Disease States

This is where everything we’ve learned comes together. A urinalysis result isn’t just a list of numbers and names; it’s a pattern, a “liquid fingerprint” that points directly toward specific disease processes

As a laboratory scientist, you do not diagnose the patient. Your critical role is to perform an accurate analysis and recognize these classic patterns. You are the one who provides the physician with the objective data they need to make the right diagnosis

Let’s review the major disease states and the classic urinalysis profile you would expect to see for each

Glomerular Diseases

These diseases involve damage to the glomerulus, the kidney’s primary filter. The urinalysis picture changes depending on how the glomerulus is damaged

Nephrotic Syndrome

  • The Problem: The glomerular membrane is severely damaged, losing its negative charge and becoming highly permeable to large molecules, especially albumin
  • The Urinalysis “Fingerprint”
    • Physical: High specific gravity. Urine may appear “milky” or opalescent
    • Chemical: Massive Proteinuria (4+ or >3.5 g/day). This is the defining characteristic
    • Microscopic: The findings here are classic and pathognomonic:
      • Oval Fat Bodies: RTE cells that have absorbed lipids
      • Fatty Casts: Casts containing embedded fat droplets
      • Free Fat Globules: Often seen as “Maltese cross” formations under polarized light
  • The “Why”: The damaged glomerulus leaks huge amounts of protein. The liver tries to compensate by producing more proteins, including lipoproteins. These fats leak through the glomerulus, are absorbed by RTE cells (becoming oval fat bodies), and get trapped in casts

Acute Glomerulonephritis (Nephritic Syndrome)

  • The Problem: An inflammatory process in the glomerulus causes damage and allows blood cells and some protein to leak through. A classic example is post-streptococcal glomerulonephritis
  • The Urinalysis “Fingerprint”
    • Physical: Urine is often cloudy and red-brown or “coke-colored.”
    • Chemical: Hematuria (large) and moderate Proteinuria (1+ to 2+)
    • Microscopic
      • RBC Casts: This is the hallmark of glomerulonephritis. It proves the bleeding is from the kidney
      • Dysmorphic RBCs: Misshapen RBCs damaged from passing through the faulty filter
      • Numerous RBCs and WBCs
  • The “Why”: Inflammation creates breaks in the glomerular barrier large enough for cells to pass through. The RBCs that get trapped in the tubules form the tell-tale RBC casts

Tubular Diseases and Infections

These conditions involve the renal tubules and the interstitium (the tissue surrounding the tubules)

Acute Tubular Necrosis (ATN)

  • The Problem: The cells lining the renal tubules are dying, often due to lack of oxygen (ischemia) or exposure to toxins (drugs, heavy metals)
  • The Urinalysis “Fingerprint”
    • Chemical: Mild proteinuria, may see some blood
    • Microscopic
      • Renal Tubular Epithelial (RTE) Cells: Seen singly and in sheets
      • RTE Casts: The hallmark of severe, acute tubular damage
      • Coarse and fine granular casts (representing degenerating RTE casts)
  • The “Why”: The damaged tubules are literally sloughing their dying cells into the urine. Finding these cells and casts is a direct view of this destructive process

Pyelonephritis (Upper UTI / Kidney Infection)

  • The Problem: A bacterial infection has ascended from the bladder into the kidney tissue itself, causing inflammation within the tubules
  • The Urinalysis “Fingerprint”
    • Physical: Cloudy urine, often with a foul odor
    • Chemical: Positive Leukocyte Esterase, positive Nitrite, mild proteinuria, may see blood
    • Microscopic
      • WBC Casts: This is the key finding that differentiates a kidney infection from a bladder infection
      • Numerous WBCs (often in clumps) and bacteria
  • The “Why”: The infection and inflammation are inside the kidney. Therefore, WBCs get incorporated into the Tamm-Horsfall matrix within the tubules, forming casts

Cystitis (Lower UTI / Bladder Infection)

