Synopsis
Recognise renal amyloid and MGRS, prove the deposited protein or lesion, and secure rapid nephrology–haematology treatment of the pathogenic clone.
- Amyloidosis is extracellular deposition of misfolded fibrils; renal AL amyloid commonly causes albumin-predominant proteinuria, nephrotic syndrome and progressive kidney impairment.
- MGRS describes kidney injury caused by a monoclonal immunoglobulin from a B-cell or plasma-cell clone that may be too small to meet conventional malignancy treatment criteria.
- A small paraprotein is not necessarily incidental when renal biopsy demonstrates a compatible monoclonal lesion.
Key red flags
Breathlessness, syncope, raised biomarkers, low-voltage ECG or increased ventricular wall thickness may indicate high-risk cardiac involvement.
Investigation priorities
Detect and characterise a monoclonal immunoglobulin with greater sensitivity than electrophoresis alone.
Management branches
An adult has unexplained proteinuria, CKD, nephrosis or proximal tubular dysfunction.
- Characterise urine albumin and total protein, sediment, renal trajectory and systemic features rather than relying on a dipstick.
- Request serum free light chains plus serum and urine immunofixation and review calcium, blood count and bone symptoms.
Key medicines
Clone-directed therapy for AL amyloid or MGRSThe haematology–nephrology multidisciplinary team must choose and renal-adjust the current disease-specific regimen; no single bortezomib-, antibody- or chemotherapy schedule applies to all lesions.
Loop diuretic for symptomatic oedemaTitrate the locally selected oral or intravenous preparation to congestion, renal response and blood pressure; severe nephrosis or cardiac amyloid often requires specialist-guided adjustment rather than a fixed dose.