Wajid Choudhry MD, (Rochester, NY)
Recently I have come across with an interesting case of an African
American young woman who presented with nephrotic syndrome ( 6g/d
proteinuria), benign urinary sediment and normal renal function. Renal
biopsy revealed "double glomerulopathy"; i.e., concurrent focal segmental
glomerulosclerosis and membranous nephropathy. No secondary causes of FSGS
or membranous nephropathy were identified.
Amenta et al (1) reported 2 similar cases in 1989. One had nephrotic
syndrome who responded to oral steroids with decreased proteinuria and
preserved renal function for 10 years. They concluded that concurrent FSGS
and MN has better prognosis than expected for a patient presenting with
either one.
Questions:
1. Is it true to predict better renal survival in patients with double
glomerulopathy than either one alone?
2. Is there any hypothesis to explain this phenomenon.
3. Anyone else with such experience? Published vs. unpublished data or
treatment protocols?
Reference
Amenta PS et al. Concurrent focal segmental glomerulosclerosis and
membranous nephropathy. Clin Nephrol Vol. 32 No.4-1989(173-177)
Response by members of NEPHROL John Charles Jennette MD, (University of North Carolina)
With respect to the renal biopsy finding of histologic lesions that
resemble focal segmental glomerulosclerosis concurrent with pathologic
changes indicative of membranous glomerulopathy (MG-FSGS), Wakai and
Magil published an excellent study of this pathologic phenotype in
Kidney International in February of 1992 (41:428-34).
They compared 27 patients with MG-FSGS to 25 patients with MG alone.
At the time of biopsy, MG-FSGS patients had more severe proteinuria.
Although both groups received similar treatment, the MG-FSGS group
developed renal failure (48% versus 13%) over the observation period,
that was more severe than the MG group. The renal survival at 60
months was 48% for the MG-FSGS group compared to 88% for the MG group
(p=0.025). Therefore, they concluded that the presence of FSGS lesions concurrent
with MG is a poor prognostic sign.
Parmjeet Randhawa MD, (University of Pittsburgh)
FSGS is best assumed to be secondary to membranous GN in this case unless
proven otherwise. One approach to document concurrent idiopathic FSGS in this
patient would be to measrure the circulating glomerular permeability factor
described by Savin et al (New Engl J Med 1996:334:878). The fact that FSGS is
in itself a non-specific finding in chronic glomerular disease is often
overlooked by clinicians not regularly reviewing kidney biopsies with a
pathologist.