A serum albumin of 2 g/L
| HOSP # | WARD | Victoria Hospital – Internal Medicine | |
| CONSULTANT | Jody Rusch | DOB/AGE | 30 y/o Female |
Abnormal Result
Albumin = 2 g/L
Previous Albumin results: 5 g/L; 11 g/L; 8 g/L all 3 months apart respectively.
Presenting Complaint
The patient did not present with any complaints and the bloods taken was for follow-up only.
History
Patient is known with HIV, diagnosed in 2019 with a CD4 count of 250 cells/uL at the time.
ANA, ANCA, Hepatitis B negative
C3 & C4 normal
The patient presented previously with a left renal vein thrombosis, kidney sizes 150mm and 149mm respectively.
Examination
Not available.
Laboratory Investigations
Current CD4 count= 140 cells/uL.
Urine protein:creatinine ratio of 0.42 (multiple previous values of >1.5 though)
Total Cholesterol 4.2 mmol/L
Other Investigations
Histology
MACROSCOPY:
Specimen consists of a single pale core measuring 6mm in length.
MICROSCOPY:
Glomeruli:
There are a total of 9 glomeruli present. There are no globally sclerosed glomeruli and there are no crescents present. Focal segmental lesions are present. Neutrophils are frequently identified within capillary loops (endocapillary hypercellularity). There is mild focal segmental increase in mesangial cellularity. Glomerular basement membranes appear mildly increased in thickness in areas. There are no features of collapsing FSGS. Podocytes appear prominent. Focal areas suspicious for early spike formation are noted on Jones silver stain.
Tubules:
Tubules show protein resorption droplets with focal areas of ATI. Areas of tubular atrophy and thyroidisation are present. Tubular microcysts are not a feature.
Interstitium:
Moderate lymphoplasmacytic inflammation is present.
Vessels:
Vessels appear normal.
IMMUNOHISTOCHEMISTRY:
IgA: Negative
IgG: membrane staining presnet
IgM: membrane staining present
C3: Negative
C4d: Negative
C1q: 3+ staining present, membrane and mesangial
ELECTRON MICROSCOPY:
Pending – specimen will be processed ex-wax.
PATHOLOGICAL DIAGNOSIS:
Kidney, biopsy:
- Immune complex glomerulonephritis with features suggestive of early membranous nephropathy. DDx=HIVICK. TEM pending.
- Additional acute endocapillary hypercellularity (neutrophils).
- Moderate chronic interstitial inflammation.
Electron microscopy
Ultra-thin resin sections show the presence of electron dense deposits with subepithelial and intramembranous location in keeping with membranous nephropathy.
Ehrenreich-Churg stage: 1-2
Immunohistochemistry:
IgG4: negative.
PATHOLOGICAL DIAGNOSIS:
- Features in keeping with membranous nephropathy.
Final Diagnosis
Membranous Nephropathy
Take Home Message
Severe hypoalbuminemia can occur in nephrotic syndrome. One should ascertain before authorizing such a severely deranged result, that it is not due to a sample type swop of kinds. The history of previously low albumin results was in this case confirmatory. The other features of nephrotic syndrome should also be sought, which is hypertriglyceridemia (no triglyceride value was available in this patient but the Total cholesterol was 4.2 mmol/L).
HIVICK (HIV immune complex disease of the kidney) continues to be an important cause of nephropathy in HIV-naive patients in South Africa. In contrast to HIVAN where the HIV infects the podocytes primarily, HIVICK boasts itself in the fact that it indirectly causes disease by initiating an immune response.
This approach utilizes a completely different offensive strategy that eliminates the need to directly infect the kidney one cell at a time as is the case in HIVAN.
HIVICK is an immune complex attack on the kidney that leads to a variety of histopathologic glomerular lesions: membranous, diffuse/membranoproliferative, IgA nephropathy. The unique aspect of these immune complexes is their composition involving specific HIV antigens as the source target of the antibody response. Therefore the development of HIVICK is completely dependent on the presence of active HIV viremia.
This is a very interesting read on the two diseases: https://www.medscape.com/viewarticle/840389_3