HEMATOLOGICAL PROFILE AND SERUM POTASSIUM LEVEL IN PATIENTS OF CHRONIC RENAL FAILURE AT A TERTIARY HEALTH CARE CENTER

Chronic kidney disease (CKD) is defined as kidney damage or estimated glomerular filtration rate (eGFR) of less than 60 ml/min/1.73 m for a period of 3 months or more [1]. End-Stage Renal Disease (ESRD) is the final stage of CKD characterized by progressive, irreversible deterioration in renal function resulting in fluid and electrolyte imbalance. This leads to uremia. ESRD is characterized by a decrease in GFR and evidence of less than 10% nephron function remaining [2].


INTRODUCTION
Chronic kidney disease (CKD) is defined as kidney damage or estimated glomerular filtration rate (eGFR) of less than 60 ml/min/1.73 m 2 for a period of 3 months or more [1]. End-Stage Renal Disease (ESRD) is the final stage of CKD characterized by progressive, irreversible deterioration in renal function resulting in fluid and electrolyte imbalance. This leads to uremia. ESRD is characterized by a decrease in GFR and evidence of less than 10% nephron function remaining [2].
CKD is associated with a variety of hematological abnormalities. Anemia is the most common, consistent and severe of the various hematological abnormalities [3]. According to the NKF/KDOQI guidelines (2002), anemia in Chronic Kidney Disease can be defined as hemoglobin level less than 13.0 g/dl in adult males and less than 12.0g/dl in adult females [4]. The primary cause of anemia in CKD patients is insufficient production of erythropoietin. Other factors include deficiency of iron, folate & B12, probably due to increased blood loss or nutritional insufficiency [5].
Other causes may consist of acute and chronic inflammation with impaired iron utilization, severe hyperparathyroidism (HPT) and reduced red cell life span due to uremia [5,6].
Prolonged anemia, if untreated, may lead to several physiologic disorders. The significant complications anticipated are; cardiovascular manifestations like decreased tissue oxygenation increased cardiac output, ventricular dilatation and ventricular hypertrophy, and ultimately increased mortality and morbidity. Renal insufficiency is also associated with bleeding tendency attributed to platelet dysfunction [5].
Besides genetic and pathological factors, certain environmental factors may also be responsible for development of renal insufficiency. Presently, the number of studies on hematological derangements in CKD patients is quite less, especially among the Indian population [7].
2 comparison with healthy control group at a tertiary care center located in the state of Rajasthan. Exclusion criteria: Patients suffering from primary hyperparathyroidism or Vitamin D supplementation, who underwent thyroid or parathyroid surgeries, were also excluded.

MATERIAL AND METHODOLOGY
Methodology: Blood samples were collected for all subjects enrolled in the study and subjected to analysis for renal function test (RFT) including serum urea, creatinine, potassium using dry chemistry and direct ion -selective electrode method on VITROS 5600 and hematological profile including total leucocyte count (TLC), hemoglobin (Hb), platelets count and red blood cell (RBC) count.
Statistical analysis: Results obtained were analyzed using a statistical package program (SPSS 17 Inc; Chicago II, USA) for social science. All variables were presented in the two groups as mean ± SD and compared by applying Student's t-test.

RESULTS
On the evaluation of distribution of co-morbid conditions in CKD patients, the study reported hypertension as the most common co-morbid condition associated with CKD. Out of fifty CKD patients, 29 (58%) patients had hypertension, and 4 (8%)had Diabetes mellitus.14 patients (28%) patients had both hypertension and diabetes mellitus while 3 (6%) patients suffered from other comorbidities (Fig 1).
Parameters evaluated in the study and control group are presented in (Table1).The mean Hb level of CKD group was as low as 7.50+/-1.6g/dL. Mean RBC levels were significantly lower (P < 0.0001) lower in CKD patients (3.03± 0.60) as compared to healthy subjects (5.07±0.54). Comparison of Platelets was not considerably (221.52± 83) in CKD group as compared to healthy subjects (247.73±64.80). The mean serum potassium levels were significantly higher in CKD population as compared to age-matched healthy subjects with normal kidney function (Table 1).  Table 2: CKD Patients grouped according to severity of anemia [8].

DISCUSSION
The mean age of CKD patients (38.98 ± 10.32) was comparable with that of healthy control group. However, out of 50 CKD patients, maximum number n=16 (32%) patients were in the group of 51-60 years, which is similar to the study done by Ann M et al. [7].
The significant comorbidities identified among the CKD patients were diabetes and hypertension. The observations are similar to the studies carried out by Chhetri PK et al.2009 [9]and Dash SC et al. 2006[10] where diabetes mellitus and hypertension were identified as leading causes. Coresh J et al. 2007[11] also reported that two leading causes of CKD, i.e. hypertension and diabetes, account for as much as 70% of all new cases.
Healthy kidneys produce a hormone called erythropoietin (EPO). EPO prompts the bone marrow to make red blood cells, which then carry oxygen throughout the body [12].
Anemia of chronic renal failure is multifactorial. The pathogenesis of this type of anemia has been attributed to decreased plasma erythropoietin due to renal damage, inhibitors of erythropoiesis in uremic plasma, and decreased hemoglobin oxygen affinity [13]. In addition to damage to renal site of erythropoietin production, plasma erythropoietin and erythropoiesis are further suppressed in patients with renal disease. The stimulus to erythropoietin production is less intense than in patients with comparable severe anemia due to other causes. This is because the affinity of oxygen decreases, which increases the availability of oxygen per unit of hemoglobin circulating through the kidney [13].
Usually 90%of the hormone is produced in peritubular interstitial cells of the kidney and 10% in the liver and elsewhere, there are no performed stores and the stimulus to erythropoietin production is then oxygen tension in the tissues of the kidney, erythropoietin production, therefore, increase in anemia, when hemoglobin for some reason is unable to give up oxygen usually, when atmospheric oxygen is low or when destructive cardiac or pulmonary function or damage to the renal circulating affect oxygen delivery to the kidney.
Hakim et al. [12] found the mean platelet count among ESRD patients to be significantly reduced (1.75+/-0.065 lakhs/cmm) compared to controls. Another study by Dorgalalehet al. [17] found the mean platelet count in CKD patients to be 1.72±0.9 lakhs/ cmm and reduced compared to controls. Other studies show platelet dysfunction in many cases of ESRD which predisposes the patients to bleeding [18,19].
CKD and ESRD inevitably lead to K derangements and an increased risk of adverse cardiovascular events and mortality [20]. Potassium (K) is the most abundant intracellular cation with >98% of total body K located intracellularly and <2% extracellularly.

CONCLUSION
This study showed absolute prevalence of anemia in patients of CKD. It was predominantly of the normocytic normochromic type, suggesting EPO deficiency as the primary cause. However, in some cases, the presence of abnormal cells such as fragmented RBCs, pencil cells, and macro-ovalocytes suggest other contributory factors, such as hemolysis, iron deficiency, or folate/vitamin B12 deficiency. Neutrophilic leukocytosis in some patients may be explained by the tendency towards latent or secondary infections. Although the platelet counts, bleeding, and clotting times were mostly normal in this study.

Suggestions:
In the light of this study, there is a need for nephrologists to monitor the hematological profile of CKD patients on dialysis, and treat any derangements in the same, to improve outcome for these patients.