Acute Kidney Injury

Acute kidney injury is a sudden reduction in kidney function developing over hours or days. It often occurs during another illness, after fluid loss, with urinary obstruction or through medicine related effects. Early recognition, treatment of the cause and careful control of fluid, potassium, acid balance and medicines can prevent life threatening complications.

What acute kidney injury is Acute kidney injury, usually shortened to AKI, is a sudden reduction in kidney function developing over hours or days. The kidneys become less able to remove waste, control electrolytes and maintain fluid and acid balance. The change may be mild and reversible or severe enough to require dialysis. AKI is a clinical syndrome rather than one disease. Dehydration, sepsis, medicines, inflammation and urinary obstruction can all produce the same initial loss of function. Early recognition matters because treating the cause and preventing further injury can improve recovery. The word injury does not always mean physical trauma In AKI, injury describes an acute loss of kidney function. It does not mean that the kidneys were struck or physically torn. A fall, operation or crush injury can contribute, but many episodes occur without direct trauma. Some early episodes involve reduced filtration without established structural damage. Others involve inflammation, toxic injury or death of kidney tubular cells. The same person can have several mechanisms at once, so the cause should be identified rather than inferred from the word injury. What healthy kidneys normally do Your kidneys filter blood continuously and remove many waste products through urine. They regulate sodium, potassium, water and acid balance. They also influence blood pressure, red blood cell production and bone mineral regulation. When function falls suddenly, potassium, acid, fluid and medicines can accumulate before obvious symptoms develop. AKI therefore affects the whole body and often reflects severe illness elsewhere rather than an isolated kidney problem. AKI is different from chronic kidney disease AKI develops over hours to days. Chronic kidney disease, or CKD, describes abnormalities of kidney structure or function lasting at least three months. A high creatinine found today cannot be labelled chronic without previous results or evidence of duration. Likewise, a person with established CKD can still develop a new acute deterioration. NICE specifically warns that a creatinine rise in CKD may represent AKI rather than gradual progression. The time course, previous blood tests, urine findings and clinical context separate the two patterns. AKI can occur on top of CKD AKI on CKD means that a person with chronic impairment develops an additional sudden decline. People with CKD have less kidney reserve and are more vulnerable to dehydration, infection, surgery, obstruction and medicine related changes. Their creatinine may not return fully to the previous baseline after the acute episode. Management treats the acute cause while recognising the person's usual kidney function, albuminuria, medicines and long term kidney plan. Persistent dysfunction after AKI Kidney function does not always return to baseline within a few days. Persistent impairment during the period between acute injury and the three month CKD threshold is sometimes described as acute kidney disease. This concept emphasises that recovery is a process rather than a single discharge blood result. Abnormal function lasting at least three months may meet criteria for CKD and needs an appropriate long term assessment. AKI is often silent Many people with mild AKI have no specific symptoms. It is often detected through routine blood tests during another illness. You may continue passing a normal amount of urine despite a significant creatinine rise. This is called non oliguric AKI. Other people develop reduced urine, thirst, nausea, swelling, breathlessness, drowsiness or confusion. Symptoms alone cannot determine the stage or cause, so blood tests and urine monitoring remain essential. Creatinine is a marker, not a toxin diagnosis Creatinine is a waste product produced mainly by normal muscle metabolism and removed largely by the kidneys. When filtration falls, serum creatinine usually rises. Clinicians compare the current result with a previous baseline rather than relying only on the laboratory reference range. Creatinine can lag behind the actual kidney injury. A major fall in filtration may have occurred before the blood level rises clearly. Muscle mass, amputation, frailty, diet and some medicines affect creatinine, so the result measures kidney function indirectly and does not identify the cause. Why eGFR can mislead during AKI Estimated glomerular filtration rate, or eGFR, is calculated from serum creatinine and personal characteristics. The calculation assumes that creatinine is reasonably stable. That assumption is false when creatinine is rising or