  • The Problem: A bacterial infection is confined to the bladder
  • The Urinalysis “Fingerprint”
    • Physical/Chemical: Same as pyelonephritis (cloudy, positive LE, positive Nitrite)
    • Microscopic: Numerous WBCs and bacteria. Crucially, NO casts are present.
  • The “Why”: The inflammation is only in the bladder, not in the renal tubules where casts are formed. The absence of casts is as significant as their presence

Metabolic Disorders

These systemic diseases manifest powerfully in the urine

Diabetes Mellitus

  • The Problem: High blood sugar (hyperglycemia) overwhelms the proximal tubule’s ability to reabsorb glucose. In severe, uncontrolled cases (ketoacidosis), the body resorts to burning fat for energy
  • The Urinalysis “Fingerprint”
    • Chemical: Positive Glucose. In diabetic ketoacidosis (DKA), you will also see strong positive Ketones
    • Physical: High specific gravity (due to dissolved glucose), pale color (due to polyuria)
    • Microscopic: Not specific, but yeast is a common finding, as it thrives in the sugary environment
  • The “Why”: Blood glucose exceeds the renal threshold (~180 mg/dL). Ketones are the acidic byproducts of fat metabolism

Diabetes Insipidus

  • The Problem: The body either doesn’t produce enough Antidiuretic Hormone (ADH) or the kidneys can’t respond to it
  • The Urinalysis “Fingerprint”
    • Physical: Very low Specific Gravity (<1.005) that remains low even if the patient is dehydrated. Pale/colorless urine and a large volume (polyuria)
    • Chemical/Microscopic: Otherwise unremarkable
  • The “Why”: Without ADH, the collecting ducts cannot reabsorb water. All the water from the filtrate is flushed out, resulting in a large volume of very dilute urine

Liver and Biliary Tract Disorders

The urinalysis provides a critical, non-invasive window into liver function by measuring bilirubin and urobilinogen

Liver Disease (e.g., Hepatitis, Cirrhosis)

  • The Problem: Damaged liver cells cannot properly process bilirubin and cannot clear urobilinogen from the portal circulation
  • The Urinalysis “Fingerprint”
    • Chemical: Positive Bilirubin and Increased Urobilinogen (normal is a low positive; this would be a high positive)
    • Microscopic: In severe liver failure, you may find leucine and tyrosine crystals

Biliary Obstruction (e.g., Gallstone, Tumor)

  • The Problem: A blockage prevents conjugated bilirubin from entering the intestines from the bile duct
  • The Urinalysis “Fingerprint”
    • Chemical: Strongly positive Bilirubin and Negative/Absent Urobilinogen
  • The “Why”: This pattern is pathognomonic. Conjugated bilirubin backs up from the obstructed bile duct into the blood and spills into the urine. Since no bilirubin reaches the intestine, no urobilinogen can be formed to be reabsorbed and excreted. This combination is a powerful clue

Putting It All Together: From Data to Diagnosis

This is the culmination of your training as a urinalysis expert. In this final step, you move beyond identifying individual elements to recognizing diagnostic patterns. A single result is just a clue; the combination of results is the “liquid fingerprint” of a disease

An isolated WBC count suggests inflammation, but when combined with a positive leukocyte esterase, nitrite, and crucially, WBC casts, it tells a specific story of pyelonephritis. Remove the casts from that picture, and the story changes to a bladder infection (cystitis). This one microscopic finding changes the entire clinical picture, diagnosis, and treatment plan

Is there massive proteinuria with oval fat bodies and fatty casts? You’re looking at nephrotic syndrome. Is it heavy hematuria with RBC casts and dysmorphic RBCs? That’s the classic profile of glomerulonephritis

Your role is to see these patterns, to connect the dots between the color, the chemicals, and the cells. By presenting this complete, cohesive picture, you transform a list of results into a powerful diagnostic tool, guiding the physician straight to the heart of the patient’s condition