3.2 Acute Kidney Injury, Chronic Kidney Disease & Electrolyte Imbalances
Key Takeaways
- Prerenal AKI is characterized by a BUN/Creatinine ratio > 20:1, Urine Osmolality > 500 mOsm/kg, and FENa < 1%.
- The most common cause of intrinsic AKI is Acute Tubular Necrosis (ATN), often showing muddy brown casts on urinalysis.
- Hyperkalemia management prioritizes cardiac membrane stabilization with IV calcium gluconate before initiating measures to shift or excrete potassium.
- Hyponatremia must be corrected slowly (limit < 8 mEq/L per 24 hours) to prevent osmotic demyelination syndrome.
- In Chronic Kidney Disease, secondary hyperparathyroidism develops due to phosphate retention and decreased synthesis of 1,25-dihydroxyvitamin D.
Acute Kidney Injury, Chronic Kidney Disease & Electrolyte Imbalances
Nephrology constitutes a cornerstone of clinical internal medicine on the SMLE. A solid mastery of acute kidney injury (AKI) differentiation, chronic kidney disease (CKD) staging and systemic complications, glomerulonephropathies, and emergency electrolyte management protocols is vital.
Acute Kidney Injury (AKI): Categorization & Diagnostic Metrics
AKI is defined by KDIGO criteria as an increase in serum creatinine by ≥0.3 mg/dL within 48 hours, an increase in serum creatinine to ≥1.5 times baseline within 7 days, or urine volume <0.5 mL/kg/h for 6 consecutive hours.
Prerenal, Intrinsic, and Postrenal AKI Differentiation
| Diagnostic Parameter | Prerenal Azotemia | Intrinsic AKI (ATN) | Postrenal Azotemia |
|---|---|---|---|
| Primary Pathophysiology | Hypoperfusion without structural parenchymal damage (hypovolemia, CHF, sepsis). | Direct parenchymal damage (ischemic or nephrotoxic ATN, AIN, Glomerulonephritis). | Urinary tract obstruction (BPH, stones, tumors, neurogenic bladder). |
| BUN / Serum Creatinine Ratio | > 20 : 1 (Enhanced urea reabsorption driven by aldosterone/ADH). | < 15 : 1 (Impaired tubular reabsorption of urea). | Variable (>20:1 early; <15:1 late). |
| Fractional Excretion of Na+ (FENa) | < 1% (Functional tubules conserve Na+ to restore volume). | > 2% (Damaged tubules lose ability to reabsorb Na+). | Variable (>2% late). |
| Urine Sodium (mEq/L) | < 20 mEq/L | > 40 mEq/L | > 40 mEq/L |
| Urine Osmolality | > 500 mOsm/kg (Concentrated urine). | < 350 mOsm/kg (Isosthenuria; loss of concentration ability). | < 350 mOsm/kg |
| Urinalysis Microscopy | Benign or Hyaline Casts. | Muddy Brown Granular Casts (ATN); WBC Casts/Eosinophils (AIN); RBC Casts (Glomerulonephritis). | Normal sediment or WBCs/RBCs/Crystals. |
| Diagnostic Test of Choice | Volume challenge (IV fluid trial). | Renal biopsy (if etiology unclear). | Renal Ultrasound (demonstrates Hydronephrosis). |
Glomerular Diseases: Nephrotic vs. Nephritic Syndromes
- Nephrotic Syndrome: Marked by severe proteinuria (>3.5 g/24 hours), Hypoalbuminemia (<3.0 g/dL), Generalized Edema (anasarca), and Hyperlipidemia / Lipiduria (Maltese cross fatty casts). Major complications: Hypercoagulability (loss of Antithrombin III in urine) leading to renal vein thrombosis, and increased infection risk (loss of immunoglobulins).
- Minimal Change Disease: Most common in children. Effacement of podocyte foot processes on Electron Microscopy (EM). Responds dramatically to corticosteroids.
- Focal Segmental Glomerulosclerosis (FSGS): Most common in adults of African descent, HIV patients, and IV drug users. Sclerosis in subset of glomeruli. Poor response to steroids; high rate of progression to ESRD.
- Membranous Nephropathy: Spike and dome appearance on silver stain; subepithelial immune complex deposits. Strongly associated with anti-PLA2R antibodies, solid organ malignancies, and HBV/HCV.
- Nephritic Syndrome: Marked by Hematuria (dysmorphic RBCs and RBC Casts), moderate proteinuria (<3 g/day), Hypertension, and Oliguria.
- Post-Streptococcal Glomerulonephritis (PSGN): 1-3 weeks after Group A Strep pharyngitis or impetigo. Low C3 complement, elevated ASO titers. Subepithelial "humps" on EM.
- IgA Nephropathy (Berger Disease): Most common cause of primary glomerulonephritis worldwide. Recurrent gross hematuria occurring concurrently (1-2 days) with an upper respiratory infection. Normal complement levels.
