Urinalysis Master Diagnostic Algorithm
Introduction: The Underutilized Diagnostic Tool
Urinalysis remains one of the most powerful diagnostic tools in clinical medicine, yet is often ordered but not carefully interpreted. A methodical, stepwise approach to urinalysis—dipstick interpretation followed by microscopic analysis—reveals specific pathophysiologic processes occurring within the kidneys and urinary tract. This guide teaches pattern recognition for urinalysis as a diagnostic window into renal disease [1].
Urinalysis is not a screening test—it is a targeted diagnostic tool. The findings must be integrated with BMP, renal function, imaging, and serologic markers to construct a differential diagnosis.
Part 1: Dipstick Analysis
The Seven Key Dipstick Parameters
1. pH (4.5–8.0 normal)
| pH | Causes | Clinical Significance |
|---|---|---|
| Acidic (< 5.5) | Meat-based diet, metabolic acidosis, diarrhea | Favors uric acid stone formation |
| Neutral (6.5–7.0) | Mixed diet, normal | Normal range |
| Alkaline (> 7.5) | Vegetarian diet, UTI (urease-producing organisms), alkali therapy, respiratory alkalosis | Favors phosphate/calcium stone formation (triple phosphate) |
Clinical Pearl: Urine pH interpretation requires timing—pH changes rapidly if specimen sits at room temperature (bacteria consume acids, pH rises).
2. Specific Gravity (1.005–1.030)
| SG Value | Interpretation | Clinical Significance |
|---|---|---|
| 1.005–1.010 (Low) | Dilute urine | Polyuria, DI, overhydration, acute tubular necrosis |
| 1.010–1.020 (Normal) | Concentrated urine | Normal renal concentrating ability |
| > 1.020 (High) | Very concentrated urine | Prerenal azotemia, dehydration, SIADH, acute glomerulonephritis |
High SG with low osmolality is paradoxical and suggests presence of osmotically active particles: glucose (DM, Fanconi), protein (nephrotic syndrome), contrast (post-CT), lipids.
3. Protein (Dipstick: Negative–3+)
| Dipstick Result | Approximate Quantity | Pathophysiology |
|---|---|---|
| Negative | < 150 mg/day | Normal or excellent renal function |
| Trace–1+ | 150–300 mg/day | Borderline; quantify with UPCR or 24h collection |
| 2+ | 500 mg/day | Likely glomerular disease; warrants investigation |
| 3+ | 1,000 mg/day | Nephrotic-range proteinuria (> 3.5 g/day) |
| 4+ | > 1,000 mg/day | Massive proteinuria; almost always glomerular disease |
Dipstick Limitations: - Detects albumin best; misses immunoglobulin light chains, Bence Jones protein - False positives: concentrated urine, alkaline urine, blood contamination - False negatives: dilute urine, non-albumin proteinuria
Quantification Methods: - 24-hour urine protein (gold standard; cumbersome) - Spot urine protein-to-creatinine ratio (UPCR) (preferred; more convenient) - UPCR mg/g = (urine protein mg/dL / urine Cr mg/dL) × 100 - UPCR 100–300 mg/g = microalbuminuria (early diabetic/hypertensive disease) - UPCR > 300 mg/g = macroalbuminuria - UPCR > 3,500 mg/g = nephrotic-range
4. Blood on Dipstick (Negative–3+)
| Finding | Interpretation | Differential |
|---|---|---|
| Blood + RBCs on microscopy | True hematuria | Glomerular (casts, proteinuria), IgAN, ANCA, post-infectious, trauma, stones, malignancy |
| Blood + NO RBCs on microscopy | Hemoglobinuria (free Hb) | Intravascular hemolysis (malaria, PNH, severe burns) |
| Blood + NO RBCs + dark urine | Myoglobinuria | Rhabdomyolysis, severe myositis |
| Blood + lots of RBCs + casts | Glomerulonephritis | PSGN, IgAN, lupus, ANCA-associated |
The dipstick is exquisitely sensitive for blood (detects heme-containing compounds) but not specific (can detect Hb, myoglobin). Always confirm with microscopy. If blood 3+ but no RBCs on microscopy → think hemolysis or rhabdo.
