Section 8.1: Acute Kidney Injury & Chronic Kidney Disease

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1 Foundations - Biostatistics & Study Design

1.1 Study Designs & Clinical Trials 1.2 Hypothesis Testing & Statistical Significance 1.3 Measures of Association & Diagnostic Accuracy

2 Foundations - Epidemiology & Literature Interpretation

Section 2.1: Epidemiology & Risk Measures Section 2.2: Interpretation of Medical Literature & Ads Section 2.3: Preventive Medicine & Screening Guidelines

3 Foundations - Ethics & Communication

3.1 Medical Ethics & Patient Autonomy 3.2 Professionalism & Communication Skills 3.3 Legal Medicine & Informed Consent

4 Foundations - Patient Safety & Systems

Section 4.1: Patient Safety & Error Reduction Section 4.2: Quality Improvement & Systems-Based Practice Section 4.3: Healthcare Delivery Systems & Transitions of Care

5 Cardiovascular Management

5.1 Ischemic Heart Disease & Myocardial Infarction 5.2 Heart Failure & Cardiomyopathies 5.3 Arrhythmias & Conduction System Disorders 5.4 Vascular Diseases & Hypertension Management

6 Respiratory Management

Section 6.1: Obstructive Lung Diseases Section 6.2: Restrictive & Interstitial Lung Diseases Section 6.3: Infectious Pulmonary Diseases Section 6.4: Pulmonary Vascular & Pleural Diseases

7 Gastrointestinal & Hepatic Management

Esophageal & Gastric Disorders Intestinal & Colorectal Disorders Hepatic, Biliary, & Pancreatic Diseases Nutritional & Malabsorptive Syndromes

8 Renal, Urinary, & Endocrine Management

Section 8.1: Acute Kidney Injury & Chronic Kidney Disease Section 8.2: Fluid, Electrolyte, & Acid-Base Disorders Section 8.3: Diabetes Mellitus & Metabolic Syndrome Section 8.4: Thyroid, Adrenal, & Pituitary Disorders

9 Neurology, Special Senses, & Behavioral Health

9.1 Cerebrovascular Disease & Stroke 9.2 Neurodegenerative & Demyelinating Disorders 9.3 Psychiatric Emergencies & Substance Use Disorders 9.4 Common Mood, Anxiety, & Psychotic Disorders

10 Obstetrics & Gynecology

10.1 Antepartum Care & Pregnancy Complications 10.2 Intrapartum Management & Postpartum Care 10.3 Gynecology & Breast Disorders

11 Pediatrics, Human Development, & Multisystem Care

11.1 Normal Development & Childhood Immunizations 11.2 Common Pediatric & Neonatal Illnesses 11.3 Multisystem & Rheumatologic Diseases

12 Skin, Musculoskeletal, & CCS Case Management

Section 12.1: Common Dermatologic Presentations Section 12.2: Acute & Chronic Musculoskeletal Injuries Section 12.3: Computer-Based Case Simulations (CCS) Strategy

Section 8.1: Acute Kidney Injury & Chronic Kidney Disease

Key Takeaways Explain This Topic AI

AKI is staged by KDIGO criteria based on serum creatinine rise or urine output decline; Stage 3 represents a threefold rise in creatinine, creatinine ≥4.0 mg/dL, anuria for ≥12 hours, or RRT initiation.

Prerenal AKI presents with FeNa < 1% (or FeUrea < 35% with diuretics) and a BUN/Cr ratio > 20:1, while ATN shows muddy brown casts, FeNa > 2%, and a BUN/Cr ratio of 10-15:1.

Emergent hemodialysis indications (AEIOU) include refractory metabolic acidosis, severe hyperkalemia with ECG changes, toxic alcohol/lithium ingestion, refractory volume overload, and symptomatic uremia.

Anemia of CKD is managed with iron supplementation to target TSAT > 30% and ferritin > 500 ng/mL, followed by ESAs to target a hemoglobin of 10.0-11.0 g/dL.

CKD-mineral bone disorder management involves dietary phosphate restriction, phosphate binders (non-calcium preferred if hypercalcemic), active vitamin D, and calcimimetics like cinacalcet.

Last updated: July 2026

Acute Kidney Injury: Staging and Diagnostic Framework

Acute kidney injury (AKI) is a rapid decline in glomerular filtration rate resulting in nitrogenous waste accumulation. The KDIGO guidelines standardize AKI staging: Stage 1 is a serum creatinine (Cr) rise of 1.5–1.9 times baseline (or ≥0.3 mg/dL within 48 hours) or urine output (UO) <0.5 mL/kg/h for 6–12 hours. Stage 2 is a serum Cr increase of 2.0–2.9 times baseline or UO <0.5 mL/kg/h for ≥12 hours. Stage 3 is a serum Cr increase of ≥3.0 times baseline, a Cr increase to ≥4.0 mg/dL, initiation of renal replacement therapy (RRT), or UO <0.3 mL/kg/h for ≥24 hours (or anuria for ≥12 hours).

The diagnostic workup begins by categorizing AKI into prerenal, intrinsic, or postrenal etiologies.

