Key Clinical Formulas & Scores
CrCl (mL/min) = [(140 - Age) ร Weight (kg)] / [72 ร Serum Creatinine]
ร 0.85 (if female)
Used for: drug dosing (vancomycin, aminoglycosides, DOACs), CKD staging
Limitations: overestimates in obesity, underestimates in elderly/muscle wasting
eGFR (mL/min/1.73mยฒ) = 175 ร (Scr)^(-1.154) ร (Age)^(-0.203)
ร (0.742 if female) ร (1.212 if African American)
CKD-EPI 2021: preferred equation (removes race coefficient)
Stages: G1 (โฅ90), G2 (60-89), G3a (45-59), G3b (30-44), G4 (15-29), G5 (<15)
FENa (%) = [(Urine Na ร Plasma Cr) / (Plasma Na ร Urine Cr)] ร 100
FENa <1%: prerenal (volume depletion, heart failure)
FENa >2%: intrinsic renal (ATN)
FENa 1-2%: indeterminate
Useful when patient on diuretics (then use FEurea instead)
FEurea (%) = [(Urine Urea ร Plasma Cr) / (Plasma Urea ร Urine Cr)] ร 100
FEurea <35%: prerenal
FEurea >50%: intrinsic renal (ATN)
More reliable than FENa when patient is on diuretics
Stage 1: SCr rise โฅ0.3 mg/dL within 48h OR 1.5-1.9 ร baseline OR UO <0.5 mL/kg/hr ร 6h
Stage 2: SCr 2.0-2.9 ร baseline OR UO <0.5 mL/kg/hr ร 12h
Stage 3: SCr โฅ3.0 ร baseline OR โฅ4.0 mg/dL OR RRT OR UO <0.3 mL/kg/hr ร 24h OR anuria ร 12h
CKD staging: GFR + albuminuria (A1 <30, A2 30-300, A3 >300 mg/g)
Core Concepts
Acute Kidney Injury (AKI)
Prerenal (most common, 60-70%): decreased renal perfusion (hypovolemia, heart failure, sepsis, renal artery stenosis). BUN/Cr ratio >20:1, FENa <1%, urine osmolality >500. Intrinsic: ATN (ischemic or nephrotoxic), glomerulonephritis, interstitial nephritis, thrombotic microangiopathy. Urine sediment: muddy brown granular casts (ATN), RBC casts (GN), WBC casts/eosinophils (AIN). Postrenal: obstruction (BPH, stones, malignancy, retroperitoneal fibrosis). Ultrasound: hydronephrosis. Treatment: address underlying cause, avoid nephrotoxins, fluid management, dialysis if indicated (AEIOU: Acidosis, Electrolyte, Intoxications, Overload, Uremia).
Chronic Kidney Disease (CKD)
Definition: eGFR <60 for โฅ3 months OR kidney damage (albuminuria, structural) for โฅ3 months. Etiologies: diabetes (most common), hypertension, glomerulonephritis, PKD. Complications: anemia (EPO deficiency โ treat with erythropoiesis-stimulating agents), CKD-MBD (hyperphosphatemia, hypocalcemia, elevated PTH โ treat with phosphate binders, calcitriol, cinacalcet), metabolic acidosis, hyperkalemia, CVD (leading cause of death). Progression: ACEi/ARB for renoprotection (especially with proteinuria), SGLT2 inhibitors (dapagliflozin, empagliflozin), blood pressure control (<130/80), HbA1c target ~7%.
Glomerular Diseases
Minimal change disease: nephrotic syndrome (proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia), normal LM, effacement on EM. Responds to corticosteroids. Membranous nephropathy: anti-PLA2R antibodies, subepithelial deposits. FSGS: segmental scarring, HIV/obesity-related. IgA nephropathy: most common GN worldwide, mesangial IgA deposits, gross hematuria after URI. Post-streptococcal GN: low C3, subepithelial humps, self-limited. Rapidly progressive GN: crescents on biopsy, treat aggressively.
Clinical Case Studies
Case 1: Prerenal AKI from Sepsis
Patient: 70-year-old male, urosepsis, BP 85/50, HR 110. Creatinine 2.8 (baseline 0.9). BUN/Cr = 28. Urine osmolality 520 mOsm/kg. FENa = 0.8%. Urine sediment: hyaline casts.
Diagnosis: Prerenal AKI (septic, hypovolemic). KDIGO Stage 2 (2.8/0.9 = 3.1x baseline).
Management: Aggressive IV fluid resuscitation (balanced crystalloids 30 mL/kg). Norepinephrine if MAP <65 after fluids. Broad-spectrum antibiotics within 1 hour. Avoid nephrotoxins (NSAIDs, aminoglycosides). Monitor urine output hourly, daily creatinine. Most prerenal AKI reverses within 48-72 hours if perfusion restored. If no recovery: renal ultrasound to exclude obstruction, consider ATN vs other intrinsic causes.
Case 2: Diabetic Nephropathy
Patient: 55-year-old male, type 2 diabetes ร 15 years, HbA1c 8.5%, hypertension, gradual creatinine rise over 2 years. eGFR 42 mL/min/1.73mยฒ. UACR 850 mg/g. Fundoscopy: diabetic retinopathy. No hematuria.
Diagnosis: Diabetic kidney disease โ CKD G3a A3.
Management: ACE inhibitor (lisinopril) or ARB (losartan) โ renoprotective independent of BP effect. SGLT2 inhibitor (dapagliflozin 10 mg daily) โ proven to slow CKD progression (DAPA-CKD trial). Blood pressure target <130/80 mmHg. Statin for CVD risk reduction. Nephrology referral for CKD management, preparation for renal transplant evaluation if progressing. Annual monitoring: eGFR, UACR, retinal exams, foot exams.
Case 3: Hyperkalemia Emergency
Patient: 65-year-old male, CKD stage 4, presents with muscle weakness, palpitations. K = 7.2 mEq/L. ECG: peaked T waves, widened QRS complex. Currently on lisinopril, spironolactone, and ibuprofen.
Diagnosis: Life-threatening hyperkalemia (K >6.5 with ECG changes).
Management: (1) Cardiac stabilization: IV calcium gluconate 1 g over 2-3 minutes (protects myocardium, works in minutes, lasts 30-60 min). (2) Shift K into cells: regular insulin 10 units IV + D50W 25g, albuterol nebulizer 10-20 mg, sodium bicarbonate if acidemic. (3) Remove K from body: sodium zirconium cyclosilicate or patiromer (chronic), furosemide if volume overloaded, dialysis if severe/refractory. Discontinue ACEi, spironolactone, NSAIDs. Long-term: dietary K restriction, loop diuretic, patiromer.
Practice Questions
A: CrCl = [(140-60) ร 70] / [72 ร 1.5] = 5600/108 = 51.9 mL/min. CKD stage G3a (eGFR 45-59).
A: FENa = [(15 ร 3.5) / (138 ร 120)] ร 100 = 52.5/16560 ร 100 = 0.32%. FENa <1% suggests prerenal etiology.
A: Diabetes mellitus (diabetic nephropathy) โ accounts for ~40-50% of ESRD cases. Hypertension is the second leading cause (~25-30%).
A: Minimal change disease (MCD). Normal light microscopy, negative immunofluorescence, diffuse podocyte foot process effacement on EM. Most common cause of nephrotic syndrome in children, responds well to corticosteroids.
A: ACE inhibitor or ARB (renoprotective independent of blood pressure lowering). Add SGLT2 inhibitor (dapagliflozin or empagliflozin) โ proven to reduce CKD progression and CV events (DAPA-CKD, EMPA-KIDNEY trials).