falling quickly. A reported eGFR during AKI should therefore be interpreted cautiously and should not be used as though it describes a steady state. Medicine dosing during rapidly changing function often requires clinical judgement, repeat tests and pharmacist or specialist advice. Urine output provides an early signal Falling urine output can reveal AKI before creatinine rises. Oliguria means urine output below 0.5 millilitres per kilogram per hour. NICE uses persistence beyond six hours in adults as one AKI detection criterion. Low urine output can also result from dehydration, obstruction, shock or an incorrectly positioned catheter without established kidney damage. Conversely, normal urine volume does not exclude AKI. Output and creatinine provide related but different information. The KDIGO definition The widely used KDIGO definition identifies AKI when serum creatinine rises by at least 26 micromoles per litre within 48 hours. It also identifies AKI when creatinine rises to at least 1.5 times baseline, known or presumed to have occurred within seven days. A urine output below 0.5 millilitres per kilogram per hour for at least six hours also meets the adult definition. Only one criterion is required. The definition detects a change in function but does not explain why it occurred. Stage 1 AKI Stage 1 is the least severe KDIGO category, but it is still clinically important. It includes a creatinine rise to 1.5 to 1.9 times baseline or an increase of at least 26.5 micromoles per litre. The urine output criterion is below 0.5 millilitres per kilogram per hour for six to twelve hours. Stage 1 can progress, and even apparently reversible episodes are associated with increased future kidney and cardiovascular risk. Stage 2 AKI Stage 2 includes a creatinine rise to 2.0 to 2.9 times baseline. It also includes urine output below 0.5 millilitres per kilogram per hour for at least twelve hours. The stage indicates greater severity and a higher risk of complications than stage 1. It does not mean that dialysis is automatically needed or that the kidneys cannot recover. Stage 3 AKI Stage 3 is the most severe KDIGO category. It includes a creatinine rise to at least three times baseline, a rise to at least about 354 micromoles per litre in an acute context, or starting renal replacement therapy. It also includes urine output below 0.3 millilitres per kilogram per hour for at least 24 hours or no urine for at least twelve hours. NICE advises nephrology discussion within 24 hours for stage 3 AKI and immediate specialist referral when dialysis indications are present. How staging is used When creatinine and urine output criteria produce different stages, clinicians use the higher stage. Staging helps communicate severity, monitoring needs and prognosis. It does not identify whether the cause is dehydration, inflammation, toxicity or obstruction. A person with stage 1 disease and dangerous hyperkalaemia can need more urgent treatment than someone with stage 3 criteria who is stable and recovering. The pre renal, intrinsic and post renal framework A traditional framework divides causes into pre renal, intrinsic renal and post renal groups. Pre renal causes reduce blood flow or effective perfusion before blood reaches the filtering units. Intrinsic causes damage structures within the kidney. Post renal causes block urine flow after it has been formed. This is a useful organising model, not three watertight boxes. Sepsis, heart failure and medicines often produce mixed mechanisms. Pre renal AKI Pre renal AKI develops when kidney perfusion is insufficient to maintain filtration. Early in the process, kidney tissue may remain structurally intact and function can improve rapidly when circulation is restored. If severe or prolonged hypoperfusion continues, tubular cells can become injured and the process can evolve into intrinsic acute tubular injury. Clinicians assess the whole circulation rather than assuming that every raised creatinine needs intravenous fluid. Dehydration and volume loss Vomiting, diarrhoea, fever, poor intake and excessive sweating can reduce circulating volume. Blood loss, burns, high output stomas and excessive urinary losses can have the same effect. Clues include thirst, dry mucosa, postural dizziness, low blood pressure and reduced urine, but no single sign measures volume accurately. Older people and people relying on others for drinks can deteriorate quickly because access to fluid may be limited. Sepsis and severe infection Sepsis is a major cause of AKI. Low blood pressure, abnormal blood vessel tone, inflammation and microcirculatory changes can all contribute. Kidney injury can occur in sepsis even when a dramatic period of low blood pressure was not recorded. Treatment includes urgent infection management, appropriate fluids, antibiotics, source control and circulatory support. A rising creatinine during sepsis is a marker of organ dysfunction and should not be treated