Pathophysiology
P-II-13. Kidney disease, Case 5
腰疾患 症例5
Case report / complaints:
- 48-year-old woman
- Painless swelling of the feet (started 2 months ago), started from the ankles; now the legs, thighs and external genitals are swollen
- Her face is swollen in the morning
- Her urine is foamy
- Difficulty in breathing is getting worse
- 20 kg weight gain (in 4 months)
- Untreated diabetes, no smoking, no drinking, no drug use
Diagnostic evaluation:
- Blood pressure: 153/87 mmHg
- Pulse: 90/min
- Pitting edema: legs, upper extremities, labia majora
- Temperature: 36.0 °C
- Dull percussion sounds, diminished breathing sounds on both sides
- Oxygen saturation: 98%
- X-ray, CT: pleural effusion, ascites
- Normal heartbeat sounds, no murmurs, normal position of apical impulse; echocardiography: negative
- No sign of chronic liver disease
- No neurological deficits
- Ophthalmic examination: severe non-proliferative diabetic retinopathy
Laboratory (blood):
- Haemoglobin (Hb): 95 g/L
- Haematocrit (HTK): 30%
- MCV: 95 fL
- White blood cell count (WBC): 4.7 × 10⁹/L
- Thrombocytes (PLT): 330 × 10⁹/L
- Sodium (Na⁺): 141 mmol/L
- Potassium (K⁺): 4.0 mmol/L
- Urea: 7.1 mmol/L
- Creatinine: 112 μmol/L
- Glucose: 9.8 mmol/L
- HbA1c: 11%
- Total protein: 55 g/L
- Albumin: 20 g/L
- Cholesterol: 15.2 mmol/L
- Triglycerides: 2.7 mmol/L
- ASAT: 20 U/L
- ALAT: 9 U/L
- CRP: 3 mg/dL
Laboratory (urine) — chemistry test strip:
- Bilirubin: neg
- Urobilinogen: normal
- Ketone: 50 mg/dL
- Vitamin C: neg
- Glucose: 500 mg/dL
- Protein: 500 mg/dL
- RBC: neg
- pH: 7.5
- Nitrite: neg
- White blood cell (LEU): neg
- Specific gravity: 1.042
- Turbidity: clear
- Colour: yellow
Urine sediment:
- Red blood cell (RBC): 11.4 /uL
- White blood cell (WBC): 13.2 /uL
- Hyaline cast: 20.7
- Pathologic cast: 1.8
- Epithelial cell: 30.8
- Bacterium: 321.2
- Coccus: 321.2
- Mucus: 338.8
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “Painless swelling … ankles … legs, thighs and external genitals”; “face is swollen in the morning” | Generalized pitting oedema/anasarca → severe hypoalbuminaemic state |
| “urine is foamy”; urine protein 500 mg/dL | Massive proteinuria — the defining feature of nephrotic syndrome |
| Albumin 20 g/L; total protein 55 g/L (low) | Hypoalbuminaemia from urinary protein loss → reduced oncotic pressure → oedema |
| Cholesterol 15.2, triglycerides 2.7 mmol/L | Hyperlipidaemia — a classic component of the nephrotic syndrome |
| “severe non-proliferative diabetic retinopathy”; HbA1c 11% | Advanced diabetic microvascular disease → points to diabetic nephropathy as the cause |
| Echo negative; “No sign of chronic liver disease” | Excludes cardiac and hepatic causes of the oedema/low albumin |
| Pleural effusion + ascites; 20 kg gain in 4 months | Fluid accumulation in serous cavities from the severe hypoalbuminaemia |
Key Points
- Diagnosis: Nephrotic syndrome due to diabetic nephropathy (advanced/overt stage).
- Nephrotic tetrad: Massive proteinuria, hypoalbuminaemia, oedema (anasarca), and hyperlipidaemia.
- Cause clue: Long-standing poorly controlled diabetes with severe retinopathy strongly supports diabetic glomerulosclerosis.
- Exclusions: Normal echocardiography and no liver disease rule out cardiac/hepatic causes of oedema.
- Pathophysiology: Diabetic glomerular damage → heavy albumin loss → low plasma oncotic pressure → fluid shift into tissues and serous cavities (effusion, ascites).
一問一答
▶How is nephrotic-range proteinuria defined?
Protein loss >3.5 g/24h.
▶What is the classic tetrad of nephrotic syndrome?
Massive proteinuria, hypoalbuminaemia, oedema, and hyperlipidaemia.
▶What is the diagnosis in a diabetic woman with anasarca, foamy urine, heavy proteinuria, and low albumin?
Nephrotic syndrome, here due to diabetic nephropathy.
▶Why does foamy urine occur in nephrotic syndrome?
High protein content in the urine lowers surface tension, producing foam.
▶What is the mechanism of oedema in nephrotic syndrome?
Urinary albumin loss → hypoalbuminaemia → reduced plasma oncotic pressure → fluid shifts into tissues.
▶Why does this patient have pleural effusion and ascites?
Severe hypoalbuminaemia allows fluid to accumulate in serous cavities (anasarca).
▶Why does hyperlipidaemia develop in nephrotic syndrome?
Low oncotic pressure stimulates hepatic lipoprotein synthesis and lipid clearance is reduced.
▶Why does severe diabetic retinopathy support diabetic nephropathy as the cause here?
Diabetic micro-vascular complications tend to coexist, so advanced retinopathy points to diabetic glomerulosclerosis.
▶How do a normal echocardiogram and absence of liver disease help here?
They exclude cardiac and hepatic causes of oedema and low albumin, pointing to a renal cause.
▶Why are nephrotic patients hypercoagulable / at risk of thrombosis?
Urinary loss of anticoagulant proteins (e.g. antithrombin III) and increased clotting factors promote venous thrombosis.
▶Why are nephrotic patients more susceptible to infections?
Urinary loss of immunoglobulins and complement factors impairs immune defence.
▶Why does this patient have a 20 kg weight gain over 4 months?
It reflects fluid retention/oedema, not true tissue mass gain.
▶Why does this patient have worsening dyspnoea?
Pleural effusions and fluid overload reduce lung expansion and gas exchange.
▶How does nephrotic syndrome differ from nephritic syndrome?
Nephrotic = heavy proteinuria, hypoalbuminaemia, oedema; nephritic = haematuria, hypertension, mild proteinuria, and red-cell casts.
▶Why is the morning facial/periorbital swelling typical of nephrotic oedema?
The low-pressure periorbital tissues accumulate fluid overnight when recumbent.
▶Why is this patient mildly anaemic (Hb 95 g/L)?
Chronic kidney disease reduces erythropoietin, and protein loss contributes to anaemia.
▶What general treatment measures are used in nephrotic syndrome?
Salt/fluid restriction and diuretics for oedema, RAAS blockade to reduce proteinuria, lipid lowering, and treating the underlying cause.
▶What does pitting oedema reaching the genitals indicate about severity?
Severe, generalized fluid overload (anasarca) from profound hypoalbuminaemia.
▶Why is the urine specific gravity high (1.042) in this patient?
Heavy proteinuria and glucosuria increase urine solute content, raising specific gravity.
▶Why does proteinuria itself accelerate kidney damage?
Filtered protein is toxic to tubular cells and promotes interstitial inflammation and fibrosis.