THE ROLE OF RAAS BLOCKADE IN COEXISTING IgA NEPHROPATHY AND MINIMAL CHANGE DISEASE: A CASE REPORT

 

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https://storage.unitedwebnetwork.com/files/1099/a6fe014014631f025e21b73e15e20378.pdf
THE ROLE OF RAAS BLOCKADE IN COEXISTING IgA NEPHROPATHY AND MINIMAL CHANGE DISEASE: A CASE REPORT

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Chung-Mao
Yuan
Chung-Mao Yuan Chungmeow.med@gmail.com Kaohsiung Armed Forces General Hospital Department of Internal Medicine Kaohsiung City Taiwan *
Chi-Hao Liu colinliu1201@gmail.com Kaohsiung Armed Forces General Hospital Division of Nephrology, Department of Internal Medicine Kaohsiung City Taiwan -
 
 
 
 
 
 
 
 
 
 
 
 
 

IgA nephropathy (IgAN) is the most common form of primary glomerular disease in Asia. It usually presents with hematuria, although presentation with nephrotic syndrome is rare. Minimal change disease (MCD), on the other hand, accounts for approximately 10-15% of adult primary nephrotic syndrome. In rare patients with IgAN presenting with nephrotic syndrome, renal biopsy may reveal features of both IgAN and MCD, termed MCD-IgAN. According to current guidelines, the first-line therapy of IgAN is renin–angiotensin–aldosterone system (RAAS) blockade, whereas glucocorticoids are the standard of care for MCD. Treatment for MCD-IgAN generally follows the approach used for MCD.

We report a 22-year-old male who presented with rapid-onset lower limb edema, hypoalbuminemia (1.9 g/dL), heavy proteinuria (9.8 g/day) and preserved renal function. Elevated blood pressure was also noted at presentation. We prescribed glucocorticoid, angiotensin receptor blocker (ARB) and loop diuretics initially. Renal biopsy was performed and demonstrated diffuse mesangial deposition of IgA on immunofluorescence (IF). Marked foot process effacement with moderate epithelial microvillous transformation was seen on electron microscopy (EM). The pathological findings were compatible with MCD-IgAN.

Following the initial treatment, the patient showed rapid clinical improvement. Proteinuria decreased to 1.2 g/day on the 7th day, and the patient was discharged on the 14th day of admission. However, the disease relapsed rapidly (proteinuria 8.4 g/day), necessitating readmission just 12 days after ARB was discontinued during outpatient follow-up. Upon the second time of admission, we administered ARB again, and proteinuria quickly decreased to 0.9 g/day on the 8th day, leading to symptomatic improvement.

This case highlights the importance of renal biopsy in nephrotic syndrome with atypical features such as hypertension. Moreover, although current guidelines do not specifically recommend RAAS blockade for MCD-IgAN, our observation suggests that ARB therapy may play an important role in the treatment of MCD-IgAN, just as it dose in IgAN.

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