as an isolated laboratory problem. Heart failure and kidney perfusion Heart failure can reduce forward blood flow to the kidneys. Venous congestion can also raise pressure around the kidneys and reduce filtration. A person may have AKI while visibly fluid overloaded, with swollen legs and pulmonary oedema. Giving extra fluid automatically can worsen breathing and congestion. Withholding every diuretic can also be harmful. Assessment considers blood pressure, congestion, weight, oxygenation, heart function and response to treatment. Liver disease and effective circulating volume Advanced liver disease can cause marked vasodilation and reduced effective blood flow to the kidneys despite total body fluid excess. Infection, bleeding, diuretics and large volume fluid shifts can precipitate AKI. Hepatorenal syndrome is a specific functional kidney failure pattern associated with advanced cirrhosis after other causes are assessed. Management requires liver and kidney expertise because ordinary fluid replacement alone may be ineffective or harmful. Haemorrhage, shock and major surgery Major bleeding reduces oxygen and blood delivery to kidney tissue. Trauma, gastrointestinal bleeding, obstetric haemorrhage and operative blood loss can therefore cause AKI. Emergency and major intraperitoneal surgery increase risk, especially with sepsis, hypovolaemia, diabetes, CKD or heart failure. Treatment restores circulation, controls bleeding and maintains oxygen delivery while avoiding excessive fluid accumulation. Intrinsic renal AKI Intrinsic AKI results from disease within the kidney tissue. The affected structure may be the tubules, glomeruli, interstitium or renal blood vessels. Urine findings, medicine exposure, systemic features and the time course help narrow the cause. Many intrinsic disorders need early nephrology input because delayed immune or cause specific treatment can lead to permanent damage. Acute tubular injury and acute tubular necrosis Acute tubular injury is the commonest intrinsic pattern in hospitalised adults. It can follow prolonged hypoperfusion, sepsis, major surgery, pigment release or direct nephrotoxins. The traditional term acute tubular necrosis, or ATN, remains widely used, although not every case involves widespread cell death. Recovery depends on the severity, ongoing insults and the person's previous kidney reserve. Supportive care allows surviving tubular cells to repair. Sepsis related tubular injury is multifactorial Septic AKI is not simply dehydration. Inflammation, altered microcirculation, venous congestion, medicines and haemodynamic changes can act together. A fluid challenge may help genuine hypovolaemia, but repeated fluid without evidence of responsiveness can produce pulmonary oedema. Frequent reassessment is more important than applying one fixed volume to every person. Glomerulonephritis Glomerulonephritis is inflammation of the kidney's filtering units, called glomeruli. Possible clues include blood and protein on urine testing, swelling, high blood pressure and a rapid creatinine rise. A purpuric rash, coughing blood, sinus symptoms, joint symptoms or systemic inflammation can suggest vasculitis or another multisystem disease. Urgent nephrology assessment is needed because kidney biopsy and immune treatment may be time critical. Acute interstitial nephritis Acute interstitial nephritis is inflammation of the tissue surrounding kidney tubules. Medicines are common triggers, including some antibiotics, proton pump inhibitors and NSAIDs. Infection and autoimmune disease can also contribute. Fever, rash and raised eosinophils form a classic pattern but are absent in many cases. Management identifies and stops the likely trigger when safe, treats complications and considers specialist assessment or corticosteroid treatment in selected cases. Rhabdomyolysis and pigment injury Rhabdomyolysis is rapid breakdown of skeletal muscle, releasing myoglobin and other intracellular contents. Crush injury, prolonged immobility, seizures, extreme exertion, heat illness, drugs and some medicines can trigger it. Muscle pain, weakness and dark urine may occur, but the full combination is not always present. Creatine kinase, potassium, calcium, phosphate and kidney function require urgent monitoring because hyperkalaemia and AKI can develop quickly. Renal vascular causes Blood vessel disorders can reduce kidney perfusion or damage the small vessels within the kidneys. Examples include renal artery occlusion, malignant hypertension, thrombotic microangiopathy and some forms of vasculitis. Low platelets, anaemia from red cell destruction, severe hypertension or pain may provide clues. These conditions are uncommon but can progress rapidly and require urgent specialist investigation. Post renal AKI Post renal AKI occurs when urine flow is obstructed after filtration. Obstruction raises pressure within the urinary tract and can reduce filtration in the affected kidney. AKI