5. Leukocyte Esterase (Negative or Positive)
| Result | Interpretation | Significance |
|---|---|---|
| Positive | WBCs present (from neutrophils) | UTI, pyelonephritis, acute interstitial nephritis, contamination |
| Negative | No WBCs or very few | Absence of pyuria; helps rule out UTI/AIN |
Limitations: False negatives if immunosuppressed (unable to mount WBC response); false positives from contamination.
6. Nitrites (Negative or Positive)
| Result | Interpretation |
|---|---|
| Positive | Gram-negative bacteria (E. coli, Klebsiella, Proteus); highly specific for UTI |
| Negative | Gram-positive bacteria, anaerobes, Pseudomonas (all nitrite-negative); does NOT rule out UTI |
Pearl: Positive leukocyte esterase + positive nitrites = high likelihood of bacterial UTI (~95%). Negative nitrites does NOT exclude UTI.
7. Glucose (Dipstick: Negative–4+)
| Finding | Threshold | Significance |
|---|---|---|
| Negative | < 5 mg/dL | Normal (renal threshold ~180 mg/dL plasma) |
| Positive (any grade) | > 5 mg/dL | Plasma glucose > renal threshold (160–180) OR abnormal proximal tubular reabsorption (Fanconi, SGLT2i) |
Additional Dipstick Parameters
| Parameter | Normal | Pathologic | Interpretation |
|---|---|---|---|
| Ketones | Negative | Positive | DKA, starvation ketosis, high-fat diet |
| Bilirubin | Negative | Positive | Bilirubinuria (conjugated bilirubin in urine); suggests liver disease/biliary obstruction |
| Urobilinogen | Trace–0.1 mg/dL | Elevated | Hemolysis, liver disease; absent in biliary obstruction |
Part 2: Microscopy Interpretation
Specimen Preparation and Quality
- Fresh urine only (< 2 hours old ideally)
- Centrifuged: 5 mL at 1,500 rpm × 5 min
- Low power (LPF, 10×): 10–15 fields for casts, crystals, large structures
- High power (HPF, 40×): 5–10 fields for cells, bacteria, small crystals
Casts: The “Renal Cell Express”
Golden Rule: Finding ANY casts in urine = casts came from kidneys (not contamination)
Cast Types and Pathophysiology
| Cast Type | Composition | Clinical Significance | Associated Findings |
|---|---|---|---|
| Hyaline | Tamm-Horsfall (uromodulin) only | Normal if < 2–3/LPF; increased in dehydration, fever, exercise, acidosis | Often asymptomatic |
| RBC | RBCs trapped in matrix | ALWAYS pathologic; glomerulonephritis | Hematuria, proteinuria, dysmorphic RBCs, acanthocytes |
| WBC | WBCs in matrix | Pyelonephritis, acute interstitial nephritis, lupus | Pyuria, bacteriuria, systemic symptoms |
| Muddy Brown/Granular | Cellular debris, degenerated organelles | Acute Tubular Necrosis (ATN); the “muddy brown” is pathognomonic | Acute rise in Cr, FeNa > 2%, muddy casts |
| Waxy/Broad | Uromodulin + proteinaceous material | Chronic kidney disease; indicates slowed urine flow/long tubular transit | Chronic Cr elevation, narrow casts also present |
| Fatty | Lipids, oval fat bodies (lipid-laden epithelial cells) | Nephrotic syndrome | Heavy proteinuria, hyperlipidemia, lipiduria |
| Crystalline | Specific crystal types (see table below) | Stone-forming tendency; Fanconi; toxic medication (sulfadiazine, ampicillin) | Acidic/alkaline pH, relevant medication history |
Cells and Cellular Elements
| Element | Normal | Pathologic | Interpretation |
|---|---|---|---|
| RBCs | 0–3/HPF | > 3/HPF = hematuria | Glomerular if dysmorphic/acanthocytes; non-glomerular if isomorphic |
| WBCs | 0–5/HPF (female); 0–2/HPF (male) | > 5/HPF = pyuria | UTI, pyelonephritis, AIN, lupus |
| Epithelial cells (renal tubular) | 0–1/HPF | > 2–3/HPF | Tubular injury (ATN, drug toxicity, reflux) |
| Epithelial cells (squamous) | Common (contamination) | Should be ignored if > 5–10/HPF | Vaginal/skin contamination; invalidates specimen |
| Bacteria | Absent | Present | UTI if symptomatic + nitrites/LE positive |
| Yeast | Absent | Rare | Vaginal candidiasis (female) or contamination |
| Trichomonads | Absent | Rare | Trichomoniasis (sexually transmitted) |
Dysmorphic RBCs (irregular shape, membrane protrusions) indicate glomerular origin; isomorphic RBCs (uniform, regular shapes) indicate non-glomerular hematuria (stones, tumors, trauma).
