Chronic kidney disease (CKD) is a global public health crisis with progressive and irreversible decline in renal function [1]. It is often precipitated by underlying comorbidities, most notably hypertension and diabetes mellitus [2]. It is associated with exceptionally high all-cause cardiovascular mortality [3]. Clinical guidelines from StatPearls and KDIGO define CKD as an estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m² for 3 or more months [4,5]. With the progressive loss of renal parenchyma, the kidneys are unable to clear metabolic waste, regulate fluid balances, or synthesise essential hormones [6,7]. Haematological abnormalities such as normocytic normochromic anaemia are seen in most patients and worsen with the progression of the disease [8,9]. Anaemia in CKD is multifactorial with the contributing factors being deficiency of erythropoietin (EPO), peripheral resistance to erythropoiesis-stimulating agents [10] and abnormal iron metabolism [11]. At the same time, retention of uremic solutes induces severe biochemical alterations [12,13]. CKD-mineral and bone disorder (CKD-MBD) is characterised by hypocalcaemia and hyperphosphatemia, which results from impaired phosphate excretion and decreased active vitamin D synthesis [14,15]. If left untreated, these disturbances lead to secondary hyperparathyroidism, aggravating vascular calcifications and clinical outcome [16]. The objective of the present study was to systematically determine the clinical prevalence and severity of haematological and biochemical derangements in CKD patients in a tertiary care center, thereby generating local data that can guide effective clinical interventions.

Study Design and Setting A cross-sectional observational study was carried out in the Department of General Medicine, Navodaya Medical College, a tertiary care teaching hospital, Raichur, Karnataka. The study was conducted in a pre-determined period of 18 months. Study Population and Selection Criteria The study cohort was 50 adult patients (N = 50) attending the inpatient and outpatient department. Consecutive purposive sampling was used to select patients according to the following criteria: • Inclusion Criteria: Adult patients (>18 years) with a diagnosis of Chronic Kidney Disease (Stage III-V). The stage was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, and the Glomerular Filtration Rate (eGFR) was estimated by the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation. • Exclusion Criteria: Patients who had acute kidney injury (AKI) or acute-on-chronic renal failure were strictly excluded to avoid confounding physiologic variables. Patients with a history of active malignancies, acute hemorrhagic events, active systemic infections, recent blood transfusions (within the last 3 months) or who were currently receiving targeted erythropoiesis-stimulating agents (ESAs) or heavy iron infusion therapy were also excluded from the analysis. Methods and Data Collection in Laboratory Detailed sociodemographic data, clinical history, and physical examination findings were recorded on a pretested semi-structured proforma. Sample Collection Fasting venous blood (5 mL) was collected from each participant’s antecubital vein under strict aseptic conditions. The sample was poured into two sterile vacutainers, EDTA (Ethylenediaminetetraacetic acid) tube for haematological analysis and a plain serum separator tube (SST) for biochemical evaluation. All samples were transported to the central laboratory in the cold chain and processed within 2 hours of collection to prevent artifactual changes and to ensure cellular integrity. Haematological Parameters: Haematological profiling (e.g., flow cytometry and direct current impedance principles) was performed using a fully automated 6-part haematology analyser. The parameters considered were: • Haemoglobin concentration (Hb) (determined by the cyanide-free photometric method) • Total Red Blood Cell (RBC) Count • White Blood Cell (WBC) count, total • Number of platelets • Haematocrit (HCT) Biochemical Parameters The serum was separated by centrifugation at 3000 rpm for 10 min. The biochemical assays were estimated on a fully automated chemistry analyser [17] using standard colorimetric and enzymatic principles: • Blood Urea: Measured by the Urease-GLDH (Glutamate Dehydrogenase) enzymatic UV method. • Serum Creatinine: Measured by the modified kinetic Jaffe method. • Serum Calcium: Estimated by Arsenazo III colorimetric end point method. • Serum Phosphorus: Phosphomolybdate UV method (estimated). Data analysis: Data were entered in Microsoft Excel and statistically analysed using appropriate Statistical software. Statistical significance in all tests was defined as a p-value < 0.05.