Prerenal AKI arises from renal hypoperfusion without structural parenchymal damage. Key causes include hypovolemia (hemorrhage, GI losses), decreased effective circulating volume (heart failure, cirrhosis), and hemodynamically mediated impairment (NSAIDs constricting the afferent arteriole, or ACE inhibitors/ARBs dilating the efferent arteriole). Diagnostic indicators include a fractional excretion of sodium (FeNa) < 1%, a fractional excretion of urea (FeUrea) < 35% (highly useful in patients receiving loop diuretics), urine sodium < 20 mEq/L, high urine osmolarity (>500 mOsm/kg), and a Blood Urea Nitrogen (BUN) to creatinine ratio > 20:1. Urinalysis typically reveals benign hyaline casts. Management focuses on restoring renal perfusion via isotonic crystalloids, optimizing cardiac output, and discontinuing offending drugs.

Intrinsic AKI involves structural damage to the renal parenchyma, subclassified into tubular, interstitial, glomerular, or vascular diseases. Acute Tubular Necrosis (ATN) is the most common cause in hospitalized patients, precipitated by ischemic or toxic injuries. Exogenous nephrotoxins include aminoglycosides, cisplatin, amphotericin B, and radiocontrast media. Endogenous toxins include myoglobin from rhabdomyolysis. Laboratory findings in ATN show a FeNa > 2% (FeUrea > 50%), urine sodium > 40 mEq/L, urine osmolarity < 350 mOsm/kg, and a BUN to creatinine ratio of 10–15:1. Urinalysis characteristically reveals "muddy brown" granular casts. Treatment is supportive, focusing on fluid balance and avoiding nephrotoxins.

Acute Interstitial Nephritis (AIN) is an immunologically mediated inflammatory infiltration of the renal interstitium, typically drug-induced (beta-lactams, cephalosporins, sulfonamides, NSAIDs, proton pump inhibitors). The classic triad of fever, rash, and eosinophilia is rare. Urinalysis demonstrates sterile pyuria, white blood cell casts, and eosinophiluria. Management relies on drug discontinuation; systemic corticosteroids may be initiated if kidney function fails to improve within several days.

Glomerulonephritis presents with hematuria, dysmorphic red blood cells, RBC casts, variable proteinuria, and hypertension. Diagnostics require serological workup (complements, ANA, ANCA, anti-GBM) and renal biopsy.

Postrenal AKI results from mechanical obstruction of urine outflow (BPH, neurogenic bladder, bilateral nephrolithiasis, pelvic tumors). Renal ultrasound is the initial imaging of choice, demonstrating hydronephrosis. Management necessitates urgent decompression via Foley or suprapubic catheter for lower tract obstruction, and ureteral stents or percutaneous nephrostomy tubes for upper tract obstruction. Following relief of obstruction, clinicians must monitor for post-obstructive diuresis. Severe cases require replacing 50% of hourly urine output with 0.45% saline to avoid volume depletion.

Indications for Emergent Renal Replacement Therapy

In the acute setting, the decision to initiate emergent hemodialysis is guided by clinical and laboratory parameters, summarized by the "AEIOU" mnemonic:

Acidemia: Severe metabolic acidosis (pH < 7.1) refractory to medical therapy.

Electrolytes: Severe, refractory hyperkalemia (K > 6.5 mEq/L) or rising levels with associated ECG changes (peaked T waves, QRS widening).

Intoxication: Ingestion of dialyzable toxins (methanol, ethylene glycol, lithium, salicylates, theophylline).

Overload: Volume overload (pulmonary edema) refractory to high-dose diuretics.

Uremia: Symptomatic uremia (pericarditis, encephalopathy, neuropathy, or uremic bleeding due to platelet dysfunction).

Chronic Kidney Disease: Complications and Management

Chronic kidney disease (CKD) management focuses on slowing progression and treating complications. Anemia of CKD results from impaired erythropoietin production. Clinicians must first rule out and treat iron deficiency. Iron stores are assessed via transferrin saturation (TSAT) and serum ferritin; iron repletion is indicated if TSAT is ≤ 30% and ferritin is ≤ 500 ng/mL. Once iron is optimized, erythropoiesis-stimulating agents (ESAs) are initiated if hemoglobin (Hb) falls below 10 g/dL, targeting a range of 10.0–11.0 g/dL. Exceeding 11.0 g/dL increases the risk of stroke, venous thromboembolism, and cardiovascular events.

Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) pathophysiology begins with phosphate retention due to declining GFR. Hyperphosphatemia directly stimulates parathyroid hormone (PTH) secretion and binds free ionized calcium, causing hypocalcemia. Simultaneously, loss of renal mass impairs 1-alpha-hydroxylase activity, reducing active 1,25-dihydroxyvitamin D (calcitriol) and decreasing intestinal calcium absorption. The combination of hypocalcemia, hyperphosphatemia, and low calcitriol stimulates the parathyroid glands to hyper-secrete PTH, causing secondary hyperparathyroidism.

Treatment is stepwise: dietary phosphate restriction (800–1000 mg/day) and phosphate binders. Calcium-based binders (calcium acetate or calcium carbonate) are used if calcium is normal; non-calcium-based binders (sevelamer carbonate or lanthanum carbonate) are preferred if hypercalcemia or vascular calcification is present. Active vitamin D analogs (calcitriol, paricalcitol, doxercalciferol) are administered to suppress PTH once phosphate is controlled. Calcimimetics (cinacalcet) increase the sensitivity of parathyroid calcium-sensing receptors, reducing PTH without elevating calcium or phosphorus levels.