Crystals: Identifying Stone-Forming Tendency and Toxicity
| Crystal Type | pH | Associated Condition | Clinical Pearl |
|---|---|---|---|
| Calcium oxalate | Acidic | Hyperoxaluria, ethylene glycol toxicity | Envelope-shaped (diagnostic); elevated in ethylene glycol poisoning |
| Calcium phosphate/apatite | Alkaline | Normal variant, stone former | Appear as amorphous granules |
| Uric acid | Acidic | Gout, tumor lysis, dehydration | Rhomboid or needle-shaped; increase in acidosis |
| Struvite (magnesium ammonium phosphate) | Alkaline | UTI with urease producers (Proteus); chronic struvite stones | “Coffin-lid” shaped; always indicates infection |
| Cystine | Acidic | Cystinosis (rare inherited disorder); cystine stones | Pathognomonic hexagonal shape; strongly suggests cystinosis |
| Sulfonamide/Sulfadiazine | Variable | Drug-induced nephropathy (TMP-SMX, sulfadiazine) | Needle-shaped; associated with fever, rash (AIN) |
| Bilirubin | Any | Hemolysis, liver disease | Rare; biliary obstruction prevents bilirubin excretion |
| Myoglobin/Hemoglobin | Any | Rhabdomyolysis, hemolysis | Dark (tea-colored) urine; associated with hypokalemia |
Bacteria and Organisms
| Organism | Morphology | Associated Condition |
|---|---|---|
| Bacteria (rods) | Gram-negative coccobacilli | E. coli, Klebsiella, Proteus (UTI) |
| Cocci | Clusters or pairs | Staphylococcus, Streptococcus |
| Trichomonads | Motile, flagellate | Trichomoniasis |
| Yeast | Budding forms | Candidiasis (especially with glycosuria) |
| Sperm | Motile (fresh specimen) | Semen contamination |
Part 3: Systematic Diagnostic Algorithm
The Five-Question Diagnostic Cascade
URINALYSIS INTERPRETATION FLOWCHART
│
├─ Question 1: Is there HEMATURIA (RBCs > 3/HPF)?
│ ├─ YES → Is there PROTEINURIA and CASTS?
│ │ ├─ YES → GLOMERULONEPHRITIS (See Differential Table)
│ │ │ └─ Pattern: Dysmorphic RBCs, RBC casts, proteinuria
│ │ │ Differential: IgAN, post-infectious GN, lupus, ANCA
│ │ │
│ │ └─ NO → NON-GLOMERULAR HEMATURIA
│ │ └─ Pattern: Isomorphic RBCs, NO casts, no proteinuria
│ │ Differential: Stones, malignancy, trauma, benign hematuria
│ │
│ └─ NO
│
├─ Question 2: Is there PROTEINURIA (dipstick positive)?
