Acute kidney injury (AKI) is a sudden fall in kidney function over hours to days, shown by a rise in serum creatinine and/or a drop in urine output. It is often reversible. Chronic kidney disease (CKD) is abnormal kidney structure or function present for more than 3 months, and it is usually progressive.
Causes of AKI
| Category | Mechanism | Examples |
|---|
| Prerenal (most common) | Reduced blood flow to the kidneys | Dehydration, hypovolemia, hemorrhage, heart failure, sepsis, shock; NSAIDs or ACE inhibitors/ARBs in a volume-depleted client |
| Intrarenal (intrinsic) | Damage to kidney tissue | Acute tubular necrosis (prolonged ischemia, nephrotoxins such as aminoglycosides, vancomycin, iodinated contrast), glomerulonephritis, lupus nephritis, interstitial nephritis, rhabdomyolysis |
| Postrenal | Obstruction to urine outflow | Stones, enlarged prostate, tumors, blocked catheter |
Prerenal AKI that is not corrected can progress to intrarenal damage.
Classic course of AKI (from acute tubular necrosis)
- Oliguric phase — urine output < 400 mL/day; retention of fluid, potassium, and waste → hyperkalemia, metabolic acidosis, fluid overload, uremia (some forms are non-oliguric)
- Diuretic phase — output rises (can be several liters/day) → risk of dehydration, hypokalemia, hyponatremia
- Recovery phase — function improves over weeks to months; some clients progress to CKD
Leading causes of CKD: diabetes and hypertension, then glomerulonephritis, polycystic kidney disease, chronic pyelonephritis/obstruction.
What failing kidneys stop doing explains CKD complications:
- Excreting water, sodium, potassium, acid, phosphate, and nitrogen wastes → fluid overload, hypertension, hyperkalemia, metabolic acidosis, uremia
- Producing erythropoietin → anemia
- Activating vitamin D → hypocalcemia, hyperphosphatemia, secondary hyperparathyroidism, bone disease (CKD-mineral and bone disorder)
- Clearing drugs → drug accumulation and toxicity
Fluid and cardiovascular
- Edema, weight gain, hypertension, crackles, jugular venous distension, dyspnea
- Or, in prerenal AKI: hypotension, tachycardia, dry mucous membranes
Hyperkalemia — muscle weakness, paresthesia, dysrhythmias; ECG: peaked T waves, prolonged PR, widened QRS, sine-wave pattern, ventricular fibrillation or asystole
Uremia (advanced disease)
- Neurologic: fatigue, decreased concentration, memory impairment, lethargy, asterixis, peripheral neuropathy, restless legs, seizures, coma
- GI: anorexia, nausea, vomiting, metallic taste, uremic (ammonia) breath
- Skin: pruritus, pallor, dry skin, easy bruising; uremic frost (rare, late)
- Uremic pericarditis — chest pain, pericardial friction rub
- Kussmaul respirations with metabolic acidosis
- Bleeding tendency (platelet dysfunction)
Anemia — fatigue, pallor, dyspnea on exertion
KDIGO AKI staging (use the higher stage met by either criterion)
| Stage | Serum creatinine | Urine output |
|---|
| 1 | 1.5–1.9 × baseline (known or presumed within the prior 7 days), or rise ≥ 0.3 mg/dL (≥ 26.5 µmol/L) within 48 h | < 0.5 mL/kg/h for 6–12 h |
| 2 | 2.0–2.9 × baseline | < 0.5 mL/kg/h for ≥ 12 h |
| 3 | ≥ 3.0 × baseline, or creatinine ≥ 4.0 mg/dL (≥ 353.6 µmol/L), or start of kidney replacement therapy | < 0.3 mL/kg/h for ≥ 24 h, or anuria ≥ 12 h |
CKD staging (KDIGO — by cause, GFR, and albuminuria)
| GFR category | eGFR (mL/min/1.73 m²) | Description |
|---|
| G1 | ≥ 90 | Normal or high (with kidney damage) |
| G2 | 60–89 | Mildly decreased |
| G3a | 45–59 | Mildly to moderately decreased |
| G3b | 30–44 | Moderately to severely decreased |
| G4 | 15–29 | Severely decreased |
| G5 | < 15 | Kidney failure |
Albuminuria categories (UACR): A1 < 30 mg/g (< 3 mg/mmol), A2 30–300 mg/g (3–30 mg/mmol), A3 > 300 mg/g (> 30 mg/mmol). eGFR is calculated with the race-free CKD-EPI 2021 equation; cystatin C can be added for confirmation.
