HEMATOLOGICAL EFFECTS AND CARDIAC DERANGEMENT IN END STAGE RENAL DISEASE - A RETROSPECTIVE ANALYSIS

Abstract

Anemia is one of the major disorders needing great attention in public. Anemia free India is a national project with a motto nourish, prevent and protect. According to NFHS 2024 67% children and 59% of adolescent girls are anemic. The WHO reports prevalence of anemia in 40% of children aged 6-59 months and 30% in 15-49 years. While iron deficiency and folic acid deficiency have been the major factors in malnutrition contributing to anemia, defective absorption of the supplemented nutrients is the second major problem. The prevalence of chronic kidney disease is in the exponential trend and Rounik tadulkar et al have estimated 13.24% prevalence in India. This data is further worrying and poses major threat to the management of anemia in the masses. Anemia refers to reduction in red cell mass or reduced hemoglobin and decreased oxygen carrying capacity of blood to tissues. It has significant effects on respiratory and cardiovascular systems and generalised effects due to reduced tissue oxygenation. This study is a retrospective analysis of hematological aspects of kidney disease derived from data in end stage renal disease patients who presented for renal transplantation. Reduced production and impaired morphology, increased destruction are all the changes that could cause anemia in chronic kidney disease. Apart from tissue oxygenation, anemia in ESRD causes associated coagulation abnormalities and significant cardiac dysfunction. Study of red cell width distribution enables to notify increased anisocytosis that provokes hemolysis and anemia. Through erythropoietin from juxtaglomerular apparatus takes the brunt of causation. Several uremic toxins attack various levels and components of anemia.

Methods: The case records, laboratory and echocardiogram reports of the patients who attended the preanesthetic clinic were scrutinised and the selected aforesaid parameters were noted. The results were tabulated and analysed.

RESULTS

Hemoglobin, red cell width and platelets showed negative correlation with r value of -0.015 with creatinine levels. A lower hemoglobin and PCV was associated with poor ejection fraction (p=0.01) and raised RVSP (P=0.05) .The values of ejection fraction and PCV showed p= 0.011, red cell width vs RVSP depicted p= 0.076, packed cells with EF showed p = 0.011, LA diameter with ejection fraction showed p= 0.004. Hemoglobin and ejection fraction showed a significant p value = 0.007.

CONCLUSION

Anemia in chronic kidney disease progresses with severity of the renal dysfunction. Erythropoietin, the cytokine hormone which is the major attribute of anemia, the production of which is directly proportional to the glomerular mass. Oxygen delivery to peripheral tissues is determined by red cell mass. The red cell mass is controlled by variations in production of erythropoietin by negative feedback loop. This response of erythropoiesis production requires iron, vitamin B12 and folic acid as cofactors. Inefficient erythropoiesis due to vitamin B12 and folic acid causes megaloblastic anemia and iron deficient erythropoiesis leads to microcytic anemia. The red cell width distribution increases leading to hemolysis, tissue hypoxia and associated with raised RVSP (P= 0.076). This study includes hematological indices which have been analysed for right and left heart parameters that conclude severity of cardiac dysfunction to be associated with severe anemia. Poor PCV and hemoglobin associated with LVEF (p=0.01). Red cell width distribution with RVSP P = 0.076, LA diameter negatively correlating with hemoglobin p-0.06 and PCV (r= 0.18) signify strong association of cardiac involvement with anemia of ESRD. Correction of anemia appears to halt the progress of cardiac involvement which has been determined as the major cause of morbidity and mortality in patients with end stage renal disease.