usually requires obstruction of both kidneys, obstruction below the bladder outlet, or obstruction of a solitary functioning kidney. Prompt drainage can produce substantial recovery, but prolonged obstruction can cause permanent damage and infection. Stones A ureteric stone can cause severe loin pain radiating towards the groin, nausea and blood in the urine. One blocked ureter does not usually cause AKI when the other kidney functions normally. Bilateral stones, a solitary kidney or severe pre existing CKD can make obstruction much more dangerous. Fever or sepsis with an obstructed urinary tract suggests an infected obstructed kidney and requires urgent drainage. Prostate and bladder outlet obstruction An enlarged prostate can obstruct urine leaving the bladder. Symptoms may include poor stream, hesitancy, incomplete emptying, frequency, overflow leakage or inability to pass urine. Chronic retention can be painless and present with kidney impairment rather than dramatic bladder pain. A bladder scan and urinary catheter can identify and relieve lower tract retention, followed by investigation of the cause. Tumours and pelvic disease Tumours in the bladder, prostate, cervix, uterus, bowel or retroperitoneum can compress or invade the urinary tract. Pelvic fibrosis, blood clots and previous radiotherapy can also obstruct urine flow. Symptoms may include haematuria, pelvic pain, weight loss or altered urinary function, but obstruction can be silent. Imaging and urgent urological planning are needed when upper tract obstruction contributes to AKI. Catheter blockage A blocked, kinked or displaced urinary catheter can mimic anuria and cause bladder retention. Clinicians check the tubing, bag position, bladder fullness and catheter patency before assuming that the kidneys have stopped producing urine. Flushing or replacing a catheter should follow trained clinical procedures because trauma and infection are possible. Persistent absent urine after a catheter problem is corrected requires urgent reassessment. Who is at higher risk Risk rises with age 65 or over, previous AKI and pre existing CKD. Diabetes, heart failure, liver disease, cancer, frailty and neurological or cognitive impairment also increase vulnerability. Sepsis, hypovolaemia, urinary obstruction, critical illness and major surgery can trigger rapid deterioration. Risk factors do not prove that AKI is present. They lower the threshold for checking creatinine and monitoring urine output. Why older age increases risk Kidney reserve commonly falls with age, and older adults are more likely to have CKD, heart disease and several medicines. Thirst perception, mobility and access to drinks may be reduced during illness. A smaller muscle mass can produce a deceptively modest creatinine despite a major decline in filtration. Assessment should compare with the person's baseline and functional change rather than assuming deterioration is normal ageing. Diabetes and AKI Diabetes can increase AKI risk through CKD, vascular disease, infection and dehydration from high glucose. Vomiting, diarrhoea or reduced intake can make glucose lowering medicines unsafe even before a creatinine result is available. AKI can cause some medicines to accumulate and increase hypoglycaemia, lactic acidosis or ketoacidosis risk. A personalised diabetes sick day plan should accompany kidney related medicine guidance. Medicines can contribute in different ways Some medicines directly injure kidney structures. Others reduce filtration pressure during dehydration or accumulate when kidney function falls. Calling every medicine nephrotoxic is inaccurate and may make people stop treatments that protect the heart or kidneys long term. The correct response is a structured medication review considering indication, current circulation, kidney function, potassium and safer alternatives. Any medicine that is paused needs a documented restart plan. NSAIDs NSAIDs include ibuprofen, naproxen and diclofenac. They inhibit prostaglandins that help keep the afferent kidney arteriole open during reduced circulation. During dehydration, heart failure or CKD, this can reduce blood flow into the glomerulus and precipitate AKI. NSAIDs can also cause acute interstitial nephritis, sodium retention, hypertension and hyperkalaemia. Over the counter availability does not make them safe for everyone. People at high risk should discuss suitable pain relief with a clinician or pharmacist. ACE inhibitors and ARBs ACE inhibitors and angiotensin receptor blockers dilate the efferent arteriole leaving the glomerulus. This lowers pressure inside the filter and helps protect kidneys with albuminuria over the long term. It can also reduce filtration during severe dehydration, sepsis or hypotension. These medicines are not simply kidney poisons. They improve outcomes in heart failure, hypertension and proteinuric CKD. NICE advises considering temporary interruption during vomiting, diarrhoea or sepsis