Internal Medicine · Year 3 · from Internal Medicine

Case 2: Nephrotic Syndrome

Patient Presentation

A 45-year-old man with a history of type 2 diabetes mellitus for 15 years presents with facial swelling worse in the morning and leg swelling that progresses throughout the day. He notes his urine has been "foamy" for several months. He denies dyspnea, orthopnea, or chest pain.

Vital Signs

  • Blood Pressure: 142/88 mmHg
  • Heart Rate: 76 bpm
  • Respiratory Rate: 14/min
  • Oxygen Saturation: 98% on room air
  • Temperature: 36.9°C

Physical Examination

  • General: Periorbital edema, mild facial puffiness
  • Cardiovascular: No JVD, normal S1/S2, no murmurs or gallops
  • Pulmonary: Clear to auscultation
  • Abdomen: Mild ascites, no hepatosplenomegaly
  • Extremities: 2+ pitting edema to knees bilaterally

Initial Workup

  • Urinalysis: 4+ protein, oval fat bodies, fatty casts
  • Spot urine protein/creatinine ratio: 8.5 g/g
  • Serum albumin: 1.8 g/dL (normal 3.5-5.0)
  • Total cholesterol: 342 mg/dL
  • Creatinine: 1.6 mg/dL
  • HbA1c: 8.2%

Clinical Image

Figure 2: Urine microscopy showing an oval fat body with characteristic "Maltese cross" pattern under polarized light, pathognomonic for nephrotic syndrome.

Image Source: Educational illustration for teaching purposes.

Questions

  1. What defines nephrotic syndrome?
  • A) Proteinuria >1 g/day, hypoalbuminemia, edema
  • B) Proteinuria >3.5 g/day, hypoalbuminemia, hyperlipidemia
  • C) Hematuria, proteinuria, hypertension
  • D) Proteinuria >500 mg/day, hyperlipidemia, lipiduria
  1. What is the primary mechanism of edema in nephrotic syndrome?
  • A) Increased capillary hydrostatic pressure
  • B) Decreased plasma oncotic pressure
  • C) Lymphatic obstruction
  • D) Sodium retention by the kidney
  1. What is the most likely underlying cause of nephrotic syndrome in this patient?
  • A) Minimal change disease
  • B) Focal segmental glomerulosclerosis
  • C) Diabetic nephropathy
  • D) Membranous nephropathy
  1. Why are patients with nephrotic syndrome at increased risk for thromboembolism?
  1. What is the role of ACE inhibitors in managing this patient's proteinuria?

Answers

  1. B) Proteinuria >3.5 g/day, hypoalbuminemia, hyperlipidemia - The classic triad of nephrotic syndrome includes massive proteinuria (>3.5 g/day), hypoalbuminemia (<3 g/dL), and hyperlipidemia. Edema and lipiduria are associated findings.
  1. B) Decreased plasma oncotic pressure - Massive urinary protein loss leads to hypoalbuminemia, reducing plasma oncotic pressure and causing fluid movement from intravascular to interstitial space per Starling forces. However, primary renal sodium retention also contributes.
  1. C) Diabetic nephropathy - Given 15 years of diabetes with suboptimal control (HbA1c 8.2%), diabetic nephropathy is the most likely cause. It is the leading cause of nephrotic syndrome and ESRD in adults in the United States.
  1. Thromboembolism risk factors in nephrotic syndrome:
  • Urinary loss of antithrombin III
  • Increased hepatic synthesis of procoagulant factors (fibrinogen, factors V, VIII)
  • Hyperviscosity from hemoconcentration
  • Platelet hyperaggregability
  • Particularly high risk of renal vein thrombosis
  1. ACE inhibitors in proteinuria:
  • Reduce intraglomerular pressure by dilating efferent arteriole
  • Decrease proteinuria by 30-50% independent of BP reduction
  • Slow progression of diabetic nephropathy
  • First-line therapy for proteinuric kidney disease
  • Monitor for hyperkalemia and acute rise in creatinine

Learning Points

  1. Starling forces govern fluid movement: edema results from increased capillary hydrostatic pressure, decreased oncotic pressure, increased capillary permeability, or lymphatic obstruction.
  1. Pitting edema suggests increased hydrostatic pressure or decreased oncotic pressure, while non-pitting edema suggests lymphedema or myxedema.
  1. Distribution of edema provides diagnostic clues: dependent edema (heart failure), periorbital edema (nephrotic syndrome, renal failure), localized edema (venous or lymphatic obstruction).
  1. BNP levels help distinguish cardiac from non-cardiac causes of edema.
  1. Treatment targets the underlying cause while providing symptomatic relief with sodium restriction and diuretics when appropriate.

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