Introduction Focal segmental glomerulosclerosis (FSGS) leads to rapidly progressive scarring or sclerosing of capillaries, deterioration of kidney function and end-stage renal disease (ESRD), and dialysis/transplantation. FSGS causes proteinuria from asymptomatic microalbuminuria to large symptomatic nephrotic syndrome, > 3,500 mg/24 h and hypertension.
Methods We treated eight patients 3 to 5 years with kidney biopsy-proven FSGS. Serial studies included proteinuria, BP, electrolytes, serum creatinine, and glomerular filtration rate (GFR) in response to combination therapy interfering with the renin-angiotensin-aldosterone system (RAAS). Medications were in four categories: angiotensin-converting enzyme inhibitors (ACE I), angiotensin receptor blockers, and selective aldosterone receptor antagonists or aldosterone receptor antagonist plus immunosuppressives, corticosteroids, and mycophenolate. Poor response to corticosteroids defined refractory. Mycophenolate was used as a last resort.
Results As medications were added, a decrease in proteinuria occurred in six of eight patients. Treatment with three drugs blocking the RAAS caused progressive reduction of BP and proteinuria, preventing rapid deterioration of GFR in all eight patients while adhering to the therapeutic regimen. In six long-term compliant patients, proteinuria and BP were reduced progressively. Two of eight patients became delinquent and noncompliant, leading to rapid reduction of GFR and subsequent hemodialysis within 6 to 9 months.
Conclusion FSGS prognosis correlates with BP and proteinuria reduction, preventing ESRD. Anti-RAAS treatment effectively reduced proteinuria and BP in eight of eight patients while compliant, slowing down the loss of GFR. Two anti-RAAS noncompliant patients had rapid deterioration of kidney function requiring hemodialysis. Patients with FSGS should be treated early and continuously with combinations of anti-RAAS medications. Frequent testing of potassium and creatinine are required. Future larger trials are in design.
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