Table 1.
Cases of CMML-Related Glomerulopathy Reported in the Literature
| Reference (Year) | No. of Patients With CMML | Clinical Presentation |
Glomerular Pathology on Biopsy | Concomitant Tubulointerstitial Findings | Therapies Instituted at Kidney Diagnosis | Change in Kidney Function After Therapy |
|---|---|---|---|---|---|---|
| Schwarze et al31 (1975) | N = 18 (postmortem kidney examination of autopsy cases of CMML) | N/A | Leukemic infiltration of glomeruli | Leukemic infiltration of cortex and medulla (N = 17), tubular atrophy, secondary uric acid diathesis, nephrocalcinosis, interstitial edema, tubular hyaline droplet change | N/A | N/A |
| Morschhauser et al27 (1995) | N = 45 | NS (N = 3), AKI (N = 1) |
AL amyloidosis (N = 1), extracapillary glomerulonephritis (N = 1) | - | VP16 and hydroxyurea | Improved in 2 patients, stable in 1 patient, and worsened in 1 patient |
| Enriquez et al28 (2008) | N = 1 | NS | Membranous glomerulopathy | - | Initially hydroxyurea or prednisone and cyclosporine then MMF | No response to hydroxyurea or prednisone or cyclosporine; MMF brought proteinuria down from 27 g/d to 1 g/d |
| Büttner-Herold et al19 (2021) | N = 4 | Hematuria (N = 2), Proteinuria (N = 4) (no cases of NS) | Endothelial damage (N = 4), mesangiolysis (N = 2), double contours (N = 4), podocytopathy >75% (N = 1), TMA (N = 1), IR-like GN (N = 1) | |||
| Belliere et al29 (2021) | N = 8 | FSGS (N = 2), extramedullary hematopoiesis (N = 3), monocyte infiltration (N = 1) | Decitabine, azacitidine, ruxolitinib | Improved in 1 patient, worsened in 2 patients, continued dialysis dependence in 1 patient | ||
| Asano et al30 (2021) | N = 1 | Subnephrotic proteinuria (2 g/g), microscopic hematuria with red cell casts, AKI | Extracapillary infiltration of CMML (diagnosed by immunostaining) | Tubulointerstitial nephritis with positive staining for MPO and CD68, positive staining for lysozyme in proximal tubule | Not discussed | Not discussed |
| Person et al21 (2021) | N = 18 (postmortem kidney findings) | N/A | Diffuse glomerulosclerosis (N = 2, both of which were post allo-HCT) | Extramedullary hematopoiesis, leukemic infiltration | N/A | N/A |
| Sun et al12 (2022) | N = 1 | AKI and NS. Proteinuria 15/d | MCD (complete foot process effacement of podocytes and no immune complex deposition) | Proximal tubular injury, focal mononuclear infiltration in the interstitium, positive lysozyme staining, and increased lysosomal granules in proximal tubular | ||
| Gipe et al20 (2023) | N = 14 | AKI, nephrotic syndrome with CKD, nonnephrotic range proteinuria with CKD | Focal global glomerulosclerosis (N = 3), FSGS (N = 2), glomerular ischemia (N = 1), acute post infectious glomerulonephritis (N = 1), minimal change disease (N = 1), myeloproliferative related neoplasm (MPN) related glomerulopathy (N = 1), IgA nephropathy (N = 1) |
Acute tubular injury, interstitial nephritis, arteriosclerosis, moderate to severe tubular atrophy and interstitial fibrosis, lysozyme-induced nephropathy, tubulointerstitial CMML infiltration | Supportive care, decitabine, hydroxyurea, and prednisone taper | Decrease in creatinine between 0.5 and 1.2 mg/dL (N = 2), 3 patients died |
Abbreviations: AKI, acute kidney injury; AL, amyloid light chain; AZA, azacytidine; CKD, chronic kidney disease; CMML, chronic myelomonocytic leukemia; DAC, decitabine; EMH, extramedullary hematopoiesis; HCT, hematopoietic cell transplant; IR-like GN, infection-related-like glomerulopathy; FSGS, focal segmental glomerulosclerosis; HU, hydroxyurea; MCD, minimal change disease; MMF, mycophenolate mofetil; N/A, not available; NS, nephrotic syndrome; PIGN, post infectious glomerulonephritis; TMA, thrombotic microangiopathy; VP16, etoposide.