2.08 CME

Nephrotic Syndrome Demystified: A Case-Based Approach

Speaker: Dr. Sandeep Huilgol

Patil Medicare Multispeciality Hospital, Bangalore

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Description

Nephrotic Syndrome Demystified: A Case-Based Approach offers a practical and engaging way to understand this complex renal condition through real-world clinical scenarios. It explores key features like heavy proteinuria, hypoalbuminemia, edema, and hyperlipidemia, helping learners connect textbook knowledge to bedside diagnosis and management. The session highlights common causes, differential diagnoses, and treatment strategies across age groups. By analyzing diverse patient cases, this approach enhances clinical reasoning and decision-making in nephrology practice.

Summary Listen

  • Nephrotic syndrome is a common presentation, differing across age groups and classified as primary or secondary, necessitating understanding for diagnosis and management. Key features include proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It's crucial to distinguish it from nephrotic-range proteinuria and nephritic syndrome, where hematuria and hypertension may be present.
  • The glomerular filtration barrier, composed of endothelial cells, basement membrane, and podocytes, plays a vital role. Podocyte injury typically causes nephrotic syndrome, while endothelial damage leads to nephritic syndrome, often involving RBCs in urine and inflammation.
  • Consequences of proteinuria include plasma protein loss, edema due to fluid leakage, hyperlipidemia from hepatic response, increased infection risk from lost immunoglobulins, and a hypercoagulable state due to loss of protein C and S.
  • Primary nephrotic syndromes, such as minimal change disease (steroid-sensitive), focal segmental glomerulosclerosis (FSGS - steroid-resistant), and membranous nephropathy, involve pathologies primarily within the kidney. Secondary causes include diabetes, malignancy, NSAID use, lupus, amyloidosis, and infections.
  • Diagnosis involves confirming proteinuria, measuring serum albumin and lipids, evaluating kidney function, and ruling out secondary causes with ANA, complement levels, and viral serology. Renal biopsy is often required if etiology is unclear.
  • Management includes steroids (prednisolone), diuretics (furosemide), IV albumin, ACE inhibitors, statins, infection control, and thrombosis prophylaxis. Complications encompass infections, thromboembolism, acute kidney injury, and steroid-related side effects.
  • Prognosis varies with the cause, with steroid-sensitive minimal change disease having an excellent outlook. Patient education about the disease, treatment, and potential side effects is critical for treatment compliance. Referral to a nephrologist is necessary for atypical presentations, treatment failure, or complications.

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