A 61-year-old male had nephrotic syndrome in association with minimal renal amyloidosis. The amyloid deposits were inconspicuous and had been initially overlooked, and the biopsy specimen was thought to show minimal glomerular changes. Accordingly he was diagnosed as having minimal change nephrotic syndrome (MCNS). Thereafter, administration of 40 mg/day of prednisolone was started. A few weeks after treatment, proteinuria decreased, but did not disappear. Four years later, he was readmitted for the treatment of the nephrotic syndrome. The second biopsy at 65 years of age revealed typical renal amyloidosis by light microscopy. Congo red staining and electron microscopy confirmed the presence of amyloid deposits. The serum A protein (SAA) level was 328 micrograms/ml. Furthermore, the first biopsy specimen revealed minimal renal amyloidosis by Congo red staining. At the time, 40 mg/day of prednisolone proved ineffective for the proteinuria. However, after methylprednisolone pulse therapy, the proteinuria decreased and the nephrotic syndrome improved. After discharge, administration of 20 mg/day of prednisolone was maintained. One year later, the patient showed no evidence of recurrence of the nephrotic syndrome and the SAA level decreased (from 328 micrograms/ml to 74.4 micrograms/ml). Prednisolone proved to have a beneficial effect on the reduction of proteinuria and SAA levels. We strongly recommend careful examination for amyloid deposits in all kidney biopsy specimens with the appearance of MCNS on older patients whose proteinuria does not respond to the administration of prednisolone.

Download full-text PDF

Source

Publication Analysis

Top Keywords

nephrotic syndrome
24
minimal renal
12
renal amyloidosis
12
amyloid deposits
12
mg/day prednisolone
12
biopsy specimen
8
administration mg/day
8
proteinuria decreased
8
congo red
8
red staining
8

Similar Publications

: Charcot-Marie-Tooth (CMT) disease is an inherited peripheral neuropathy primarily involving motor and sensory neurons. Mutations in INF2, an actin assembly factor, cause two diseases: peripheral neuropathy CMT-DIE (MIM614455) and/or focal segmental glomerulosclerosis (FSGS). These two phenotypes arise from the progressive degeneration affecting podocytes and Schwann cells.

View Article and Find Full Text PDF

: Focal segmental glomerulosclerosis (FSGS) is a pattern of kidney injury with diverse causes and pathogeneses, resulting in podocyte injury and depletion. It can be classified as primary, genetic, or secondary. Because FSGS classically has a worse prognosis in patients with nephrotic syndrome, most studies have focused on the treatment and evolution of these patients, resulting in a lack of data related to patients without nephrotic syndrome.

View Article and Find Full Text PDF

The integrity of the filtration barrier of the kidney relies on the proper composition of podocyte interdigitating foot processes. Their architecture is supported by a complex actin-cytoskeleton. Following podocyte stress or injury, podocytes encounter structural changes, including rearrangement of the actin network and subsequent effacement of the foot processes.

View Article and Find Full Text PDF

Background: Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare entity classified under the umbrella of monoclonal gammopathy of renal significance. The clinical implications of circulating monoclonal immunoglobulin (MIg), light chain restriction on immunofluorescence (IF) microscopy, histopathological pattern, and type of therapy on renal outcomes are not clearly defined.

Materials And Methods: Sixteen patients of PGNMID diagnosed between 2013 and 2020 were included from a biopsy registry of 11,459 patients at a single center.

View Article and Find Full Text PDF

Objectives: To investigate the natural product sulforaphane (SFN) in protection of membranous nephropathy (MN) by inhibiting oxidative stress-associated podocyte pyroptosis.

Materials And Methods: A passive Heymann nephritis (PHN) model was established and treated with SFN. Clinical manifestations were examined by testing 24-hr urine protein, albumin, total cholesterol, triglyceride, high-density and low-density lipoprotein levels.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!