Kidney Failure — Symptoms, Causes & Treatment | MyMedicPlus

Kidney failure occurs when the kidneys lose the ability to filter waste and excess fluids from the blood. Classified as acute kidney injury (AKI) or chronic kidney disease (CKD), it affects over 850 million people worldwide and is a leading cause of cardiovascular morbidity and premature death.Kidney failure occurs when the kidneys lose the ability to filter waste, excess fluids, and electrolytes from the blood, leading to their accumulation at dangerous levels. It is classified as acute kidney injury (AKI — abrupt onset, potentially reversible) or chronic kidney disease stage 5 (CKD G5 — progressive, irreversible, also called end-stage kidney disease/ESKD). AKI is staged by the KDIGO criteria: Stage 1 (serum creatinine 1.5–1.9x baseline or increase of 0.3 mg/dL within 48 hours), Stage 2 (2–2.9x baseline), Stage 3 (3x baseline, above 4.0 mg/dL, or initiation of renal replacement therapy). CKD affects over 850 million people worldwide — approximately 10% of the global population — with ESKD requiring renal replacement therapy affecting 2 million people globally. Cardiovascular disease is the leading cause of death in kidney failure, occurring at 10–20 times the rate of the general population.

AKI is caused by dehydration, sepsis, nephrotoxic drugs, or urinary obstruction. CKD risk factors include diabetes mellitus, hypertension, glomerulonephritis, and polycystic kidney disease. Diabetes and hypertension together account for over 60% of CKD cases globally.AKI has three broad categories: pre-renal (50–70% of cases) — reduced renal perfusion from dehydration, haemorrhage, heart failure, sepsis, or NSAIDs; intrinsic renal (25–40%) — direct kidney damage from acute tubular necrosis (most common — ischaemia or nephrotoxins including aminoglycosides, cisplatin, contrast agents, myoglobin from rhabdomyolysis), acute glomerulonephritis (ANCA vasculitis, anti-GBM disease, IgA nephropathy), acute interstitial nephritis (drug-induced — NSAIDs, PPIs, beta-lactams, allopurinol); and post-renal (5–10%) — bilateral ureteric obstruction, urethral obstruction from BPH or prostate cancer, bladder outlet obstruction. CKD causes: diabetic nephropathy (25–40% of ESKD globally — hyperglycaemia causes glomerular hypertension, basement membrane thickening, mesangial expansion, and ultimately glomerulosclerosis), hypertensive nephropathy (arteriolar nephrosclerosis — 25–30%), IgA nephropathy, polycystic kidney disease (ADPKD — PKD1/PKD2 mutations), focal segmental glomerulosclerosis (FSGS), lupus nephritis, obstructive uropathy, and reflux nephropathy.

Reduced urine output, swelling of legs and ankles, shortness of breath, fatigue, nausea, confusion, and uremic frost in advanced cases. CKD is often asymptomatic until stage 4-5 when GFR falls below 30 mL/min/1.73m2, making routine screening essential.Reduced urine output (oliguria — less than 400 mL/24 hours; anuria — less than 100 mL/24 hours), generalised oedema involving legs, ankles, periorbital area, and lungs (pulmonary oedema causing breathlessness at rest), fatigue, weakness, nausea, vomiting, and anorexia. Uraemia — the accumulation of nitrogen-containing waste products — causes pruritus (itch), metallic taste, uraemic fetor (fishy/ammonia breath odour), neuropathy, confusion, uraemic encephalopathy (in severe untreated ESKD), and pericarditis (uraemic pericarditis with friction rub — emergency indication for dialysis). Hyperkalaemia (elevated serum potassium) in AKI and ESKD causes peaked T-waves on ECG, progressing to broad QRS complexes and potentially fatal ventricular fibrillation. CKD is often asymptomatic until eGFR falls below 30 mL/min/1.73 m² (Stage G3b) — regular eGFR and ACR screening is essential in at-risk populations including diabetics and hypertensives.

Blood tests measuring serum creatinine, BUN, and eGFR confirm diagnosis. Urinalysis detects proteinuria and hematuria. Renal ultrasound evaluates kidney size and obstruction. Kidney biopsy identifies the underlying glomerular cause. eGFR staging (G1-G5) guides CKD management.Serum creatinine and eGFR (calculated using CKD-EPI 2021 equation) are the primary markers of kidney filtration function. AKI is diagnosed by rise in serum creatinine of 0.3 mg/dL (26.5 µmol/L) within 48 hours or 1.5x baseline within 7 days. Urine microscopy reveals red cell casts (glomerulonephritis), granular casts (ATN), white cell casts (interstitial nephritis or pyelonephritis), and eosinophiluria (allergic interstitial nephritis). Urine albumin-to-creatinine ratio (ACR) in CKD: A1 (below 3 mg/mmol — normal), A2 (3–30 mg/mmol — moderate proteinuria), A3 (above 30 mg/mmol — severe proteinuria, associated with rapid CKD progression). Renal ultrasound assesses kidney size (small kidneys indicate chronic scarring; large kidneys suggest polycystic kidney disease, infiltrative disease, or acute swelling), echogenicity, hydronephrosis, and obstructive causes. Kidney biopsy is the gold standard for defining the histological cause of unexplained AKI or CKD with significant proteinuria — performed by nephrology under ultrasound guidance with percutaneous needle technique.

