Clinico-biochemical and etiological profile of chronic kidney disease in a tertiary centre: a cross-sectional study

Background: Chronic kidney disease (CKD) is a global public health challenge characterized by gradual loss of kidney function and high morbidity. In India, CKD prevalence is estimated around 15–17%, with diabetes and hypertension being the leading causes. This study aimed to evaluate the clinical and biochemical profile of CKD patients in a tertiary care setting and determine the etiological spectrum of their disease. Methods: We conducted a prospective cross-sectional study of adults with CKD stages 1–5 (predominantly stages 3–5) at a tertiary hospital in southern India. Patients were enrolled over 15 months and underwent detailed clinical evaluation, laboratory investigations, and etiological assessment. Key data included demographics, comorbidities, symptoms, biochemical parameters, and CKD stage (estimated glomerular filtration rate by CKD-EPI formula). Descriptive statistics and comparative analyses (chi-square for categorical variables, ANOVA for continuous variables) were used to summarize findings. The study was carried out in accordance with STROBE guidelines. Results: A total of 90 CKD patients were analysed (mean age 56.3 ± 16.5 years; 74.4% male). Hypertension (87.8%) and diabetes mellitus (60.0%) were the most common comorbid conditions. The majority presented at advanced CKD stages: 32.2% in Stage G5 (pre-dialysis) and 26.7% in Stage G5D (on dialysis), with only ~23% in Stage 3. The leading attributed etiologies were diabetic nephropathy (37.8% of cases) and hypertensive nephrosclerosis (21.1%), followed by chronic glomerulonephritis (17.8%) and obstructive uropathy (12.2%). Clinically, the most frequent presentations were anaemia (77.8% had clinical pallor), oedema (74.4%), and dyspnoea on exertion (50%). Laboratory evaluation showed mean serum creatinine 5.7 ± 3.9 mg/dL and blood urea 85 ± 45.6 mg/dL, reflecting advanced renal failure. Electrolyte disturbances were common, including hyperkalaemia in 28% and metabolic acidosis (mean bicarbonate 19.0 ± 4.4 mmol/L). Secondary hyperparathyroidism was evident with elevated parathyroid hormone (mean ~210 pg/mL) and 41% of patients had hypocalcaemia. Comparative analysis across CKD stages demonstrated progressive worsening of anaemia, hyperkalaemia, metabolic acidosis and mineral-bone disorder parameters in more advanced stages (all p < 0.01). Conclusions: Patients at our centre predominantly presented with late-stage CKD and poorly controlled underlying conditions. Diabetic and hypertensive nephropathies accounted for the bulk of CKD etiologies. A high burden of anaemia and mineral bone disorder complications was observed. These findings underscore an urgent need for earlier detection of CKD in high-risk individuals (especially those with diabetes or hypertension) and prompt multidisciplinary care to address complications and slow disease progression.