until the clinical condition improves and stabilises, followed by a planned review and restart when appropriate. Diuretics Diuretics help remove sodium and fluid and are essential treatments for congestion and heart failure. They can contribute to AKI when they produce or worsen hypovolaemia. Stopping them automatically can worsen pulmonary oedema or venous congestion and may itself impair kidney function. The decision depends on volume status, blood pressure, heart failure severity, urine output and electrolytes. The triple whammy The term triple whammy describes an ACE inhibitor or ARB combined with a diuretic and an NSAID. The diuretic can reduce circulating volume, the ACE inhibitor or ARB lowers efferent filtration pressure, and the NSAID constricts the afferent side by blocking prostaglandins. Together, particularly during dehydration or acute illness, these effects can markedly reduce glomerular filtration. Avoid adding an over the counter NSAID to this combination without professional advice. Aminoglycosides Aminoglycoside antibiotics, including gentamicin, can directly injure tubular cells. They remain important treatments for serious infection, so the benefit can outweigh the kidney risk. Clinicians use appropriate dosing intervals, monitor drug levels and review kidney function. Risk rises with prolonged treatment, high exposure, dehydration and other nephrotoxins. Iodine based contrast media Iodine based contrast can be associated with AKI, but modern evidence shows that the risk is smaller than previously assumed in many stable adults. NICE identifies a small increased risk particularly when eGFR is below 30 millilitres per minute per 1.73 square metres. High risk people may need recent kidney tests and oral or intravenous hydration according to the setting. Emergency contrast imaging should not be delayed when delay would create a greater clinical risk, such as missing major bleeding, stroke or another life threatening diagnosis. Chemotherapy and other direct nephrotoxins Some cancer treatments can injure tubules, glomeruli or kidney blood vessels. Cisplatin, high dose methotrexate and selected targeted or immune treatments are important examples. Antiviral drugs, amphotericin, calcineurin inhibitors and crystal forming medicines can also cause AKI in particular circumstances. Specialist teams adjust dose, hydration and monitoring rather than withholding effective treatment without weighing benefit and risk. Medicines can accumulate during AKI Reduced kidney clearance can increase levels of medicines even when they did not cause the AKI. Examples include some antibiotics, opioids, pregabalin, gabapentin, lithium, digoxin and low molecular weight heparins. Accumulation can cause confusion, respiratory depression, bleeding, arrhythmia or other toxicity. Medicine doses should be reviewed repeatedly because kidney function can change from day to day during injury and recovery. Sick day guidance People at increased risk may receive personalised advice about medicines during an acute illness with vomiting, significant diarrhoea, fever, sweats or poor intake. A plan may advise temporarily pausing an ACE inhibitor, ARB, diuretic, NSAID or selected diabetes medicine when dehydration is likely. This guidance is not a universal rule for every minor illness. Evidence for blanket programmes is limited, and inappropriate interruption can worsen heart failure, blood pressure or diabetes. Follow your written plan, seek help when illness is more than mild and ensure that important medicines are reviewed and restarted after recovery. When self management is unsafe Do not rely on a sick day card if you are confused, fainting, severely breathless, passing almost no urine or unable to keep fluids down. People with heart failure, advanced CKD, pregnancy, a kidney transplant or complex medication packs often need direct clinical advice before changing treatment. Never stop insulin, essential steroids or transplant anti rejection medicines using general kidney sick day advice. Sick day guidance should include when to seek assessment, not only which tablets to pause. How AKI may present Possible symptoms include much less urine, thirst, nausea, vomiting, dizziness, tiredness, swelling and breathlessness. Severe disease can cause drowsiness, confusion, seizures or chest discomfort. These symptoms are non specific and often come from the illness causing AKI. A person at risk who becomes acutely unwell should have kidney function assessed rather than attempting to diagnose AKI from symptoms alone. Clinical examination The clinician assesses airway, breathing, circulation, consciousness and signs of sepsis or shock. Blood pressure, pulse, oxygen saturation, temperature and lying to standing symptoms help define immediate risk. The examination looks for dehydration and for fluid overload, including oedema, raised neck veins and lung crackles. The bladder, abdomen, skin, joints and neurological system