Chronic Kidney Disease & Dialysis

CKD is defined by time and function: kidney damage or an eGFR below 60 mL/min/1.73 m² persisting 3 months or more, whatever the cause. Two tests stage every patient — the eGFR from blood (CKD-EPI equation preferred) and the urine albumin-to-creatinine ratio (uACR) on an early-morning spot sample. A uACR ≥ 30 mg/g is the damage marker that makes even a preserved GFR count as CKD.

The KDIGO GFR categories to know: G1 ≥ 90 and G2 60–89 (CKD only with evidence of damage) · G3a 45–59 · G3b 30–44 · G4 15–29 · G5 < 15 — kidney failure, typically requiring dialysis or transplant. Albuminuria runs on its own axis: A1 < 30, A2 30–299, A3 ≥ 300 mg/g.

Why does CKD progress even after the original insult stops? Because the kidney’s compensation is self-destructive. As nephrons die, the survivors hyperfilter — glomerular hypertrophy and intraglomerular hypertension that injure the very nephrons doing the extra work. RAAS activation ties hypertension, proteinuria, and renal fibrosis into one loop, and intrarenal calcium-phosphate precipitation adds injury of its own. The result is ongoing fibrosis and destruction of normal kidney architecture across glomeruli, tubules, interstitium, and vessels — a vicious cycle, which is why RAAS blockade slows it.

Everything the kidney quietly does, CKD slowly undoes — and each lost function becomes a body-system problem. Anemia: less functioning renal mass means less erythropoietin, compounded by hepcidin-mediated iron dysfunction and shortened red-cell survival; it becomes common as GFR falls, affecting more than half of people in stages G4–G5. Acidosis: reduced hydrogen-ion secretion and impaired ammonium excretion let phosphate and organic acids accumulate — and chronic acidosis leaches bone (osteopenia); oral bicarbonate targeting a serum level of 23 mEq/L delays progression (per StatPearls). Fluid overload: retained salt and water expand volume into hypertension, edema, a harder-working heart, and fluid in the lungs.

Hyperkalemia is the signature electrolyte danger: dietary potassium keeps arriving while excretion falls and aldosterone resistance develops — with ACE inhibitors and nonselective beta-blockers contributing. It becomes a medical emergency above 6.5 mEq/L, because excess potassium can affect the heartbeat and cause death. Platelet dysfunction: uremia impairs platelet adhesion to the vessel wall — prolonged bleeding times, easy bruising, occult GI blood loss.

Symptomatic uremia — the toxin syndrome itself — generally waits for stages 4–5 (creatinine clearance below 10–20 mL/min): nausea, anorexia, metallic taste, pruritus, restless legs, and at the far end encephalopathy and pericarditis, the two uremic emergencies that mandate immediate dialysis.

Follow the chain and CKD-MBD stops being memorization. Falling GFR means phosphate retention. High phosphate raises FGF23 and directly suppresses the kidney’s 1-α-hydroxylase, so calcitriol (active vitamin D) falls → the gut absorbs less calcium → hypocalcemia → the parathyroids respond with secondary hyperparathyroidism, and sustained PTH strips calcium from bone: renal osteodystrophy. The lesions range from high-turnover osteitis fibrosa cystica (“brown tumors”) to low-turnover adynamic bone disease and osteomalacia — clinically, bone pain and fractures.

The same chemistry hardens arteries: an elevated calcium × phosphate product drives vascular calcification — dialysis patients develop early, extensive coronary artery calcification, and FGF23 elevation is associated with cardiovascular mortality. This is why the treatment attacks the first domino: phosphate binders with meals plus dietary phosphate restriction, active vitamin D (calcitriol and analogs) to suppress PTH, and calcimimetics (cinacalcet) that sensitize the calcium-sensing receptor.

Starting dialysis is a clinical decision, not a number: the IDEAL trial found no survival benefit for an early start (eGFR 10–14) over a late one (5–7), and no specific GFR threshold is defined. What forces the decision are the urgent indications: uremic pericarditis, uremic encephalopathy or neuropathy, refractory hyperkalemia (K⁺ > 6.5 mEq/L), refractory acidosis (pH < 7.2), fluid overload refractory to diuretics, refractory bleeding, persistent nausea/vomiting with malnutrition, and certain toxic ingestions. Planning starts earlier — at stage 4, renal-replacement options are presented and access is planned.

Hemodialysis removes wastes by diffusion (solutes move down a concentration gradient across a semipermeable membrane) and removes fluid by ultrafiltration (pressure-driven water removal), typically 3 sessions a week, about 4 hours each. Its lifeline is the access: the AV fistula is the gold standard (“Fistula First”) — a native artery-to-vein anastomosis that can take several months to heal and mature — then the synthetic AV graft, with a tunneled central catheter as last resort.

Peritoneal dialysis makes the patient’s own peritoneum the membrane: sterile dialysate is instilled through an abdominal catheter, its dextrose draws wastes and extra fluid from peritoneal vessels, and each exchange runs fill → dwell → drain. CAPD is manual exchanges through the day; CCPD uses a cycler overnight. PD is done at home — autonomy instead of thrice-weekly center visits — after dedicated training in the aseptic technique that holds its one great danger, peritonitis, at bay.