Treat underlying cause, control blood pressure with ACE inhibitors or ARBs, and manage blood glucose. SGLT2 inhibitors slow CKD progression in diabetic nephropathy. End-stage kidney disease requires renal replacement therapy: hemodialysis, peritoneal dialysis, or kidney transplant (preferred long-term option).Treat the underlying AKI cause: restore renal perfusion (IV crystalloid resuscitation for pre-renal AKI — caution in fluid-overloaded states), stop nephrotoxins (NSAIDs, ACEi/ARBs temporarily in acute illness), relieve obstruction (ureteric stenting or nephrostomy for post-renal AKI). Monitor fluid balance meticulously — daily weight, urine output measurement, fluid input/output charts. Electrolyte correction: hyperkalaemia — calcium gluconate (IV, cardioprotective), insulin-dextrose (drives K+ into cells), sodium resonium or patiromer (enteral potassium binders), haemodialysis for refractory cases. Metabolic acidosis: sodium bicarbonate replacement if bicarbonate below 15 mmol/L. For CKD progression: ACE inhibitors (ramipril) or ARBs (losartan) reduce proteinuria and slow progression — mandatory for CKD with ACR above 30 mg/mmol; SGLT2 inhibitors (dapagliflozin 10 mg — DAPA-CKD trial) reduce CKD progression by 39% and are now standard of care; finerenone (non-steroidal MRA) for diabetic CKD on ACEi/ARB. End-stage kidney disease management: haemodialysis (HD — 3–4 sessions weekly, typically 4 hours each, in hospital or home setting); peritoneal dialysis (PD — home-based, continuous or cycled — better preserved residual function); kidney transplantation — the best long-term outcome, with 5-year graft survival above 90% for living donor kidneys.

Cardiovascular disease risk is 2-10 times higher than the general population. Additional complications include anemia, mineral bone disease, hyperkalemia, metabolic acidosis, uremic pericarditis, and increased susceptibility to infection. ESRD requires lifelong renal replacement therapy.Cardiovascular disease is the leading cause of death in kidney failure — CKD patients have a 10–20 times higher cardiovascular event rate than the general population due to traditional risk factors (hypertension, diabetes) plus uraemia-specific factors (vascular calcification, endothelial dysfunction, inflammation, anaemia, fluid overload). Anaemia of CKD — normochromic normocytic, caused by reduced erythropoietin synthesis — requires erythropoiesis-stimulating agents (ESAs: darbepoetin alfa, epoetin beta) targeting haemoglobin 100–120 g/L; iron supplementation (IV iron preferred in G4–G5); oral HIF-PH inhibitors (daprodustat — NICE approved). CKD-mineral bone disorder (CKD-MBD): hyperphosphataemia, hypocalcaemia, elevated PTH (secondary hyperparathyroidism), and reduced 1,25-dihydroxyvitamin D cause renal osteodystrophy (osteomalacia, osteoporosis, osteitis fibrosa cystica) and vascular calcification — managed with phosphate binders (sevelamer, calcium carbonate), active vitamin D analogues (alfacalcidol, calcitriol), and cinacalcet. Uraemic pericarditis — an absolute indication for dialysis regardless of eGFR. Infections account for 15–20% of deaths in dialysis patients; vascular access infections (dialysis catheter-related bloodstream infections) carry high mortality.

Control diabetes and hypertension rigorously. Avoid nephrotoxic agents including NSAIDs, iodinated contrast, and aminoglycosides. Maintain adequate hydration. Undergo annual eGFR and urine albumin-to-creatinine ratio testing if diabetic or hypertensive. Smoking cessation reduces progression risk.Rigorous control of the two leading preventable causes: optimal diabetes management (HbA1c below 53 mmol/mol, 7%, reduces diabetic nephropathy progression by 25–35% — UKPDS, DCCT trials) and strict blood pressure control (below 130/80 mmHg — ACEi/ARBs mandatory for proteinuric CKD and diabetic nephropathy). Avoid nephrotoxic medications: NSAIDs (ibuprofen, naproxen, diclofenac) are contraindicated in eGFR below 30 and should be minimised at all CKD stages; aminoglycoside antibiotics require dose adjustment and therapeutic drug monitoring; IV iodinated contrast — hold metformin 48 hours before and after; gadolinium MRI contrast contraindicated in eGFR below 30 (risk of nephrogenic systemic fibrosis). Maintain adequate hydration — dehydration causes pre-renal AKI and accelerates CKD progression. Annual eGFR and urine ACR testing for all people with diabetes and hypertension — essential for early CKD detection when interventions are most effective. Smoking cessation independently reduces CKD progression risk by 30–40%.

Seek emergency assessment immediately if you or a family member experiences: sudden dramatic reduction or complete absence of urine output; rapid-onset leg, face, or body swelling; breathlessness at rest (pulmonary oedema); confusion, drowsiness, or reduced responsiveness (uraemic encephalopathy); chest pain; severe nausea, vomiting, or inability to take medications — these may indicate acute kidney injury or end-stage renal disease requiring emergency dialysis. Patients on dialysis should contact their renal unit immediately for: dialysis access problems (fistula thrombosis, catheter infection); fever or rigors (potential dialysis access infection); persistent hypotension or hypertension during dialysis; weight gain of more than 2–3 kg between sessions (fluid overload). See your GP if you have known CKD and notice deteriorating symptoms, worsening blood pressure control, or new symptoms — do not wait for routine appointments if you feel significantly unwell.