are examined when obstruction, vasculitis, infection or systemic disease is possible. Fluid balance assessment Fluid balance combines intake, urine output, vomiting, diarrhoea, drains and other losses. Daily weight can reveal accumulating or lost fluid more reliably than one examination sign. A urinary catheter may be needed for accurate output monitoring in severe illness, but it should not be inserted without a clinical indication. The aim is adequate circulation without pulmonary oedema or harmful positive fluid balance. Blood investigations Blood tests include creatinine, urea, sodium, potassium and bicarbonate. A full blood count, inflammatory markers, glucose, liver tests and a blood gas may help identify the cause and complications. Creatine kinase is measured when rhabdomyolysis is possible. Calcium, phosphate, haemolysis tests and immune tests are used when indicated. Results are repeated according to severity because potassium, acid balance and creatinine can change rapidly. Urinalysis NICE recommends urine dipstick testing for blood, protein, leucocytes, nitrites and glucose as soon as AKI is suspected or detected. Blood and protein without urinary infection or catheter trauma can suggest acute nephritis and should prompt nephrology consideration. Leucocytes and nitrites may support urinary infection but do not prove that infection caused the kidney injury. A normal dipstick does not exclude tubular injury, obstruction or haemodynamic AKI. Urine microscopy and protein measurement Microscopy can identify red cell casts, white cell casts, granular casts, crystals or other clues. Red cell casts support glomerular inflammation, while muddy brown granular casts can occur with acute tubular injury. Urine albumin to creatinine or protein to creatinine ratios quantify protein loss when glomerular disease is possible. No sediment finding should be interpreted without the history, dipstick, blood results and clinical context. Ultrasound and obstruction Ultrasound can identify hydronephrosis, bladder retention and some structural abnormalities. NICE advises urgent urinary tract ultrasound within 24 hours when the cause is unclear or obstruction risk is present. When an infected obstructed kidney is suspected, ultrasound should be immediate and performed within six hours of assessment. Ultrasound is not routinely required when a clear non obstructive cause is responding promptly to treatment. Bladder scanning and catheter assessment A bedside bladder scan estimates retained urine and can identify lower urinary obstruction. If a catheter is already present, clinicians check whether it is blocked, displaced or kinked. Catheter drainage can reveal post obstructive diuresis, where very large urine volumes follow relief of chronic obstruction. Fluid and electrolytes then require close monitoring because rapid losses can cause dehydration, sodium disturbance and further AKI. ECG and hyperkalaemia An ECG assesses the heart's electrical response when potassium is raised. Possible changes include peaked T waves, loss of P waves, widening of the QRS complex, bradycardia and dangerous ventricular rhythms. UK Kidney Association guidance recommends an urgent 12 lead ECG for hospitalised adults with potassium at least 6.0 millimoles per litre. A normal ECG does not exclude severe hyperkalaemia. The potassium level, rate of rise and clinical condition all matter. Further imaging and specialist tests CT may identify stones, tumours, haemorrhage or other abdominal disease when ultrasound is insufficient. Kidney biopsy can diagnose glomerulonephritis, interstitial nephritis and other intrinsic disorders when the result will change treatment. Immune tests may include complement, ANCA, anti GBM antibodies and immunoglobulins according to the pattern. These are targeted investigations rather than a standard panel for every episode of dehydration related AKI. Management begins with the underlying cause There is no single medicine that reverses every form of AKI. Treatment may involve restoring circulation, treating sepsis, controlling bleeding, relieving obstruction or stopping an offending medicine. Glomerulonephritis may need immunosuppression, while rhabdomyolysis requires treatment of muscle injury and electrolyte complications. Repeated reassessment determines whether kidney function and urine output are improving or whether the diagnosis needs revision. Intravenous fluid treatment Isotonic crystalloid can restore circulation when hypovolaemia is present. The volume and speed depend on blood pressure, ongoing losses, age, heart function and response. Small reassessed boluses may be safer than large unreviewed volumes in frail people or those with heart failure. Fluid is a treatment for deficient circulation, not a routine treatment for every raised creatinine. Sepsis and shock treatment Sepsis management includes prompt antimicrobials when indicated, source control, fluid assessment and close