Chronic Kidney Disease — Stages, eGFR, Dialysis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function persisting for over 3 months, with implications for health. It is staged by estimated glomerular filtration rate (eGFR): Stage 1 (eGFR above 90 mL/min with kidney damage markers), Stage 2 (eGFR 60-89), Stage 3a (45-59), Stage 3b (30-44), Stage 4 (15-29), and Stage 5 (below 15 — kidney failure requiring dialysis or transplant). CKD affects approximately 850 million people worldwide (10% of adults). It is largely silent until advanced stages, leading to late diagnosis. Diabetes and hypertension together cause 80% of CKD. CKD is now recognised as a cardiovascular risk equivalent — patients with CKD Stage 3-5 have a substantially elevated risk of dying from cardiovascular disease before ever reaching dialysis — making cardiovascular risk reduction as important as kidney-specific management in a comprehensive CKD care plan.

Diabetic nephropathy (Type 1 and Type 2 diabetes — most common cause of CKD and end-stage renal disease [ESRD] in developed countries, accounting for 40-44%); hypertensive nephrosclerosis (chronic high blood pressure causing glomerular damage — second most common, 28%); glomerulonephritis (IgA nephropathy, lupus nephritis, membranous nephropathy, FSGS); polycystic kidney disease (PKD — genetic, causing progressive cyst formation); chronic pyelonephritis (recurrent urinary tract infections); obstructive nephropathy (benign prostatic hyperplasia, kidney stones, congenital urological abnormalities); medications (NSAIDs, aminoglycosides, calcineurin inhibitors, contrast nephropathy); and cardiovascular disease (shared risk factors). Less common but clinically important causes of CKD include primary glomerulonephritis (IgA nephropathy being the most common globally), myeloma kidney (light chain cast nephropathy), renal amyloidosis, renovascular disease from renal artery stenosis, and hereditary nephropathies such as Alport syndrome and autosomal dominant polycystic kidney disease.

CKD is often asymptomatic in Stages 1-3 — detected only on routine blood/urine testing. As eGFR falls below 30-45 (Stage 3b-4), symptoms may develop: fatigue and reduced exercise tolerance (from anaemia of CKD — erythropoietin deficiency); oedema (fluid retention — ankle and periorbital swelling); hypertension (often difficult to control); nocturia and polyuria; pruritus (itching from uraemia); loss of appetite and nausea; and bone pain or fractures (renal osteodystrophy — secondary hyperparathyroidism). Stage 5 (uraemia): severe fatigue, confusion, pericarditis, pulmonary oedema, uraemic frost (urea crystals on skin — rare), and decreased consciousness. Regular kidney function monitoring (eGFR and urine ACR) allows early detection.

eGFR is calculated from serum creatinine using the CKD-EPI 2021 equation (incorporating age, sex, and creatinine — no longer uses race as a modifier). Urine albumin-creatinine ratio (ACR): above 3 mg/mmol is significant; above 30 mg/mmol is severely elevated — important marker of glomerular damage. CKD staging uses both eGFR and ACR (KDIGO 2012 classification). Additional investigations: urine microscopy (haematuria, red cell casts suggest glomerulonephritis); renal ultrasound (size, corticomedullary differentiation, obstruction, polycystic kidneys); FBC (anaemia); bone profile (calcium, phosphate, PTH — secondary hyperparathyroidism); serum potassium (hyperkalaemia risk); lipid profile (cardiovascular risk); and HbA1c (diabetic nephropathy). Renal biopsy in unexplained rapid decline or suspected glomerulonephritis.

Retarding CKD progression: ACE inhibitors (ramipril, lisinopril) or ARBs (losartan, irbesartan) reduce intraglomerular pressure and proteinuria — essential in diabetic and proteinuric CKD; target systolic blood pressure below 130 mmHg. SGLT2 inhibitors (empagliflozin/Jardiance, dapagliflozin/Forxiga, canagliflozin) provide 30-40% relative risk reduction in CKD progression and are now recommended from CKD Stage 2 regardless of diabetes status. Finerenone (non-steroidal mineralocorticoid receptor antagonist) further reduces progression in diabetic CKD. Dietary: low-protein diet (0.6-0.8 g/kg/day — reduces glomerular hyperfiltration); restrict dietary potassium (Stage 4-5); restrict phosphate (Stage 4-5); reduce sodium. Managing complications: EPO (erythropoiesis-stimulating agents) for CKD-associated anaemia; phosphate binders (calcium carbonate, sevelamer); active vitamin D (alfacalcidol, calcitriol); sodium bicarbonate for metabolic acidosis; statins for cardiovascular risk. Renal replacement therapy (Stage 5/ESRD): haemodialysis (3 sessions per week, 4 hours each), peritoneal dialysis (daily home dialysis), or kidney transplantation (superior survival and quality of life — living-donor preferred).

Untreated or rapidly progressing CKD leads to end-stage renal disease (ESRD) requiring dialysis or transplantation to sustain life. CKD is a powerful independent cardiovascular risk factor — patients with Stage 3-5 CKD are 10-100x more likely to die from cardiovascular disease than to reach dialysis. Complications of advanced CKD: anaemia (affecting quality of life, exercise, and cognitive function); secondary hyperparathyroidism and renal osteodystrophy (bone pain, fractures); hyperkalaemia (life-threatening arrhythmias); metabolic acidosis (accelerates bone loss and muscle wasting); fluid overload (hypertension, heart failure, pulmonary oedema); and uraemic encephalopathy. Global CKD burden is increasing due to rising prevalence of diabetes and hypertension.

Tight glycaemic control in diabetes (HbA1c below 53 mmol/mol) reduces diabetic nephropathy risk and progression. Blood pressure control below 130/80 mmHg using ACE inhibitors or ARBs in proteinuric CKD is the most important intervention to slow CKD progression. SGLT2 inhibitors are now recommended for all patients with CKD regardless of diabetes status. Avoid NSAID use (ibuprofen, diclofenac) regularly — they reduce renal blood flow and worsen kidney function. Stay well hydrated (adequate fluid intake reduces kidney stone formation and infection risk). Do not smoke — smoking doubles the rate of CKD progression. Attend regular CKD monitoring appointments (eGFR, ACR, blood pressure, potassium, haemoglobin). Ensure medications are reviewed regularly — many drugs require dose adjustment in CKD and some must be avoided.

See your GP for annual kidney function testing (eGFR and urine ACR) if you have diabetes, hypertension, a family history of CKD, or are aged over 60. Many people with CKD stages 1–3 are asymptomatic — the condition is detected on routine blood tests. Established CKD patients should attend all nephrology appointments to monitor eGFR trajectory and cardiovascular risk. Seek urgent assessment for: sudden decrease in urine output (less than 400 mL per day); severe leg or facial swelling; confusion or drowsiness in someone with known CKD (uraemic encephalopathy); breathlessness at rest or lying flat (pulmonary oedema from fluid overload); and severe hypertension with headache or visual disturbance. Seek emergency care for: complete absence of urine (anuria), severe vomiting preventing fluid and medication intake, chest pain, or breathlessness — these may indicate acute kidney injury superimposed on CKD or serious cardiovascular complication requiring hospitalisation.