Chronic Kidney Disease (CKD) & Systemic Complications
CKD is defined as kidney damage or eGFR <60 mL/min/1.73m² for >3 months. Diabetes Mellitus is the leading cause, followed by Hypertension.
CKD Mineral and Bone Disorder (CKD-MBD)
- Pathophysiology: Decreased GFR leads to renal phosphate retention. Concurrently, damaged proximal tubular cells fail to express 1-alpha-hydroxylase, reducing synthesis of active vitamin D (1,25-dihydroxyvitamin D / Calcitriol).
- Hypocalcemia & Secondary Hyperparathyroidism: Low calcitriol impairs intestinal calcium absorption, producing hypocalcemia. Both hypocalcemia and hyperphosphatemia directly stimulate the parathyroid glands, producing Secondary Hyperparathyroidism.
- Renal Osteodystrophy: Chronically elevated PTH causes high-turnover bone disease (osteitis fibrosa cystica), releasing bone calcium at the expense of skeletal strength.
- Management: Dietary phosphate restriction, oral Phosphate Binders (Sevelamer [non-calcium], Calcium Acetate), and Active Vitamin D analogs (Calcitriol, Paricalcitol).
Anemia of CKD
- Primarily due to decreased renal Erythropoietin (EPO) synthesis by peritubular interstitial cells. Presents as a normocytic, normochromic anemia.
- Management: Rule out iron deficiency first (ensure Transferrin Saturation >20% and Ferritin >100 ng/mL), then initiate Erythropoiesis-Stimulating Agents (ESAs) (Epoetin alfa or Darbepoetin alfa). Target hemoglobin is 10.0–11.5 g/dL (avoiding >12 g/dL due to increased stroke and thrombosis risks).
Emergency Management of Electrolyte Imbalances
Hyperkalemia (Serum K+ > 5.0 mEq/L)
Life-threatening medical emergency. ECG changes progress: Peaked T waves → PR prolongation → QRS widening → Sine wave → Ventricular Fibrillation / Asystole.
Three-Step Resuscitation Protocol:
- Step 1: Cardiac Membrane Stabilization (Immediate Action):
- IV Calcium Gluconate (10 mL of 10% solution over 2-5 mins). Membrane stabilizer; does NOT lower serum K+. Acts within 1-3 minutes.
- Step 2: Intracellular Potassium Shift (Temporary Lowering):
- IV Regular Insulin (10 Units) + 50% Dextrose (50 mL): Shifts K+ into cells within 15-30 mins.
- Nebulized Albuterol (10-20 mg): Beta-2 agonist driving intracellular K+ shift.
- IV Sodium Bicarbonate: If severe metabolic acidosis is present.
- Step 3: Total Body Potassium Excretion (Definitive Lowering):
- Loop Diuretics (IV Furosemide): For volume-overloaded patients with functioning kidneys.
- GI Cation Exchangers: Sodium Polystyrene Sulfonate (Kayexalate), Patiromer, or Sodium Zirconium Cyclosilicate (SZC).
- Emergent Hemodialysis: Gold standard for severe, refractory hyperkalemia or end-stage renal disease.
Hyponatremia (Serum Na+ < 135 mEq/L)
- Symptomatic Severe Hyponatremia (Seizures, Coma, Confusion): Treat immediately with 3% Hypertonic Saline (100 mL IV bolus over 10 mins) to rapidly elevate serum Na+ by 4-6 mEq/L and abort cerebral edema.
- Correction Speed Limit: For chronic hyponatremia, the rate of correction MUST NOT exceed 8 mEq/L in 24 hours to prevent Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).
A 68-year-old man with a history of chronic kidney disease stage 4 presents for routine follow-up. He reports generalized fatigue and occasional pruritus. His current medications include lisinopril and amlodipine. Laboratory investigations reveal a serum creatinine of 3.2 mg/dL, BUN 45 mg/dL, serum calcium 7.8 mg/dL (normal 8.4-10.2), serum phosphorus 6.5 mg/dL (normal 2.5-4.5), and an intact parathyroid hormone (PTH) level of 450 pg/mL (normal 15-65). What is the primary pathophysiological mechanism underlying this patient's elevated PTH level?
A 55-year-old male is admitted to the hospital with severe crush injuries following a motor vehicle accident. On the third day of admission, his urine output drops to 300 mL over 24 hours. Laboratory results show a serum creatinine increase from 1.1 mg/dL on admission to 3.5 mg/dL. Serum BUN is 42 mg/dL. Urinalysis reveals 2+ blood on the dipstick but only 0-2 RBCs per high-power field on microscopic examination, along with muddy brown granular casts. The fractional excretion of sodium (FENa) is calculated at 2.5%. Which of the following is the most likely diagnosis?
A 72-year-old female with a history of heart failure and chronic kidney disease is brought to the emergency department by her family due to progressive profound weakness and confusion over the past 24 hours. An ECG is immediately performed in triage and demonstrates peaked T waves and a widened QRS complex. A rapid point-of-care chemistry panel reveals a serum potassium of 7.2 mEq/L. Which of the following interventions should be administered immediately?