🧠 Interpreting Renal Function Tests:

Renal function tests aren’t just numbers — they’re clues. When interpreted thoughtfully, they can help us distinguish between dehydration, intrinsic renal disease, and post-renal obstruction.  In this post, you’ll meet patients like Tom, who presents with dehydration and rising creatinine; Aisha, whose frothy urine holds a glomerular secret; and Leo, whose “normal” labs conceal a chronic decline — all to help you decode renal results with clinical confidence. 

We’ll explore how to interpret renal function tests and urinalysis through a clinical reasoning lens — breaking down key blood and urine markers, comparing patterns across different types of kidney injury, and working through real-world cases to bring the concepts to life.

🔍 Serum Creatinine: More than just a number

Creatinine is a byproduct of muscle metabolism, excreted almost entirely by the kidneys. It’s often the first marker students latch onto — but it’s also one of the most misunderstood.

• Normal range: ~60–110 µmol/L

• Elevated? Think impaired filtration — but remember, it’s influenced by muscle mass

• High creatinine doesn’t always mean kidney failure. A 25-year-old bodybuilder with a creatinine of 120 µmol/L may be perfectly normal. A frail 80-year-old with a creatinine of 90 µmol/L might be in acute kidney injury (AKI).
• Think about baseline. Always ask: is this new? Is it trending up?
• Consider muscle mass, hydration, and medications. Trimethoprim (an antibiotic), for example, can raise creatinine without affecting GFR

🧠 Clinical reasoning tip: If creatinine has doubled from baseline, GFR has likely halved — even if the absolute number is still within the “normal” range.

💧 Urea: The dehydration clue

Urea is produced in the liver from protein metabolism and excreted by the kidneys. But unlike creatinine, it’s reabsorbed in the tubules — especially when the body is trying to conserve water.

• Normal: ~2.5–7.1 mmol/L
• Elevated? Could be dehydration, high protein intake, or renal dysfunction.
• High urea with relatively normal creatinine? Think pre-renal causes like dehydration, GI bleeding, or high protein intake.
• Low urea? Consider liver dysfunction or low protein states.

🧠 Clinical reasoning tip: A disproportionately high urea-to-creatinine ratio (>100:1 in SI units) suggests pre-renal azotaemia. A low ratio may point to intrinsic renal damage or liver disease

🧪 eGFR: A Calculated Estimate, Not Gospel

eGFR is derived from creatinine, age, sex, and body size. It’s useful for staging chronic kidney disease (CKD), but it has limitations.

• Above 90: Normal
• 60–89: Mild reduction
• Below 60: Consider chronic kidney disease
• Not reliable in pregnancy, extremes of body habitus, or rapidly changing renal function.
• Always interpret alongside clinical context and urinalysis.

🧠 Clinical reasoning tip: eGFR is best used for chronic kidney function. In AKI, it can be misleading.

⚡ Electrolytes: The Kidney’s Report Card

• Potassium: Elevated in AKI or CKD due to reduced excretion. Also watch for medications (e.g. ACE inhibitors, spironolactone).
• Sodium: Can be low in fluid overload (e.g. heart failure) or high in dehydration.
• Bicarbonate: Low in metabolic acidosis — a hallmark of advanced CKD or AKI with tubular dysfunction.

🧠 Clinical reasoning tip: A falling bicarbonate with rising potassium and urea may indicate worsening renal function or a mixed acid-base disorder.

💧 Urinalysis: A Window into the Nephrons

Urinalysis is more than a dipstick — it’s a rapid, low-cost tool that can reveal infection, glomerular disease, metabolic derangements, and more. But like all tests, it’s only useful when interpreted alongside the clinical picture.

More great details here https://litfl.com/dipstick-urinalysis/ 

🔍 Step 1: Physical Examination of Urine

• Colour
• Pale yellow: Well hydrated
• Dark amber: Dehydration
• Red/brown: Haematuria, myoglobinuria, or beetroot ingestion
• Milky/cloudy: Infection, chyluria, or crystals

• Clarity
• Clear: Normal
• Cloudy: Pyuria, crystals, or contamination
• Odour
• Sweet: Ketones (e.g. DKA)
• Foul: Infection (especially with urea-splitting organisms)

🧠 Clinical reasoning tip: A patient with dark, frothy urine and oedema? Think nephrotic syndrome — proteinuria is the likely culprit.