Other tests
- Serum creatinine and BUN (normal creatinine about 0.6–1.2 mg/dL (53–106 µmol/L), BUN 7–20 mg/dL (2.5–7.1 mmol/L)); BUN:creatinine ratio > 20:1 suggests prerenal cause
- Potassium (normal 3.5–5.0 mEq/L, same in mmol/L), bicarbonate, calcium, phosphorus, PTH, CBC, iron studies
- Urinalysis and sediment (muddy brown casts in ATN), urine sodium
- Renal ultrasound — hydronephrosis (postrenal) and small kidneys (chronic disease)
- 12-lead ECG for hyperkalemia
AKI
- Treat the cause: restore volume in prerenal AKI; relieve obstruction (catheter, stent, nephrostomy) in postrenal AKI; stop nephrotoxins
- Diuretics are not given routinely — only for fluid overload, per prescription (they do not speed recovery and are ineffective in anuria)
- Adjust all drug doses to kidney function; avoid contrast when possible
- Kidney replacement therapy for refractory hyperkalemia, acidosis, fluid overload, or uremic complications (see Topic 54)
Emergency management of hyperkalemia (e.g., K⁺ ≥ 6.5 mEq/L or any level with ECG changes)
- Stabilize the heart: IV calcium gluconate (or calcium chloride via central line) — works in minutes, does not lower K⁺; continuous cardiac monitoring
- Shift K⁺ into cells: regular insulin IV with dextrose (monitor glucose for hypoglycemia for several hours); nebulized albuterol (tachycardia); sodium bicarbonate if acidotic
- Remove K⁺: loop diuretic (if making urine), potassium binders (sodium zirconium cyclosilicate — edema from sodium load; patiromer — hypomagnesemia, separate other oral drugs by 3 hours; sodium polystyrene sulfonate — risk of intestinal necrosis), or dialysis
CKD (KDIGO 2024 principles)
- Blood pressure control — ACE inhibitor or ARB for albuminuria (monitor K⁺ and creatinine; a rise in creatinine up to about 30% can be acceptable; contraindicated in pregnancy)
- SGLT2 inhibitors for CKD with type 2 diabetes when eGFR ≥ 20, and for many clients without diabetes with albuminuria or heart failure; once started, continue even if eGFR later falls below 20 (until dialysis) — a small early eGFR dip is expected. Adverse effects: genital infections, volume depletion, euglycemic DKA; hold during acute illness per sick-day rules
- Finerenone for type 2 diabetes with albuminuria — start only if K⁺ ≤ 4.8–5.0 mmol/L and eGFR ≥ 25; monitor for hyperkalemia; contraindicated with strong CYP3A4 inhibitors
- Statin for cardiovascular risk; glucose control in diabetes
- Anemia: iron (oral or IV) first when deficient, then erythropoiesis-stimulating agents (epoetin alfa, darbepoetin) — boxed warning: higher hemoglobin targets increase risk of stroke, thrombosis, and death; do not aim for normal hemoglobin; check BP (hypertension) and iron stores
- Mineral-bone disorder: phosphate binders taken with meals (calcium acetate — hypercalcemia; sevelamer, lanthanum — GI effects); active vitamin D; calcimimetics (cinacalcet — hypocalcemia)
- Metabolic acidosis: consider treatment (e.g., sodium bicarbonate) when serum bicarbonate < 18 mmol/L
- Drug safety: avoid NSAIDs; avoid magnesium- or aluminum-containing antacids and laxatives and sodium phosphate enemas; reduce metformin dose at eGFR 30–44 and stop below 30; renally dose antibiotics and other drugs
- Plan early for kidney replacement therapy or conservative care, and refer for transplant evaluation
Listed in priority order.
