Chronic Kidney Disease

Chronic Kidney Disease (CKD) is a progressive, irreversible decline in renal function. In the UK, it is commonly caused by diabetes mellitus, hypertension, and glomerulonephritis. Diagnosis requires either a reduced eGFR (<60 mL/min/1.73m²) or evidence of kidney damage (e.g., albuminuria, structural abnormalities) that persists for more than 3 months. The NICE classification uses G-staging for eGFR (G1: ≥90, G2: 60-89, G3a: 45-59, G3b: 30-44, G4: 15-29, G5: <15) and A-staging for albuminuria (A1: <3 mg/mmol, A2: 3-30 mg/mmol, A3: >30 mg/mmol). CKD is often asymptomatic in early stages and is frequently detected during routine screening for chronic conditions. As it progresses, it leads to multisystem complications including anaemia of chronic disease, renal osteodystrophy (secondary hyperparathyroidism), and accelerated cardiovascular disease. Management prioritizes BP control, typically with ACE inhibitors or ARBs (especially if proteinuria is present), and the use of SGLT2 inhibitors which have shown significant renoprotective benefits. Patients reaching Stage G5 require preparation for Renal Replacement Therapy (RRT), including dialysis or transplantation.

Persistent injury to the renal parenchyma leads to the loss of functioning nephrons. To maintain GFR, the remaining nephrons undergo compensatory hyperfiltration, a process mediated by the renin-angiotensin-aldosterone system. While initially beneficial, this increased pressure leads to glomerular hypertension and progressive sclerosis. Over time, interstitial fibrosis and tubular atrophy occur. Failure of the endocrine functions of the kidney leads to specific complications: 1. Reduced Erythropoietin production by peritubular interstitial cells causing normocytic anaemia. 2. Failure of 1-alpha-hydroxylation of 25-hydroxyvitamin D to its active form (calcitriol), leading to hypocalcaemia. 3. Phosphate retention due to reduced filtration. Together, these cause secondary hyperparathyroidism, where the parathyroid glands overproduce PTH to normalize calcium levels, leading to high-turnover bone disease (renal osteodystrophy). Toxic metabolic waste products (uraemic toxins) eventually accumulate, affecting every organ system.

Early CKD is typically asymptomatic. Symptoms emerge in stages G4-G5 and include pruritus (itching from uraemic toxins), nausea, anorexia, and fatigue (anaemia). Fluid overload presents as peripheral oedema or dyspnoea. Signs include 'earthy' skin pallor, excoriations from scratching, and peripheral neuropathy. High blood pressure is almost universal. Complications are extensive: 1. Cardiovascular: Increased risk of MI and stroke. 2. Haematological: Anaemia and platelet dysfunction (bleeding). 3. Electrolyte: Hyperkalaemia and metabolic acidosis. 4. Mineral Bone Disorder: Bone pain and fractures. 5. Immunological: Increased susceptibility to infection. Red flags for urgent referral to a nephrologist include a GFR fall of >25% in one year, ACR >30 mg/mmol with haematuria, or resistant hypertension.

Bloods: eGFR (creatinine-based, using MDRD or CKD-EPI formula), U&Es, FBC (anaemia), HbA1c (diabetes), Bone profile (Calcium, Phosphate, PTH), Vitamin D. Urine: Albumin:Creatinine Ratio (ACR) on a first-void sample; Dipstick for haematuria. Imaging: Renal ultrasound to assess size (small kidneys suggest chronic disease, except in diabetes/PKD) and exclude obstruction. Special: Renal biopsy may be indicated if the cause is unclear and management would change.

Conservative: Smoking cessation, weight loss, salt restriction (<6g/day), and exercise. Medical: BP control (<140/90 or <130/80 if ACR >70 mg/mmol); ACE inhibitors (e.g., Ramipril) are first-line for those with diabetes or ACR >3mg/mmol. SGLT2 inhibitors (e.g., Dapagliflozin) for GFR 25-75 with albuminuria. Statins (Atorvastatin 20mg) for primary CV prevention. Treat complications: Erythropoieses-stimulating agents (ESAs) for anaemia (Hb target 100-120 g/L); Phosphate binders (e.g., Sevelamer) and Vitamin D analogues (e.g., Alfacalcidol) for bone disease. Bicarbonate for acidosis. Surgical: Arteriovenous (AV) fistula formation for haemodialysis or peritoneal dialysis catheter insertion. Kidney transplantation is the definitive treatment for ESRD.