│ ├─ Nephrotic range (> 3.5 g/24h)
│ │ ├─ Pattern: Heavy proteinuria, oval fat bodies, fatty casts, hypoalbuminemia
│ │ │ Differential: Minimal change, FSGS, membranous, diabetic
│ │ │
│ └─ Non-nephrotic (< 3.5 g/24h) with/without RBCs
│ └─ Differential: IgAN, secondary GN, CKD, hypertensive
│
├─ Question 3: Is there PYURIA (WBCs > 5/HPF)?
│ ├─ + Leukocyte esterase + Nitrites → BACTERIAL UTI
│ ├─ + Leukocyte esterase – Nitrites → Viral UTI or Sterile Pyuria
│ │ └─ Sterile pyuria differential: Tuberculosis, AIN, glomerulonephritis
│ │
│ └─ – Leukocyte esterase → Rule out UTI/AIN
│
├─ Question 4: Are there CASTS?
│ ├─ RBC or WBC casts → INTRINSIC RENAL DISEASE
│ ├─ Muddy brown casts → ACUTE TUBULAR NECROSIS (ATN)
│ ├─ Waxy/broad casts → CHRONIC KIDNEY DISEASE
│ └─ Hyaline casts alone → Usually benign (if < 2/LPF)
│
└─ Question 5: Are there CRYSTALS or UNUSUAL ELEMENTS?
├─ Calcium oxalate → Stone former, ethylene glycol toxicity
├─ Cystine → Cystinosis (rare)
├─ Sulfonamide → Drug-induced AIN (TMP-SMX, sulfadiazine)
└─ Myoglobin + dark urine → RhabdomyolysisDiagnostic Patterns by Clinical Scenario
Pattern 1: Acute Glomerulonephritis (AGN)
| Finding | Significance |
|---|---|
| RBC casts | Hallmark finding; proves glomerular origin |
| Dysmorphic RBCs | Indicates glomerular damage |
| Proteinuria | Often 2–3+ (can be nephrotic; 5–10 g/day) |
| RBC count | Moderate to numerous |
| WBC casts or RBC casts | Variable |
| Hyaline casts | Often present |
Associated BMP findings: ↑ Cr, ↓ GFR, ↑ K (if severe oliguria), hypervolemia
Differential by serologies/clinical context: - Post-infectious GN: Young, recent infection (throat, skin), complement low - IgA nephropathy: Recurrent hematuria, IgA dominant on biopsy - ANCA-associated: Systemic symptoms, ANCA positive - Lupus: Systemic symptoms, ANA/anti-dsDNA positive
Pattern 2: Nephrotic Syndrome
| Finding | Significance |
|---|---|
| Heavy proteinuria | 3+–4+ dipstick (> 3.5 g/24h) |
| Oval fat bodies | Lipid-laden tubular epithelium; pathognomonic |
| Fatty casts | Lipid-containing casts |
| No RBC casts | Distinguishes from membranoproliferative GN |
| Hyaline casts | Often numerous |
| Minimal hematuria | < 5 RBCs/HPF (absent or trace blood) |
Associated findings: Hypoalbuminemia, hyperlipidemia, edema, heavy proteinuria on quantification
Differential: - Minimal change disease: Young, sudden onset, excellent prognosis - Focal segmental glomerulosclerosis (FSGS): Partially responsive to steroids; worse prognosis - Membranous nephropathy: Older, anti-PLA2R antibodies, insidious onset - Diabetic nephropathy: Long DM history, concurrent diabetic retinopathy, proteinuria without RBCs
Pattern 3: Acute Tubular Necrosis (ATN)
| Finding | Significance |
|---|---|
| Muddy brown/dark granular casts | Pathognomonic for ATN |
| Renal tubular epithelial (RTE) cells | From desquamated tubules |
| RTE cell casts | Desquamated cells in casts |
| Coarse granular casts | Debris from necrotic tubules |
| Minimal or absent RBCs | Unlike glomerular disease |
| Minimal proteinuria | < 1+ dipstick (< 500 mg/day) |
| High urine osmolality | Often > 400 (kidney trying to concentrate) |