- Treat and monitor hyperkalemia — continuous ECG, report peaked T waves or arrhythmias; prepare calcium gluconate first when ECG changes are present, then insulin/dextrose; recheck K⁺ and glucose
- Manage fluid volume
- Daily weight (most accurate fluid indicator), strict intake and output, hourly output in critical AKI
- Assess edema, lung sounds, JVD, BP; observe for pulmonary edema
- Fluid restriction as prescribed (often previous 24-h output + about 500 mL for insensible loss in oliguria); sodium restriction
- In the diuretic phase, watch for dehydration and hypokalemia
- Monitor labs — creatinine, BUN, electrolytes, bicarbonate, hemoglobin, calcium, phosphorus
- Protect the kidneys — avoid nephrotoxins, check drug doses, ensure hydration before contrast when prescribed, monitor vancomycin/aminoglycoside levels
- Prevent infection (a leading cause of death in AKI) — aseptic technique, avoid unnecessary urinary catheters
- Safety for uremia — neurologic checks, seizure and fall precautions, bleeding precautions
- Skin and mouth care for pruritus and uremic breath; preserve arm veins (avoid venipuncture and IVs in the nondominant arm in CKD G4–G5 for possible future access, and avoid PICC lines — use a hand vein or a tunneled small-bore central line if needed)
- Diet (CKD not on dialysis)
- Sodium < 2 g/day
- Protein about 0.8 g/kg/day (avoid high-protein intake > 1.3 g/kg/day); higher protein is needed once on dialysis
- Potassium limits if hyperkalemic — high sources include bananas, oranges, potatoes, tomatoes, dried fruit, and salt substitutes (potassium chloride); leaching and boiling vegetables lowers potassium
- Phosphorus limits — dairy, cola drinks, processed foods with phosphate additives; take binders with meals
- Fluid limits as directed; ice chips, sugar-free gum or candy, and good mouth care help thirst
- Medication safety: no NSAIDs, herbal supplements, or over-the-counter antacids and laxatives without checking; tell every provider about kidney disease
- Monitor BP and weight at home; report weight gain, swelling, reduced urine, shortness of breath, palpitations, confusion
- Glucose control for diabetes; smoking cessation; vaccines (influenza, pneumococcal, hepatitis B)
- Discuss treatment choices early: hemodialysis, peritoneal dialysis, transplant, or conservative care
- Hyperkalemia with ECG changes — cardiac arrest risk
- Pulmonary edema from fluid overload
- Metabolic acidosis — Kussmaul breathing, low bicarbonate
- Uremic pericarditis (friction rub, chest pain) → cardiac tamponade (hypotension, muffled heart sounds, JVD, pulsus paradoxus)
- Uremic encephalopathy — confusion, seizures
- Anemia and cardiovascular disease — the leading cause of death in CKD
- GI bleeding; infection; calciphylaxis (painful skin necrosis) in advanced CKD-MBD
- Drug toxicity from reduced clearance
- AKI causes: prerenal (reduced perfusion — dehydration, hypovolemia, shock), intrarenal (ATN, nephrotoxins, GN, lupus), postrenal (obstruction)
- KDIGO AKI stage 1: creatinine ≥ 0.3 mg/dL rise in 48 h or 1.5× baseline, or urine < 0.5 mL/kg/h for 6 h
- CKD = abnormal kidney function > 3 months; G5 = eGFR < 15; staging includes albuminuria (A1–A3)
- Oliguric phase: hyperkalemia, acidosis, fluid overload; diuretic phase: dehydration and hypokalemia
- Hyperkalemia with ECG changes: calcium gluconate first (protects the heart), then insulin + dextrose (shift), then removal
- Diuretics are not routine in AKI — only for fluid overload per prescription
- Low erythropoietin → anemia; ESAs: do not target normal hemoglobin (stroke, thrombosis risk)
- CKD-MBD: high phosphorus, low calcium; binders with meals
- Uremia: decreased concentration and memory, pruritus, nausea, pericarditis
- Daily weight is the best fluid indicator; avoid NSAIDs; BP control slows progression
- Diet: sodium < 2 g/day, protein 0.8 g/kg/day before dialysis; limit potassium and phosphorus as needed
Country Notes
United States
- eGFR is reported using the race-free CKD-EPI 2021 equation; creatinine in mg/dL.
- Kidney failure treated with dialysis or transplant qualifies most clients for Medicare coverage regardless of age.
Philippines
- Creatinine is often reported in µmol/L (1 mg/dL ≈ 88.4 µmol/L) and BUN as urea in mmol/L — confirm units before staging.
- Diabetes, hypertension, and chronic glomerulonephritis are major causes of kidney failure; access to nephrology care and dialysis varies by region, so early detection and BP and glucose control in primary care are emphasized.
- Heat exposure and dehydration in outdoor workers, and unsupervised use of herbal products and NSAIDs, are practical AKI risks to ask about.