Pathophysiology
P-II-12. Kidney disease, Case 4
腰疾患 症例4
Diagnostic evaluation:
- 57-year-old man
- Type 2 diabetes (diagnosed two years ago)
- 173 cm, 110 kg (BMI: 36.8)
- He used to consume alcohol regularly; he stopped drinking 2 years ago
- Untreated diabetes, no smoking, no drinking, no drug use
- Further disease: hypothyroidism
- Blood pressure: 168/100 mmHg
- Pulse: 84/min
- Physical examination: no thyroid gland enlargement
- Ophthalmological examination: no retinopathy
- Cardiovascular examination: negative, no signs of peripheral vascular damage
Laboratory (blood):
- Haemoglobin (Hb): 120 g/L
- Haematocrit (HTK): 38%
- MCV: 97 fL
- White blood cell count (WBC): 6.2 × 10⁹/L
- Thrombocytes (PLT): 210 × 10⁹/L
- Sodium (Na⁺): 139 mmol/L
- Potassium (K⁺): 4.2 mmol/L
- Urea: 5 mmol/L
- Creatinine: 106.1 μmol/L
- Glucose: 9.4 mmol/L
- HbA1c: 9.8%
- Total protein: 70 g/L
- Albumin: 41.0 g/L
- Cholesterol: 14.7 mmol/L
- Triglycerides: 2.3 mmol/L
- TSH: 1.2 mU/L
Laboratory (urine) — chemistry test strip:
- Bilirubin: neg
- Urobilinogen: normal
- Ketone: 5 mg/dL
- Vitamin C: neg
- Glucose: 150 mg/dL
- Protein: 25 mg/dL
- RBC: neg
- pH: 7.5
- Nitrite: neg
- White blood cell (LEU): neg
- Specific gravity: 1.001
- Turbidity: clear
- Colour: yellow
Urine sediment:
- Red blood cell (RBC): 4.4 /uL
- White blood cell (WBC): 1.3 /uL
- Hyaline cast: 3.1
- Bacterium: 68.2
- Coccus: 68.2
- Mucus: 357.7
U-albumin: 250 mg/24-h
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “Type 2 diabetes”; HbA1c 9.8%; glucose 9.4; “Untreated diabetes” | Poorly controlled type 2 diabetes — the underlying cause of kidney injury |
| U-albumin 250 mg/24-h | Moderately increased albuminuria (microalbuminuria) → the earliest sign of diabetic nephropathy |
| Blood pressure 168/100 mmHg | Hypertension — both a driver and a consequence of diabetic kidney disease |
| Creatinine 106 µmol/L; urea 5 (near-normal) | Renal filtration still largely preserved → early-stage nephropathy |
| BMI 36.8; cholesterol 14.7 mmol/L; triglycerides 2.3 | Obesity and dyslipidaemia → metabolic syndrome accelerating vascular/renal damage |
| “no retinopathy”; strip protein only 25 mg/dL | Early disease — microvascular complications not yet advanced; dipstick still misses microalbuminuria |
Key Points
- Diagnosis: Early (incipient) diabetic nephropathy — diabetic kidney disease at the microalbuminuria stage.
- Key marker: Moderately increased albuminuria (250 mg/24-h) with still-preserved GFR.
- Drivers: Poor glycaemic control (HbA1c 9.8%), hypertension, obesity, and dyslipidaemia.
- Pathophysiology: Chronic hyperglycaemia → glomerular hyperfiltration and basement-membrane/mesangial changes → albumin leak.
- Significance: Microalbuminuria is the earliest detectable and potentially reversible stage — a window for tighter glucose/BP control.
一問一答
▶What is the diagnosis in a poorly controlled diabetic with albuminuria of 250 mg/24h and preserved GFR?
Early (incipient) diabetic nephropathy at the microalbuminuria stage.
▶What is the earliest detectable clinical marker of diabetic nephropathy?
Moderately increased albuminuria (microalbuminuria), e.g. 30–300 mg/24h.
▶Why does a standard dipstick (protein 25 mg/dL) miss early diabetic nephropathy?
Dipsticks are insensitive to the low-level albuminuria of early disease; a specific albumin assay is needed.
▶What is the central pathophysiology of diabetic nephropathy?
Chronic hyperglycaemia causes glomerular hyperfiltration and basement-membrane/mesangial changes, leading to albumin leakage.
▶What does an HbA1c of 9.8% indicate in this patient?
Poor long-term glycaemic control, driving the kidney damage.
▶How does hypertension relate to diabetic nephropathy?
It is both a driver and a consequence — high BP accelerates glomerular injury, and kidney disease raises BP.
▶Why is microalbuminuria considered a critical window in management?
It is the earliest, potentially reversible stage — tighter glucose and BP control can slow or halt progression.
▶Which drug class is preferred to reduce albuminuria and protect the diabetic kidney?
ACE inhibitors or angiotensin-receptor blockers (RAAS blockade).
▶How do ACE inhibitors/ARBs reduce intraglomerular pressure?
They dilate the efferent arteriole, lowering glomerular hyperfiltration pressure and albumin leak.
▶Why does a near-normal creatinine (106 µmol/L) not exclude diabetic nephropathy?
In early disease GFR is still preserved; albuminuria precedes any rise in creatinine.
▶How do obesity and dyslipidaemia (cholesterol 14.7) contribute to this patient's kidney risk?
They are components of metabolic syndrome that accelerate vascular and renal damage.
▶Why is the absence of retinopathy notable in assessing diabetic nephropathy?
Retinopathy and nephropathy often coexist; its absence suggests early disease, and overt nephropathy without retinopathy should prompt considering other renal causes.
▶What characteristic glomerular lesion is associated with diabetic nephropathy?
Nodular glomerulosclerosis (Kimmelstiel–Wilson nodules).
▶What is the natural progression of untreated diabetic nephropathy?
Microalbuminuria → overt proteinuria → declining GFR → end-stage renal disease.
▶Why does urine glucose (150 mg/dL) appear in this patient?
Hyperglycaemia exceeds the renal threshold for glucose reabsorption, causing glucosuria.
▶What is glomerular hyperfiltration in early diabetes?
An early increase in GFR/intraglomerular pressure that injures the glomeruli over time.
▶Besides glucose control, what BP target/strategy helps protect the kidney in diabetes?
Strict blood pressure control, preferably with RAAS blockade (ACEi/ARB).
▶How should albuminuria be screened/monitored in diabetic patients?
With the urine albumin-to-creatinine ratio (or 24h albumin), performed regularly.
▶Why is the low urine specific gravity (1.001) potentially significant?
It can indicate impaired urinary concentrating ability, an early sign of tubular dysfunction.
▶Why is treating dyslipidaemia important in diabetic kidney disease?
Lipid lowering reduces cardiovascular risk and may slow progression of vascular/renal injury.