physiological monitoring. Vasopressors may be required in critical care when blood pressure remains inadequate despite appropriate fluid resuscitation. Antibiotic selection and dosing should account for changing kidney function. Delaying sepsis treatment to complete a renal investigation can be dangerous. Relieving urinary obstruction Lower tract retention may improve after urinary catheterisation. Upper tract obstruction can require a ureteric stent or nephrostomy to drain the kidney. NICE advises immediate urological referral for pyonephrosis, bilateral upper tract obstruction, an obstructed solitary kidney or obstruction causing AKI complications. When stenting or nephrostomy is required for upper tract obstruction with AKI, it should be performed as soon as possible. Treating intrinsic kidney disease Suspected vasculitis, glomerulonephritis, acute interstitial nephritis or myeloma related disease should be discussed with nephrology promptly. Treatment may include stopping a trigger, corticosteroids, other immune therapy, plasma exchange in selected situations or disease specific cancer care. Kidney biopsy is sometimes needed before treatment, but life threatening pulmonary kidney disease may require urgent action. Specialist care balances the danger of immune treatment against the risk of irreversible kidney loss. Medication optimisation Clinicians review prescribed, over the counter and complementary medicines at the start of AKI. Potential contributors may be paused, doses adjusted and alternatives selected. The review also identifies medicines that accumulate and medicines whose interruption could cause harm. Discharge information should state clearly which drugs remain stopped, which restart, when blood tests are due and who is responsible. Diuretics do not cure AKI Loop diuretics can increase urine output but do not repair injured nephrons or improve survival routinely. NICE advises against using them simply to treat AKI. They can be useful for fluid overload or oedema while dialysis is being arranged or during recovery. A rise in urine after a diuretic does not prove that filtration has recovered. Low dose dopamine is not kidney protection Low dose dopamine was historically used in an attempt to increase renal blood flow. Evidence does not show that it prevents or treats AKI, and it can cause arrhythmia and other harm. NICE advises not offering low dose dopamine for AKI. Circulatory support should instead follow evidence based fluid and vasopressor management. Hyperkalaemia Potassium is essential for nerve and muscle function, including the heart's electrical activity. AKI reduces potassium excretion. Tissue breakdown, acidosis and potassium raising medicines can worsen the rise. Hyperkalaemia may cause weakness, tingling or palpitations, but it is often asymptomatic until a dangerous rhythm occurs. Moderate or severe hyperkalaemia during AKI is a medical emergency requiring rapid confirmation, ECG assessment and treatment. Emergency hyperkalaemia treatment Intravenous calcium protects the heart when toxic ECG changes are present but does not remove potassium. Insulin with glucose shifts potassium temporarily into cells, and nebulised salbutamol can provide additional temporary movement. Potassium is removed through urine, gastrointestinal binders or dialysis according to the clinical situation. Repeated potassium and glucose monitoring is essential because treatment can wear off and insulin can cause hypoglycaemia. Fluid overload and pulmonary oedema When the kidneys cannot excrete sodium and water, fluid accumulates in tissues and the circulation. Swollen legs, rapid weight gain, raised neck veins and worsening blood pressure can occur. Pulmonary oedema causes severe breathlessness, low oxygen, crackles and sometimes pink frothy sputum. Oxygen, ventilatory support, diuretics and urgent dialysis may be required when fluid overload does not respond to medical treatment. Metabolic acidosis The kidneys normally excrete acid and regenerate bicarbonate. AKI can produce metabolic acidosis, especially when shock, sepsis or tissue hypoxia adds lactic acid. Severe acidosis can impair heart function, worsen potassium movement and cause deep rapid breathing, confusion or circulatory instability. Treatment corrects the cause and circulation. Dialysis is considered when severe acidosis does not respond to medical management. Uraemia Uraemia describes the clinical effects of retained waste products and disordered kidney function rather than one urea threshold. Possible features include nausea, vomiting, loss of appetite, itching, confusion, drowsiness, seizures and bleeding tendency. Uraemic encephalopathy means brain dysfunction caused by severe kidney failure. Uraemic pericarditis causes inflammation around the heart and may produce chest pain or a pericardial rub. Both are urgent dialysis indications. When dialysis is needed NICE advises immediate referral for renal replacement therapy when