Associated findings: Acute rise in Cr, oliguria, FeNa > 2%, “dirty” urine appearance
Causes: Ischemia (shock, sepsis), nephrotoxins (aminoglycosides, contrast, NSAIDs with volume depletion), rhabdomyolysis
Pattern 4: Pyelonephritis
| Finding | Significance |
|---|---|
| Pyuria | WBCs > 5/HPF, often numerous |
| WBC casts | Pathognomonic if present; casts from collecting duct |
| Bacteria | Rods (gram-negative) most common |
| Nitrites | Positive if gram-negative organism |
| Leukocyte esterase | Positive |
| Proteinuria | Usually trace–1+ (< 500 mg/day) |
| Hematuria | Trace to 1+ (microscopic) |
Associated findings: Fever, flank pain, CVA tenderness, elevated WBC, elevated CRP/ESR
Pattern 5: Acute Interstitial Nephritis (AIN)
| Finding | Significance |
|---|---|
| Sterile pyuria | WBCs without bacteria; LE positive, nitrites negative |
| WBC casts | If present, confirms renal involvement |
| RTE cells | Tubular epithelial shedding |
| Eosinophiluria | (Special stain: Hansel stain); suggests drug-induced |
| Proteinuria | Usually mild (trace–1+); nephrotic is unusual |
| Minimal hematuria | May be absent or trace |
| Normal or mildly elevated casts | Hyaline predominant |
Associated findings: Acute Cr rise (often > 50% increase), fever, rash (if drug), recent NSAID/antibiotic use
Causes: NSAIDs, β-lactams (PCN, cephalosporins), diuretics, PTIs (omeprazole), anticonvulsants
Pattern 6: Chronic Kidney Disease (CKD)
| Finding | Significance |
|---|---|
| Waxy/broad casts | Indicate slowed urine flow; advanced CKD |
| Granular casts | Fine or coarse; reflect chronic tubular atrophy |
| Mild proteinuria | Usually < 1+ (< 1 g/day), unless secondary cause |
| Minimal hematuria | Absent or trace; may be present in FSGS/IgAN |
| Minimal or absent RBC casts | Unlike active glomerulonephritis |
| Hypocellular sediment | Few cells overall |
Associated findings: Chronic Cr elevation, small kidneys on imaging, anemia (CKD-related)
Urine Electrolytes and Functional Indices
Urine Sodium (UNa) and Chloride (UCl)
| Finding | Interpretation | Clinical Significance |
|---|---|---|
| UNa < 10–20 mEq/L | Sodium avid | Pre-renal azotemia, hepatic encephalopathy, heart failure |
| UNa > 40 mEq/L | Sodium wasting | Intrinsic renal disease, diuretic use, advanced CKD |
| UCl < 10 mEq/L | Chloride-responsive alkalosis | Vomiting, NG suction (volume depletion) |
| UCl > 10 mEq/L | Chloride-resistant alkalosis | Primary hyperaldosteronism, diuretic use |
Fractional Excretion of Sodium (FeNa)
$$FeNa = \frac{(UNa × Plasma Cr)}{(Plasma Na × Urine Cr)} × 100$$
| FeNa | Interpretation | AKI Type |
|---|---|---|
| < 1% | Sodium avid; intact tubular function | Pre-renal azotemia (volume depletion, shock, heart failure) |
| > 2% | Sodium wasting; tubular dysfunction | Intrinsic renal disease (ATN, GN, AIN, contrast nephropathy) |
| 1–2% | Gray zone; clinical judgment required | Early ATN or severe pre-renal |
FeNa < 1% in oliguria strongly suggests pre-renal; FeNa > 2% suggests intrinsic disease. However, FeNa can be falsely low in heart failure/cirrhosis and falsely high in elderly/CKD. Clinical context is paramount.
