Acute Kidney Injury

What happens when the kidneys fail?

Less waste is removed → toxic levels build up in blood, kidneys can’t regulate fluid/electrolytes/pH → fluid retention → edema → BP changes (often hypertension).

What happens to BUN and creatinine levels during kidney failure?

Both increase because kidneys are not filtering properly.

What does high creatinine indicate?

Poor kidney filtration / decreased GFR.

How can you roughly estimate decline in kidney function?

Initial creatinine ÷ current creatinine.

Why do kidneys require oxygen?

They need adequate oxygen to function; low O₂ causes tissue damage and worsens kidney disease.

How can kidney failure affect oxygen levels?

Fluid overload affects breathing + reduced EPO results in fewer RBCs → lower oxygen delivery.

Compare onset of AKI vs CKD.

AKI = sudden; CKD = gradual.

Reversibility of AKI vs CKD.

AKI reversible if treated early; CKD permanent/irreversible.

Common causes of AKI.

Shock, dehydration, nephrotoxins, obstruction.

Common causes of CKD.

Diabetes, hypertension, chronic infections.

GFR changes in AKI vs CKD.

AKI: may recover; CKD: continually declines over time.

What is Prerenal AKI?

Caused by reduced blood flow to kidneys (dehydration, low CO, hypotension, blood loss).

What happens in Prerenal AKI?

Low perfusion → ↓ GFR → can cause ischemic injury if untreated.

What is Intrinsic AKI?

Direct kidney tissue damage (ATN, infections, cystic disease, ischemia, nephrotoxins).

What happens in Intrinsic AKI?

Nephron destruction → ↓ filtration → ↑ BUN/creatinine.

What is Postrenal AKI?

Obstruction after the kidney (stones, BPH, neurogenic bladder).

What happens in Postrenal AKI?

Urine backs up → hydronephrosis → tissue damage → ↓ filtration.

What is Acute Tubular Necrosis (ATN)?

Death of tubular epithelial cells in renal tubules due to ischemia or toxins.

Causes of ACUTE TUBULAR NECROSIS?

1. Ischemia
2. Nephrotoxins
3. Obstruction in tubules

What happens in ATN?

Sloughed cells block tubules → obstruct flow → ↓ GFR → ↑ BUN/Cr → oliguria/anuria.

Is ATN reversible?

Yes, if treated early; prolonged ATN can cause chronic damage.

What is CKD?

Irreversible, progressive loss of kidney function lasting >3 months.

Why does CKD worsen over time?

Loss of nephrons causes remaining nephrons to overwork → hypertrophy → further damage.

Common causes of CKD?

Diabetes (most common), hypertension, atherosclerosis, polycystic kidney disease.

What is renal osteodystrophy?

Bone disease from low vitamin D activation → hypocalcemia → PTH release → bone breakdown.

What causes edema and hypertension in CKD?

Kidneys can't excrete sodium → Na and water retention → ↑ fluid volume.

Why does CKD cause hyperkalemia?

Kidneys can't excrete potassium.

Dangers of hyperkalemia?

Dysrhythmias, cardiac arrest, muscle weakness.

Why does CKD cause anemia?

Low erythropoietin (EPO) → ↓ RBC production.

Symptoms of CKD anemia?

Fatigue, pallor, dizziness, SOB.

Why does CKD cause bone problems?

Low vitamin D activation → ↓ Ca absorption → secondary hyperparathyroidism.

Why is metabolic acidosis common in CKD?

Kidneys can't excrete acid or reabsorb bicarbonate.

What is uremia?

Buildup of nitrogenous wastes → ↑ Cr and BUN → systemic symptoms.

What symptoms occur with uremia?

Headache, nausea, vomiting, metallic taste, anorexia, weakness.

Cardiovascular complications in CKD?

Hypertension, heart disease, dysrhythmias (from hyperkalemia).

GI manifestations of CKD?

Nausea, vomiting, halitosis, weight loss, anorexia, ulcers.

Why does CKD cause pruritus?

Urea crystals and mineral deposits accumulate in the skin.

Neurologic symptoms of advanced CKD?

Peripheral neuropathy, restless legs, confusion, seizures (uremic encephalopathy).

Why does CKD increase infection risk?

Suppressed immune function and decreased WBC activity.

Why does CKD increase bleeding risk?

Platelet dysfunction and decreased platelet count.

Why is hyperkalemia dangerous?

Can cause fatal cardiac arrhythmias.

What causes fluid retention in CKD?

Poor sodium/water excretion → edema → pulmonary congestion → hypertension.

Why does metabolic acidosis occur in CKD?

Kidneys can't excrete hydrogen ions or make bicarbonate.

Why does bone disease occur in CKD?

Phosphorus retention ↓ calcium → PTH release → bone breakdown.

Sodium restriction in CKD?

<2000 mg/day.

Why limit potassium in CKD?

To prevent dangerous hyperkalemia.

Why limit phosphorus?

To prevent bone damage and hyperphosphatemia.

Why is protein moderated?

Too much increases nitrogenous waste; too little causes muscle loss.

Why monitor albumin?

Low albumin → fluid shifts → edema.

Why use antihypertensives in CKD?

To protect kidneys and control BP.

Why use diuretics in CKD?

To decrease fluid overload.

Purpose of EPO therapy?

Treat anemia by increasing RBC production.

What is hemodialysis?

Blood is filtered through a machine and returned to the body; done 3x/week.

What is peritoneal dialysis?

Uses the peritoneal membrane to filter waste; performed at home.

What daily monitoring should CKD patients do?

Urine output, weight, BP.

When should CKD patients call the provider?

Sudden weight gain, swelling, low urine output, SOB.

Why is medication adherence crucial?

Prevents disease progression and complications.

Why is diet compliance important?

Helps control fluid, electrolytes, BP, and slows CKD progression.

what is normal gfr

90 or higher