🧪 Step 2: Dipstick Chemistry — What Each Parameter Tells You

Parameter	What It Detects	Clinical Reasoning
Protein	Albuminuria	Persistent proteinuria suggests glomerular disease. Trace can be normal post-exercise or febrile illness.
Blood	Haematuria or myoglobin	Microscopic haematuria may be benign (e.g. exercise) or serious (e.g. malignancy, GN). Myoglobinuria in rhabdomyolysis.
Leukocytes	Pyuria	Suggests inflammation or infection. False positives with contamination.
Nitrites	Bacterial conversion of nitrates	Positive = likely UTI with Gram-negative organisms. Negative doesn’t rule it out.
Glucose	Glycosuria	Diabetes mellitus, stress hyperglycaemia, or proximal tubule dysfunction (Fanconi syndrome).
Ketones	Fat metabolism	DKA, starvation, low-carb diets.
pH	Acid-base status	Acidic in metabolic acidosis; alkaline in UTIs with Proteus or Klebsiella.
Specific Gravity	Concentrating ability	High = dehydration; low = impaired concentrating ability (e.g. diabetes insipidus).

🧠 Clinical reasoning tip: Positive nitrites + leukocytes = UTI likely. But if only leukocytes are present, consider sterile pyuria (e.g. chlamydia, TB, interstitial nephritis).

🔬 Step 3: Microscopy (if available)

• Casts
• Hyaline: Often normal
• RBC casts: Glomerulonephritis
• WBC casts: Pyelonephritis or interstitial nephritis
• Granular or muddy brown: Acute tubular necrosis
• Crystals
• Calcium oxalate: Common, may be normal
• Uric acid: Gout, tumour lysis
• Triple phosphate: Alkaline urine, UTI with urea-splitting organisms
• Cells
• RBCs: Glomerular vs non-glomerular haematuria
• WBCs: Infection or inflammation
• Epithelial cells:   Contamination or tubular injury

🧠 Clinical reasoning tip: RBC casts = glomerular origin. Free RBCs without casts? Think lower tract source (e.g. bladder, ureter).

🧩 Case-Based Reasoning

🧑‍⚕️ Case 1: Tom, 68 — Vomiting and Poor Oral Intake

Presentation:

• 3-day history of nausea, vomiting, and reduced fluid intake
• Dry mucous membranes, postural hypotension

Bloods:

• Creatinine: 145 µmol/L (baseline 90)
• Urea: 18 mmol/L
• Na⁺: 148 mmol/L
• K⁺: 4.8 mmol/L
• Bicarb: 28 mmol/L

Urinalysis:

• Colour: Dark amber
• Specific gravity: 1.030
• Protein: Negative
• Blood: Negative
• Ketones: +
• Nitrites/Leukocytes: Negative

  Why the results look this way:

Tom’s presentation is classic for pre-renal acute kidney injury — where there’s no intrinsic kidney damage, but renal perfusion is reduced due to volume depletion. The high urea reflects increased reabsorption in the proximal tubule as the kidneys try to conserve water. Creatinine is also elevated, but less so, leading to a high urea-to-creatinine ratio — a hallmark of pre-renal states. The hypernatraemia and elevated specific gravity show that his kidneys are responding appropriately by concentrating urine to retain fluid. Ketones indicate catabolism from poor intake, adding a metabolic clue to the clinical picture.

Interpretation

This is a classic pre-renal AKI picture. The high urea:creatinine ratio, hypernatraemia, and concentrated urine (high specific gravity) all point to dehydration. The presence of ketones suggests a catabolic state from prolonged fasting.

🧠 Teaching point: In pre-renal AKI, the kidneys are structurally intact — they’re just underperfused. The urine is concentrated, and there’s no protein or blood because the glomeruli are still functioning.

👩‍⚕️ Case 2: Aisha, 45 — Fatigue and Frothy Urine

Presentation:

• 2-week history of fatigue, ankle swelling, and frothy urine
• Mild periorbital oedema

Bloods:

• Creatinine: 110 µmol/L
• Urea: 6.5 mmol/L
• Albumin: 28 g/L
• Cholesterol: 7.2 mmol/L

Urinalysis:

• Colour: Pale yellow, frothy
• Protein: +++
• Blood: +
• Specific gravity: 1.020
• Microscopy: RBC casts, dysmorphic RBCs

 Why the results look this way

Aisha’s findings suggest glomerulonephritis with nephrotic features. The heavy proteinuria results from increased glomerular permeability due to inflammation or immune complex deposition, allowing albumin to leak into the urine. Hypoalbuminaemia and hyperlipidaemia follow as the liver compensates for protein loss. The frothy urine is a classic sign of high urinary protein content. RBC casts form when red cells leak into the nephrons and get trapped in Tamm–Horsfall protein secretions in the tubules — indicating the bleeding originates at the glomerulus, not from lower down the tract. Her creatinine is not markedly elevated yet, but early glomerular pathology often precedes a drop in GFR

Interpretation

This is consistent with glomerulonephritis, likely nephritic-nephrotic overlap. Heavy proteinuria, hypoalbuminaemia, and RBC casts point to glomerular inflammation and damage.

