6.4 Acute Kidney Injury & Renal Replacement Therapies

Acute Kidney Injury: Causes and Phases

Acute kidney injury (AKI) is an abrupt decline in kidney function, classified by location of the cause:

• Prerenal (about 55%): anything that decreases renal perfusion — hypovolemia, heart failure, sepsis, hypotension. The kidneys themselves are healthy; labs show a BUN-to-creatinine ratio above 20:1, low urine sodium, and concentrated urine. It reverses if perfusion is restored quickly.
• Intrarenal: direct parenchymal damage — acute tubular necrosis (ATN) from prolonged ischemia or nephrotoxins (aminoglycosides, amphotericin B, iodinated contrast, rhabdomyolysis pigments), plus glomerulonephritis and interstitial nephritis. Muddy brown granular casts on urinalysis point to ATN.
• Postrenal: obstruction of urine flow — benign prostatic hyperplasia, bilateral stones, strictures, tumors. A bladder scan and renal ultrasound identify it; relieving the obstruction (catheter, stent, nephrostomy) often restores function.

AKI classically moves through four phases. The onset (initiating) phase spans the insult until oliguria begins. The oliguric phase (urine output under 400 mL/day, lasting roughly 1 to 2 weeks) carries the highest mortality: expect hyperkalemia, fluid overload with hypertension and pulmonary edema, metabolic acidosis, and rising BUN and creatinine. The diuretic phase brings recovering tubular function with output of 1 to 3 liters (sometimes up to 5 liters) per day — the risk flips to dehydration, hypotension, and hypokalemia. The recovery (convalescent) phase may last up to a year, and some patients never regain full function.

Hyperkalemia (potassium above 5.0 mEq/L) is the most dangerous complication. Watch for peaked T waves, widened QRS, and prolonged PR interval on the ECG, plus muscle weakness. Treatment sequence: IV calcium gluconate first to stabilize the cardiac membrane (it does not lower potassium), then IV regular insulin with dextrose to shift potassium into cells, plus adjuncts like sodium bicarbonate or nebulized albuterol; potassium-removing binders (sodium polystyrene sulfonate, patiromer, sodium zirconium cyclosilicate) and dialysis definitively remove potassium from the body.

Chronic Kidney Disease: Stages and Complications

Chronic kidney disease (CKD) is irreversible, progressive loss of function staged by glomerular filtration rate (GFR):

Leading causes are diabetes and hypertension. Complications and their management:

• Anemia: failing kidneys produce less erythropoietin. Treat with erythropoiesis-stimulating agents (epoetin alfa) plus iron; current targets hold hemoglobin around 10 to 11.5 g/dL — full normalization increases cardiovascular risk.
• Renal osteodystrophy (CKD-MBD): the failing kidney retains phosphate and activates less vitamin D, so calcium falls and parathyroid hormone rises (secondary hyperparathyroidism), leaching calcium from bone. Give phosphate binders (calcium acetate, sevelamer) with meals, restrict dietary phosphorus, and use active vitamin D analogs.
• Hyperkalemia: restrict dietary potassium and avoid salt substitutes (potassium chloride).
• Fluid overload and hypertension: sodium and fluid restriction plus diuretics; cardiovascular disease is the leading cause of death in CKD.
• Uremic symptoms: nausea, pruritus, fatigue, pericarditis (friction rub), and encephalopathy signal the need for dialysis.

Diet teaching: limit sodium, potassium, and phosphorus; protein is moderated before dialysis (about 0.6 to 0.8 g/kg/day) but increased on dialysis (about 1.2 g/kg/day) to replace dialytic losses.

Hemodialysis and Vascular Access

Hemodialysis circulates blood through a dialyzer to remove solutes and fluid, typically three times weekly. Access options, in order of preference: arteriovenous (AV) fistula (best long-term patency, lowest infection risk — needs weeks to months to mature), AV graft, and tunneled central catheter (highest infection risk, last resort).

Access protection rules are heavily tested:

• Never take blood pressure, draw blood, or insert an IV in the access arm. Post signs and teach the patient.
• Palpate a thrill and auscultate a bruit every shift — their absence suggests thrombosis; notify the provider immediately.
• No tight clothing, jewelry, or restraints on the access arm; teach the patient to check the thrill daily and avoid sleeping on that arm.
• After dialysis, hold pressure on needle sites and assess for bleeding.

Intradialytic complications: hypotension is most common (rapid fluid removal — pause ultrafiltration, give a saline bolus per protocol, lower the head of the bed), muscle cramps, and dialysis disequilibrium syndrome (rapid solute shifts cause cerebral edema — headache, nausea, confusion; more common in new patients with very high BUN). Weigh the patient before and after treatment, and check whether antihypertensives should be held before dialysis.

Peritoneal Dialysis

Peritoneal dialysis (PD) uses the patient's peritoneum as the membrane: dialysate is instilled, dwells, and drains out as effluent, which should be clear and pale yellow. Cloudy effluent with fever, abdominal pain, and rebound tenderness signals peritonitis — the most common PD complication. Obtain a culture of the effluent, notify the provider, and anticipate antibiotics, often instilled into the dialysate; do not stop exchanges unless ordered.

Other essentials: use strict aseptic technique with a mask during exchanges, warm the dialysate (never in a microwave — use a warming device per facility), and compare outflow to inflow — retained fluid suggests outflow obstruction from constipation, catheter migration, or fibrin; repositioning and bowel regimens help. Monitor glucose because dextrose-based dialysate is absorbed, and check blood pressure and weight trends.

Indications for Dialysis: AEIOU

Emergent dialysis indications are remembered with the mnemonic AEIOU:

• A — Acidosis: severe metabolic acidosis refractory to medical management.
• E — Electrolytes: refractory hyperkalemia (especially with ECG changes).
• I — Ingestions/Intoxications: dialyzable toxins such as lithium, salicylates, methanol, ethylene glycol, and metformin-associated lactic acidosis.
• O — Overload: fluid overload with pulmonary edema unresponsive to diuretics.
• U — Uremia: symptomatic uremia — pericarditis, encephalopathy, uremic bleeding, intractable nausea.

Post-Transplant Basics

Kidney transplantation requires lifelong immunosuppression — typically a calcineurin inhibitor (tacrolimus or cyclosporine; monitor trough levels — both are nephrotoxic at high levels), an antiproliferative (mycophenolate), and corticosteroids. Teach that missing doses invites rejection. Rejection signs include fever, pain or tenderness over the graft, rising creatinine, decreasing urine output, weight gain, and flu-like symptoms — report immediately, because early treatment can save the graft. Infection risk is high: avoid live vaccines, practice meticulous hygiene, and avoid grapefruit, which raises calcineurin inhibitor levels.

Nephrotoxic Drug Awareness

Protect remaining renal function by recognizing nephrotoxins:

• NSAIDs — reduce renal perfusion via prostaglandin inhibition; avoid in CKD and AKI.
• Aminoglycosides (gentamicin) and vancomycin — dose by renal function and monitor trough levels.
• Amphotericin B — classic tubular toxin.
• Iodinated contrast — prehydrate with IV fluids, use the lowest dose, and hold metformin for about 48 hours after contrast to avoid lactic acidosis.
• ACE inhibitors/ARBs — helpful long-term for proteinuria but can worsen function during hypoperfusion and raise potassium.

Always check renal function before administering these agents, ensure adequate hydration, and question nephrotoxic orders in patients with rising creatinine.