hyperkalaemia, metabolic acidosis, uraemic complications, fluid overload or pulmonary oedema do not respond to medical treatment. Dialysis may also support selected poisonings or severe metabolic problems under specialist care. The decision is based on the person's complete condition, trajectory and treatment response. A single creatinine, urea or potassium value should not determine dialysis in isolation. Forms of renal replacement therapy Intermittent haemodialysis removes waste, potassium and fluid over several hours. Continuous haemofiltration or haemodiafiltration removes them more gradually and is often used in haemodynamically unstable intensive care patients. Peritoneal dialysis can be used in selected settings, including where other resources are limited. Dialysis for AKI is often temporary, but some people have incomplete recovery and continue long term kidney replacement therapy. When nephrology input is needed Immediate nephrology or critical care referral is required when dialysis indications are present. NICE advises discussion within 24 hours for stage 3 AKI, no clear cause, inadequate response, complications, renal transplant or CKD stage 4 or 5. Possible vasculitis, glomerulonephritis, interstitial nephritis or myeloma also needs early specialist input. A clear reversible cause that responds promptly may be managed without routine nephrology referral, provided monitoring and follow up are safe. Recovery can be rapid or prolonged Some people recover within days after dehydration or obstruction is corrected. Acute tubular injury may take weeks, and severe AKI can require temporary dialysis. During recovery, urine output can become very high before the kidneys regain normal concentrating ability. Fluid, potassium, sodium and medicine doses still need monitoring while creatinine falls. Not everyone returns to the old baseline Recovery may be complete, partial or absent. Older age, severe or prolonged AKI, previous CKD, recurrent injury and critical illness increase the risk of incomplete recovery. A lower creatinine after discharge does not guarantee that kidney structure and future risk have returned to normal. The episode should remain documented in the medical record and influence future prescribing and acute illness planning. Follow up after discharge NICE quality standards advise a clinical review within three months after hospital discharge, or sooner when the risk of poor outcomes is higher. People with heart failure, poor kidney recovery, advanced CKD, recurrent AKI or ongoing dialysis may need review within days or weeks. Follow up includes kidney function, blood pressure, medication reconciliation and a plan for ongoing monitoring. Urine albumin or protein assessment can identify persistent kidney damage when clinically appropriate. Restarting medicines after AKI Medicines stopped during AKI should not remain discontinued by default. ACE inhibitors, ARBs and diuretics may provide major long term benefits for heart failure, blood pressure and albuminuric CKD. The indication, blood pressure, potassium, volume status and degree of recovery determine when and how they restart. Clear communication between hospital, GP, pharmacy and the person taking the medicine prevents both premature restart and harmful permanent omission. Future risk after AKI An AKI episode increases the risk of recurrent AKI, CKD, cardiovascular disease and death. Risk rises with greater stage and duration, but even stage 1 disease is not completely benign. Follow up and prevention are therefore part of AKI treatment rather than optional extras. Future clinicians should know about the episode before surgery, contrast imaging or prescribing potentially kidney relevant medicines. Reducing future risk Maintain adequate fluid intake during ordinary health unless you have been given a restriction for heart, liver or kidney disease. Seek early advice for significant vomiting, diarrhoea, fever, poor intake, reduced urine or worsening breathlessness. Avoid unplanned NSAID use and keep an up to date medicine list. Use an individual sick day plan where appropriate, and confirm when temporarily paused medicines should restart. The main safety message AKI is usually a complication of another problem rather than a diagnosis that ends the investigation. The immediate priorities are recognising severity, treating the cause, balancing fluid carefully and preventing potassium, acid, fluid and medicine complications. Reduced urine, pulmonary oedema, severe hyperkalaemia, uraemic symptoms and deterioration require urgent escalation. Recovery does not end at discharge because medication review and kidney follow up reduce future harm.

AKI is a rapid change in kidney function, not a diagnosis that explains its own cause. Safe care identifies the pre renal, intrinsic or obstructive process, balances fluid and medicines carefully, treats dangerous complications promptly and arranges follow up after apparent recovery.