Kidney Failure — Causes, Stages, Dialysis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Kidney failure is the loss of kidney function sufficient to cause symptoms, metabolic disturbances, and inability to sustain life without renal replacement therapy. It is classified as: acute kidney injury (AKI) — sudden reduction in kidney function over hours to days, often reversible if the cause is treated promptly; and chronic kidney disease (CKD) — progressive, irreversible loss of kidney function over months to years, classified by estimated glomerular filtration rate (eGFR) into Stages 1-5. End-stage kidney disease (ESKD, Stage 5 CKD — eGFR below 15 mL/min/1.73m2) requires renal replacement therapy (RRT: dialysis or transplantation) or conservative management to sustain life. CKD affects approximately 10-15% of the global adult population (850 million people), with diabetes and hypertension being the two leading causes. Kidney disease is often asymptomatic until advanced stages — making screening of high-risk groups essential.

CKD causes: diabetic nephropathy (most common globally — 30-40% of ESKD); hypertensive nephrosclerosis (second most common); chronic glomerulonephritis (IgA nephropathy most common worldwide); polycystic kidney disease (autosomal dominant ADPKD — most common hereditary kidney disease); obstructive uropathy (prostatic hypertrophy, kidney stones); reflux nephropathy from recurrent UTIs in childhood; lupus nephritis; and analgesic nephropathy. AKI causes (pre-renal/renal/post-renal): pre-renal — hypovolaemia (dehydration, haemorrhage), sepsis, cardiorenal syndrome; renal — acute tubular necrosis (from ischaemia or nephrotoxins: aminoglycoside antibiotics, contrast agents, NSAIDs), glomerulonephritis, interstitial nephritis, vasculitis; post-renal — ureteric obstruction (bilateral, or single kidney), bladder outlet obstruction. Risk factors for CKD progression: poor glycaemic control, uncontrolled hypertension, proteinuria, recurrent AKI, and smoking.

Early and mild CKD (Stages 1-3) is often asymptomatic — detected only on blood and urine testing. Symptoms develop progressively as eGFR falls below 30 mL/min. Uraemic symptoms from toxin accumulation: fatigue and generalised weakness, nausea, vomiting and anorexia (leading to malnutrition and weight loss), metallic taste, itching (pruritus — from urea deposition and calcium phosphate in skin), restless legs syndrome, and peripheral neuropathy. Fluid overload: ankle and leg oedema, breathlessness from pulmonary oedema, and hypertension (from volume expansion and reduced renal renin regulation). Anaemia of chronic kidney disease (from reduced erythropoietin production): pallor, fatigue, and breathlessness. Metabolic bone disease (from impaired vitamin D activation and secondary hyperparathyroidism): bone pain and fracture risk. Urinary symptoms: oliguria (reduced urine output — below 400 mL/day in AKI or ESKD), nocturia (early CKD — concentrating defect). Uraemic emergencies: pericarditis, encephalopathy, and life-threatening hyperkalaemia (potassium above 6.5 mmol/L — cardiac arrhythmia risk).

CKD diagnosis requires abnormalities of kidney structure or function persisting for more than 3 months. eGFR (estimated glomerular filtration rate): calculated from serum creatinine, age, sex, and race using the CKD-EPI equation — CKD stages: Stage 1 (eGFR ≥90, with markers of kidney damage), Stage 2 (eGFR 60-89), Stage 3a (eGFR 45-59), Stage 3b (eGFR 30-44), Stage 4 (eGFR 15-29), Stage 5 (eGFR below 15 — kidney failure). Urine albumin-to-creatinine ratio (ACR): quantifies proteinuria — ACR above 3 mg/mmol indicates CKD with additional cardiovascular and renal progression risk. Urine dipstick and microscopy: haematuria (glomerulonephritis, stone, malignancy), casts (AKI — granular casts: ATN; red cell casts: glomerulonephritis). Blood tests: electrolytes (hyperkalaemia, acidosis), phosphate, calcium, PTH (secondary hyperparathyroidism), FBC (anaemia), albumin. Renal ultrasound: small echogenic kidneys (CKD), cysts (ADPKD), obstruction (hydronephrosis), asymmetric kidneys (renal artery stenosis). Renal biopsy: indicated for unexplained rapid decline in eGFR, heavy proteinuria, or suspected glomerulonephritis to guide immunosuppressive treatment decisions.