🧠 Teaching point: RBC casts are pathognomonic for glomerular bleeding. Dysmorphic RBCs suggest they’ve been distorted passing through the glomerular basement membrane.

👴 Case 3: Leo, 82 — Confusion and Falls

Presentation:

• Found on the floor, confused, no clear history
• Background of hypertension and osteoarthritis

Bloods:

• Creatinine: 95 µmol/L
• Urea: 7.2 mmol/L
• eGFR: 48 mL/min
• Na⁺: 132 mmol/L
• K⁺: 5.2 mmol/L
• Bicarb: 20 mmol/L

Urinalysis:

• Colour: Cloudy
• Protein: +
• Blood: +
• Nitrites: Negative
• Leukocytes: +
• Microscopy:   WBCs, epithelial cells, no casts

 Why the results look this way:

Leo shows signs of chronic kidney disease (CKD), likely from longstanding comorbidities like hypertension. His eGFR is reduced, which reflects decreased nephron mass and filtration capacity, even though his creatinine appears “normal” — a common pitfall in elderly patients with low muscle mass. The mild proteinuria and hematuria suggest ongoing chronic damage. The hyponatraemia could be dilutional from impaired free water clearance, and the elevated potassium and low bicarbonate reflect reduced excretory and buffering capacity. The urinalysis hints at possible infection or interstitial nephritis (sterile pyuria), but epithelial cells might also suggest contamination — highlighting the importance of collection technique.

Interpretation:

This is likely CKD with a possible superimposed UTI. The eGFR suggests Stage 3b CKD. The urinalysis shows sterile pyuria — possibly due to interstitial nephritis, contamination, or atypical infection.

🧠 Teaching point: In elderly patients, CKD may be under-recognised if creatinine is “normal.” Always check eGFR and consider urinalysis findings in context — especially when cognitive changes are present.

🧠 Comparing AKI Types: Pre-Renal vs Intrinsic vs Post-Renal

Feature	Pre-Renal AKI	Intrinsic (Renal) AKI	Post-Renal AKI
Cause	↓ Renal perfusion (e.g. dehydration, heart failure)	Direct nephron damage (e.g. ATN, glomerulonephritis)	Obstruction (e.g. stones, BPH, tumour)
Onset	Rapid, reversible if treated early	Variable, often slower	Variable, may be intermittent
Volume status	Hypovolaemic or low effective volume	Often euvolaemic	Variable; may have bladder distension
Urea:Creatinine ratio	>100:1 (SI units)	~40–100:1	Variable
Urine sodium	<20 mmol/L (kidneys conserving Na⁺)	>40 mmol/L (tubular dysfunction)	Variable
Urine osmolality	>500 mOsm/kg (concentrated)	<350 mOsm/kg (dilute)	Variable
Urinalysis	Bland or mild proteinuria	Active sediment: casts, protein, blood	May show haematuria or crystals
Microscopy	Normal or hyaline casts	Granular (“muddy brown”) casts, RBC/WBC casts	Crystals, transitional cells
Response to fluids	Improves rapidly	No improvement	No improvement unless obstruction relieved
Imaging	Normal kidneys	Normal or swollen kidneys	Hydronephrosis, bladder distension

🧩 Clinical Reasoning in Action

• Pre-renal AKI: Think of Tom — dry, tachycardic, high urea:creatinine, concentrated urine. Kidneys are structurally fine but underperfused.
• Intrinsic AKI: Think of Aisha — proteinuria, RBC casts, rising creatinine. The glomeruli are inflamed or damaged.
• Post-renal AKI: Imagine an elderly man with BPH, low urine output, and bilateral hydronephrosis on ultrasound. Obstruction is the key.

🧠 Teaching tip: If the urinalysis is bland but the creatinine is rising, always ask: is this pre-renal or post-renal? If the urine is “active” (casts, protein, blood), think intrinsic.

Wrapping Up

Understanding renal function tests and urinalysis isn’t about memorising numbers — it’s about learning to interpret clues in context. These investigations offer a snapshot of kidney health, hydration, systemic illness, and more. For first-year students, the goal isn’t mastery overnight but developing habits of clinical reasoning: questioning what each result means, comparing it against the clinical picture, and recognising patterns. With practice, these pieces start to form a clearer picture — and that’s where real diagnostic insight begins.

🧠 Clinical Pearls

• Always interpret results in clinical context — a raised creatinine in a muscular young man may be normal.
• Trend values over time — one-off results can mislead.
• Hydration status can skew urea and creatinine.
• Don’t forget pre-renal, renal, and post-renal causes when thinking through abnormalities.