Table 1.

Clinico-pathologic data in the 12 patients with THSD7A-associated idiopathic membranous nephropathy

No.Age, yrSexAnti-PLA2R AbUrinary Protein, g/24 hAlbumin, g/LSerum Creatinine, mg/dleGFR, ml/min per 1.73 m2aHemoglobin, g/dlCholesterol, mg/dlBP, mmHgPathologic DataMain Treatments and Prognosis
Sclerosis, %StagesTA/IFbTreatmentsResponseTime to Response, moRelapseKidney DysfunctioncTime to Last Follow-Up, mo
376Male13171.266111d309100/7013 (4 of 30 G)II1P+CTXPR9no024
764Male19231.127313309140/9517 (2 of 12 G)I1P+CTXPR3yes018
879Male17211.91367d232130/6025 (4 of 16)II2P+CTXPR6no08
9e47Female4240.6016714155140/8011 (1 of 9)I1ACEI/ARBsCR12no024
10e20Male4420.7913713348120/806 (2 of 32)I1ACEI/ARBsCR10no041
  • Ab, antibody; TA, tubular atrophy; IF, interstitial fibrosis; +, positive; ACEI/ARBs, angiotensin converting enzyme inhibitor/angiotensin II receptor blocker; CR, complete remission; NR, no remission; —, no data; G, glomeruli; P, prednisone; CTX, cyclophosphamide; PR, partial remission; CNI, calcinerin inhibitor.

  • a eGFR was calculated using the Modification of Diet in Renal Disease Study equation adjusted for Chinese populations (24): eGFR = 175 × (plasma creatinine)−1.234 × age−0.179 × 0.79 (if female).

  • b Semiquantitative scoring is graded according to the percentage of interstitial area involved: 0, 0%; 1, 5%–25%; 2, 25%–50%; 3, >50%.

  • c Kidney dysfunction was defined as eGFR decreased >30% from baseline and below 60 ml/min per 1.73 m2.

  • d Anemia was explained by late referral and long-term hypoalbuminemia with negative finding by endoscopies of colon and stomach, and recovered soon after partial remission with supportive and immunosuppressive treatments.

  • e Patients without circulating anti-THSD7A antibodies but enhanced expression of THSD7Aantigen in glomeruli.