CKD progression slowing: treat underlying cause, achieve tight blood pressure control (target below 130/80 mmHg — or below 120/80 with significant proteinuria), ACE inhibitor or ARB (reduces proteinuria and slows CKD progression independently of BP — first-line in diabetic and proteinuric CKD), SGLT2 inhibitors (dapagliflozin, empagliflozin — landmark DAPA-CKD and EMPA-KIDNEY trials demonstrated 40-50% reduction in CKD progression and cardiovascular events), tight glycaemic control in diabetes (HbA1c below 7%). Finerenone (non-steroidal mineralocorticoid antagonist) reduces CKD progression and cardiovascular events in diabetic CKD. Anaemia: erythropoiesis-stimulating agents (ESA — darbepoetin, epoetin) with IV iron supplementation target Hb 100-120 g/L. Secondary hyperparathyroidism: phosphate binders, active vitamin D (alfacalcidol), and calcimimetics (cinacalcet) for severe HPT. AKI management: remove nephrotoxins, treat cause, fluid resuscitation where appropriate, early nephrology review. Renal replacement therapy: haemodialysis (3x weekly, typically 4-hour sessions, via AV fistula or tunnelled line); peritoneal dialysis (home-based, continuous cycles); kidney transplantation (best long-term outcomes — 50-60% reduction in mortality vs dialysis; living donor preferred; requires lifelong immunosuppression).

Cardiovascular disease is the leading cause of death in CKD, with patients on haemodialysis having a 10-20 times higher cardiovascular mortality than age-matched general population — driven by hypertension, fluid overload, anaemia, hyperphosphataemia, and uraemic toxin-mediated endothelial dysfunction. Hyperkalaemia (serum potassium above 6.5 mmol/L) causes fatal cardiac arrhythmias and is the most immediately life-threatening acute complication of AKI and advanced CKD. Metabolic acidosis from impaired hydrogen ion excretion accelerates muscle wasting, bone demineralisation, and CKD progression. Anaemia of chronic kidney disease from reduced erythropoietin production causes fatigue, dyspnoea, impaired cognition, and worsens cardiac outcomes. Secondary hyperparathyroidism from phosphate retention and reduced active vitamin D causes renal osteodystrophy, bone pain, pathological fractures, and vascular calcification contributing to cardiovascular events. Uraemic pericarditis, encephalopathy, and peripheral neuropathy occur in advanced untreated kidney failure. Infections are the second leading cause of death in dialysis patients due to immunological dysfunction and dialysis access site complications.

Prevent AKI: avoid nephrotoxic medications (NSAIDs, aminoglycosides, iodinated contrast) in high-risk individuals (CKD, diabetes, elderly, dehydration). Withhold ACE inhibitors and metformin during acute illness causing dehydration (sick-day rules). Screen high-risk groups for CKD annually: diabetes (eGFR and urine ACR from diagnosis), hypertension (annually), cardiovascular disease, and family history of kidney disease. Optimise cardiovascular risk factors: blood pressure, diabetes control, dyslipidaemia, smoking cessation. Low-protein diet (under 0.8 g/kg/day) may modestly slow CKD progression in advanced disease — nutritional monitoring with renal dietitian is essential. Avoid dehydration. NSAID avoidance in CKD. Ensure adequate hydration in heatwaves and exercise — particularly important for CKD patients. Kidney donation is safe for carefully selected living donors with normal kidney function and no risk factors.

Seek emergency care immediately for: inability to urinate (anuria), extreme breathlessness from pulmonary oedema, severe vomiting with known kidney disease (risk of dehydration-triggered AKI), or symptoms of hyperkalaemia (chest pain, severe muscle weakness, abnormal heart rhythm) — hyperkalaemia above 6.5 mmol/L is a cardiac emergency. See your doctor promptly for any sudden reduction in urine output, new ankle swelling, increasing breathlessness, blood or frothy urine, or worsening fatigue with known CKD. High-risk individuals (diabetes, hypertension, family history of kidney disease) should have annual kidney function screening even without symptoms. Any adult with eGFR below 30 or urine ACR above 30 mg/mmol should be managed jointly with a nephrologist.