Urine Osmolality (Uosm)
| Uosm | Interpretation | Significance |
|---|---|---|
| > 500 mOsm/kg | Concentrated urine | Intact renal concentrating ability; pre-renal pattern |
| 250–500 mOsm/kg | Moderately concentrated | Intermediate; assess clinical context |
| < 300 mOsm/kg | Dilute urine | Loss of concentrating ability; intrinsic disease, DI, overhydration |
Urine Anion Gap (UAG) [2]
UAG = (UNa + UK) − UCl
| UAG | Interpretation | Differential |
|---|---|---|
| Negative (< 0) | GI bicarbonate loss | Diarrhea (especially small bowel) → appropriate renal acidification |
| Positive (> 0) | Renal tubular dysfunction | RTA (Type 1, 2, 4); reduced GFR; kidney cannot acidify urine |
Clinical use: Differentiates causes of non-gap metabolic acidosis
Board-Level Clinical Vignettes
Vignette 1: Hematuria with Casts
A 24-year-old male college athlete presents with dark urine × 2 days post-streptococcal pharyngitis. Dipstick: 3+ blood, 2+ protein. Microscopy: Numerous dysmorphic RBCs, RBC casts, WBC casts, no bacteria.
Diagnosis: Post-infectious glomerulonephritis (PSGN)
Key findings: RBC casts (pathognomonic for GN) + dysmorphic RBCs + proteinuria + recent infection
Next steps: Serologies (ASO titer, strep Ag), complement levels (C3 often low), renal ultrasound, possibly biopsy if atypical presentation
Prognosis: Excellent in children/young adults; most recover spontaneously; dialysis if severe oliguria
Vignette 2: Heavy Proteinuria with Oval Fat Bodies
A 38-year-old woman with 2-week history of leg swelling and dark urine. Dipstick: 4+ protein. Microscopy: Numerous oval fat bodies, fatty casts, rare RBCs (< 1/HPF), no casts except fatty.
Diagnosis: Nephrotic syndrome
Likely etiology: Membranous nephropathy (most common in adults), minimal change (if young/sudden), FSGS (if African American or progressive)
Supporting findings to order: - Serum albumin (expect < 3.5 g/dL) - Lipid panel (expect elevated cholesterol/triglycerides) - 24-hour urine protein (should be > 3.5 g) - Renal ultrasound (normal-sized kidneys rule out advanced CKD) - Serologies: ANA, anti-PLA2R (membranous marker), hepatitis B/C, malignancy screening
Next: Kidney biopsy to establish diagnosis and prognosis
Vignette 3: Muddy Brown Casts in Oliguria
A 52-year-old male post-major surgery (day 1 post-op) with oliguria (urine output 200 mL/12h). Dipstick: Trace protein, trace blood. Microscopy: Numerous muddy brown granular casts, RTE cells, minimal RBCs, no bacteria.
Diagnosis: Acute tubular necrosis (ATN) — ischemic type
Mechanism: Perioperative hypotension + major surgical stress → ischemia to renal tubules
Confirm with: FeNa > 2%, urine osmolality < 400, rapid Cr rise
Management: 1. Aggressive IV hydration with normal saline (restore perfusion) 2. Avoid nephrotoxins (NSAIDs, ACE-I, aminoglycosides) 3. Monitor K, Mg, PO4 (hyperkalemia risk with oliguria) 4. Prepare for dialysis if refractory hyperkalemia, pulmonary edema, or severe acidosis 5. Most ATN improves within 5–7 days; trend urine output, daily weights
Poor prognostic sign: Ongoing muddy casts at day 3–5 post-op indicates severe injury
Vignette 4: Sterile Pyuria Post-Antibiotic
A 68-year-old female post-TMP-SMX for UTI (started 2 weeks ago) presents with fever, rash, acute Cr rise from 1.0 to 2.1. Dipstick: 1+ protein, trace blood, LE positive, nitrites negative. Microscopy: WBCs 15/HPF (no bacteria), occasional RTE cells, hyaline casts, no RBC casts.
