 25.5–44.1; range 11.5–94.4). No statistically significant differences found for ferritin concentration (P = .94), iron concentration (P = .21) or TIBC (P = .97).

Conclusions and Clinical Importance

These results indicate that an iron deficient state exists in anemic cats with CKD and is more likely functional rather than absolute.     

The Cardiac Biomarker NT-proBNP Is Increased in Dogs with Azotemia

Background: Amino‐terminal probrain natriuretic peptide (NT‐proBNP) has been proposed as a useful biomarker for heart disease in dogs. In humans, decreased glomerular filtration rate (GFR) increases NT‐proBNP. Objective: To investigate whether decreased GFR as indicated by plasma creatinine concentration is associated with increased NT‐proBNP in dogs without heart disease. Animals: Four groups of dogs: healthy (n= 39), azotemic (n= 36), heart disease (n= 37), and congestive heart failure (CHF) (n= 7) presented to 2 teaching hospitals. Methods: Prospective observational cohort study. Plasma creatinine concentration and NT‐proBNP were measured in every dog. Nonparametric tests were used to compare the differences among groups. The median and actual results for each group were compared with the manufacturer's recommended and previously published suggestions for cut‐off values for diagnosis of heart disease. Results: Median (range) plasma creatinine concentration was 1.47 (1.06–1.70), 4.36 (1.74–15.6), 1.22 (0.69–1.91), and 1.45 (0.63–1.64) mg/dL and median (range) NT‐proBNP was 118 (2–673), 556 (37–1,819), 929 (212–5,658), and 3,144 (432–5,500) pmol/L for the healthy, azotemic, heart disease, and CHF groups, respectively. Pair‐wise comparison indicated a significant difference among all groups for NT‐proBNP (P≤ .049). Plasma creatinine concentration was significantly higher in the azotemic group compared with other groups (P < .001) but there was no significant among other groups. Application of 3 recommended cut‐off values led to misclassification of dogs with azotemia as having heart disease. Conclusions: Azotemia results in NT‐proBNP being increased to concentrations reported as diagnostic of heart disease or heart failure in dogs. Care should be employed when interpreting the results of NT‐proBNP in patients with known or possible increased plasma creatinine concentration.     

鸡贫血因子病的血液病理学变化

本实验用鸡贫血病毒感染１日龄健康ＡＡ雏鸡，以未感染雏鸡为对照，在感染后７、１４、２８、３５、４２日龄检测其外周血液各种血细胞数量，血红蛋白含量，红细胞压积，红细胞平均体积，红细胞平均血红蛋白量、红细胞平均血红蛋白浓度；骨髓红系祖细胞、粒单系祖细胞（ＣＵＦ－ＧＭ）、基质成纤维祖细胞（ＣＦＵ－Ｆ）的增殖功能；血清因子和胞腺集落刺激因子（ＣＳＦ）对造血祖细胞增殖功能的影响；骨髓造血细胞分化功能；骨髓造血     

Anemia amelioration by lactose infusion during trypanosomosis could be associated with erythrocytes membrane de-galactosylation

African trypanosomosis is a potentially fatal disease that is caused by extracellular parasitic protists known as African trypanosomes. These parasites inhabit the blood stream of their mammalian hosts and produce a number of pathological features, amongst which is anemia. Etiology of the anemia has been partly attributed to an autoimmunity-like mediated erythrophagocytosis of de-sialylated red blood cells (dsRBCs) by macrophages. Lactose infusion to infected animals has proven effective at delaying progression of the anemia. However, the mechanism of this anemia prevention is yet to be well characterized. Here, the hypothesis of a likely induced further modification of the dsRBCs was investigated. RBC membrane galactose (RBC m-GAL) and packed cell volume (PCV) were measured during the course of experimental trypanosomosis in mice infected with Trypanosoma congolense (stb 212). Intriguingly, while the membrane galactose on the RBCs of infected and lactose-treated mice (group D) decreased as a function of parasitemia, that of the lactose-untreated infected group (group C) remained relatively constant, as was recorded for the uninfected lactose-treated control (group B) animals. At the peak of infection, the respective cumulative percent decrease in PCV and membrane galactose were 30 and 185 for group D, and 84 and 13 for group C. From this observed inverse relationship between RBCs membrane galactose and PCV, it is logical to rationalize that the delay of anemia progression during trypanosomosis produced by lactose might have resulted from an induction of galactose depletion from dsRBCs, thereby preventing their recognition by the macrophages.     

Cloning and tissue expression of the equine transferrin receptor

Background: Characterization of anemia in horses presents a challenge, as they do not release reticulocytes into peripheral blood. Transferrin receptor (TfR) expression is highest on erythroid cells in people and rats, and measurement of a soluble serum form (sTfR) is used to quantify erythropoiesis in these species. We hypothesized that equine TfR (eTfR) expression is similar in quantity and distribution to that in these other species and thus has potential for characterization of the regenerative response in anemic horses. Objective: This study was conducted to clone and sequence the eTfR gene and measure expression levels using quantitative real‐time PCR and immunohistochemical (IHC) staining. Methods: Total RNA from equine bone marrow was used to produce cDNA. The eTfR gene was amplified using pooled gene‐specific primers, and PCR products were sequenced. Rapid amplification of cDNA ends was used to obtain the first 22 nucleotides of the coding sequence. Quantitative PCR was performed using eTfR gene‐specific primers, and IHC staining was used to localize TfR protein expression. Results: The deduced amino acid (aa) sequence (767 aa) of the eTfR was 75–83% identical with sequences of the receptor in several other mammals. As in people and rats, eTfR mRNA expression was highest in the bone marrow, and distribution in other tissues was also similar. Conclusion: The eTfR gene is similar to that of other mammals in structure and expression levels. We hypothesize that it is also similar in function and that, following development of an immunoassay, determining sTfR concentrations will be useful for identifying the regenerative response in anemic horses.     

Study on bone marrow angiogenic mediators and inhibitors in aplastic anemia

AIM: Through detecting bone marrow angiogenic mediators and inhibitors in aplastic anemia (AA) patients,the value of angionesis in AA pathogenesis was elucidated.METHODS: The patients were divided into severe AA group (SAA,8 patients),non severe AA group (NSAA,10 patients),and normal control group (7 persons),5 patients were observed before treating (group beginning) and getting improvement (group improving).The angiogenic mediators vascular endothelial growth factor (VEGF) and bFGF were detected by ELISA,angiogenic inhibitors IFN-γ and TSP were detected by ELISA and flow cytometry,respectively.RESULTS: The levels of VEGF were lower in SAA group and NSAA group than those in control group significantly (P<0.05),the levels of IFN-γ and TSP were higher than those in control group (P<0.05),especially in SAA group (P<0.01).Compared with group beginning,the level of VEGF was higher in group improving (P<0.05),the levels of IFN-γ,TSP were lower (P<0.05),there was no obviously difference between group beginning and group improving except IFN-γ.CONCLUSION: The dropping of angiogenic mediators and the rising of angiogenic inhibitors may be one reason of reducing the number of microvessel,which result in deficiency in supporting hemapoietic stem cells by bone marrow microenvironment.