Table 1: Demographic and Clinical Profile of CKD Patients (N=50) Parameter Classification Number of Patients (n) Percentage (%) Age Group (Years) 30 - 45 10 20.0% 46 - 60 23 46.0% > 60 17 34.0% Gender Male 32 64.0% Female 18 36.0% CKD Stage Stage III 11 22.0% Stage IV 22 44.0% Stage V (ESRD) 17 34.0% The study included 50 patients. Baseline clinical and demographic characteristics are shown in Table 1. Most of the patients were seen at an advanced stage of the disease (Stages IV and V). Table 2: Evaluation of Hematological Parameters in CKD Patients Parameter Patient Mean ± SD Reference Range Hemoglobin (g/dL) 8.4 ± 1.6 12.0 - 16.0 Total RBC Count (x10⁶/µL) 3.1 ± 0.5 4.5 - 5.5 Total WBC Count (cells/mm³) 6,950 ± 1,520 4,000 - 11,000 Platelet Count (x10⁵/µL) 1.9 ± 0.7 1.5 - 4.5 Hematocrit (%) 26.1 ± 4.8 36.0 - 46.0 Hematological evaluations (Table 2) revealed universal, progressive anemia across the cohort. Mean hemoglobin and RBC counts fell significantly below standard physiological ranges. Table 3: Evaluation of Biochemical Parameters in CKD Patients Parameter Patient Mean ± SD Reference Range Blood Urea (mg/dL) 112.4 ± 34.6 15 - 40 Serum Creatinine (mg/dL) 4.8 ± 1.9 0.6 - 1.2 Serum Calcium (mg/dL) 7.8 ± 0.9 8.5 - 10.5 Serum Phosphorus (mg/dL) 5.9 ± 1.1 2.5 - 4.5 Biochemical analysis (Table 3) showcased severe uremia. Patients displayed heavily elevated serum urea and creatinine, alongside significant mineral imbalances indicative of renal osteodystrophy. Table 4: Correlation of Hematological and Biochemical Severity by CKD Stage CKD Stage Mean Hemoglobin (g/dL) Mean Serum Creatinine (mg/dL) Mean Serum Calcium (mg/dL) Stage III 9.9 ± 1.3 2.5 ± 0.6 8.6 ± 0.5 Stage IV 8.6 ± 1.2 4.7 ± 0.9 7.7 ± 0.7 Stage V 7.0 ± 0.8 7.9 ± 1.5 6.8 ± 0.6 To investigate disease progression, Table 4 maps the inverse relationship between declining kidney function (rising creatinine) and worsening hematological outcomes.

The findings of this 9-month observational study carried out in Navodaya Medical College confirm that advanced CKD basically destabilises patients’ haematological and biochemical physiology. The mean haemoglobin level in our cohort was 8.4 ± 1.6 g/dL, which indicates the degree of anaemia in the population studied. This high prevalence is consistent with the basic data presented by McClellan et al. [8] who showed that the incidence of anaemia increases exponentially as eGFR decreases. Similar severity was reported by Bishaw et al. [9] in tertiary cohorts. The pathogenesis of this anaemia is more complex than the EPO deficiency alone, and as shown by Santos et al. [10], many CKD patients have a specific erythropoietin resistance, further complicating therapeutic options. Anoshkina et al. [11] also emphasised that the decline of haematological parameters is related to systemic iron dysregulation and functional iron deficiency. Biochemically, our study showed significantly raised serum urea and creatinine levels which are the usual signs of deteriorating uremia. These measures closely correspond to progressive severity markers studied by Gupta et al. [13]. Moreover, the assessment of these ratios of metabolic waste, and creatinine clearance, provides vital prognostic information regarding the probability of patient survival and potential acute deterioration, as highlighted by researchers such as Paulus et al. [19] and Pickering et al. [20]. Also, high metabolic waste retention may directly manifest as central nervous system toxicity, contributing to the severe uremic encephalopathies described by Lockwood et al. [22]. In addition to nitrogenous waste, the disturbances in the mineral metabolism observed, i.e. hypocalcaemia (7.8 ± 0.9 mg/dL) and hyperphosphatemia (5.9 ± 1.1 mg/dL), are pathognomonic for CKD-MBD. There are detailed mechanisms reported by Murray et al. [14] and Cernaro et al. [15], which explain how progressive hyperphosphatemia suppresses active vitamin D and causes fatal cardiovascular calcifications. In a clinical setting, Abe et al. [18] showed that the calcium-phosphorus product is an independent and important predictor for poor outcomes in patients with renal impairment. These biochemical imbalances often require strict nutritional control as heavily underlined by Kim et al. [21] to decrease hypercatabolism and delay the need for continuous haemodialysis

This prospective study demonstrates the severe systemic effects of chronic kidney disease, mainly dominated by severe normocytic anaemia, uremia and disturbed mineral homeostasis (hypocalcaemia and hyperphosphatemia). These changes in haematological and biochemical parameters were directly correlated with the progression of clinical stages of CKD. Regular and careful monitoring of these laboratory parameters is critical to guide timely clinical interventions, to optimise nutritional and pharmacological management, and ultimately to reduce the substantial morbidity and mortality associated with end-stage renal disease.

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