Diagnosis: Acute interstitial nephritis (AIN) — drug-induced (TMP-SMX)
Classic triad: Fever + rash + acute kidney injury post-drug exposure
Confirm with: - Urine eosinophils (Hansel stain; eosinophiluria suggests drug-induced) - Absence of RBC casts (distinguishes from GN) - Peripheral eosinophilia (not always present) - Renal ultrasound (may show interstitial edema)
Management: 1. Immediately stop TMP-SMX (causative agent) 2. Supportive care, hydration 3. Corticosteroids if severe (prednisone 1 mg/kg/day × 3 days, taper over 2–4 weeks); benefit greatest if started early 4. Monitor Cr daily; most improve within 5–7 days after drug discontinuation 5. Avoid NSAIDs, ACE-I (further stress kidney)
Vignette 5: Cystine Crystals in Asymptomatic Adolescent
A 16-year-old male routine physical. Dipstick: Negative. Microscopy: Several pathognomonic hexagonal cystine crystals, otherwise negative findings.
Diagnosis: Cystinosis — autosomal recessive disorder of cystine transport
Significance: Cystine crystals = diagnostic for cystinosis; patient likely has progressive renal disease ahead
Next steps: 1. Check plasma cystine (elevated confirms cystinosis) 2. Slit-lamp examination for corneal cystine deposition 3. Referral to genetics and nephrology 4. Consider cysteamine therapy (chelating agent) to reduce intracellular cystine 5. Monitor for other manifestations: growth retardation, photophobia, hypothyroidism, ESRD by adolescence/early adulthood
Integration with BMP and Renal Function
Complete Picture: Urinalysis + BMP + Renal Function
| Clinical Scenario | UA Pattern | BMP Pattern | GFR/Cr | Diagnosis |
|---|---|---|---|---|
| Acute GN | RBC casts, dysmorphic RBCs, 2+ protein | Normal K initially; ↑ Cr if severe | Acute ↓ GFR | Post-infectious or primary GN |
| Nephrotic syndrome | Heavy proteinuria, oval fat bodies | ↓ Albumin, ↓ Ca, ↑ lipids | Normal–mildly ↓ | FSGS, membranous, minimal change |
| ATN (ischemic) | Muddy brown casts, RTE cells, trace protein | ↑ K, ↑ PO4, ↑ BUN/Cr ratio | Rapidly ↑ (doubling) | Post-shock, post-op, sepsis |
| Pre-renal azotemia | Concentrated urine, hyaline casts | Normal electrolytes, ↑ BUN/Cr ratio | Mildly ↑ | Volume depletion, heart failure, sepsis |
| AIN | Sterile pyuria, WBC casts, ±eosinophils | Normal electrolytes | Acute ↑ | Recent drug exposure |
| Chronic GN/CKD | Waxy casts, mild proteinuria | Chronic ↑ K, ↑ PO4, ↑ PTH (if severe) | Chronically ↓ | IgAN, FSGS, hypertensive, diabetic |
References
[1] Simerville JA, Maxted WC, Pahira JJ. “Urinalysis: a comprehensive review.” American Family Physician. 2005 Mar 15;71(6):1153-62. PubMed
[2] Fogazzi GB, Makarova E, Rampani L, et al. “Urinary microscopy as seen by nephrologists.” Clinical Chemistry and Laboratory Medicine. 1998 Dec;36(12):975-978. doi: 10.1515/cclm.1998.172 PubMed
[3] Perazella MA. “The diagnostic utility of urinary sediment examination in acute kidney injury: a brief review.” Clinical Journal of the American Society of Nephrology. 2008 Nov;3(6):1615-1619. doi: 10.2215/CJN.04640808 PubMed
[4] Berend K, de Vries AP, Gans RO. “Physiological approach to assessment of acid-base disturbances.” New England Journal of Medicine. 2014 Sep 4;371(10):932-943. doi: 10.1056/NEJMra1003327 PubMed