Open AccessC1q nephropathy developing in a case of gastric carcinoma
Author(s) -
Kiran Preet Malhotra,
Abhilash Chandra,
Saumya Shukla,
Alka Yadav,
Nuzhat Husain
Publication year - 2019
Publication title -
saudi journal of kidney diseases and transplantation/našrat amraḍ wa zira'aẗ al-kulaẗ
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.268
H-Index - 30
eISSN - 2320-3838
pISSN - 1319-2442
DOI - 10.4103/1319-2442.275493
Subject(s) - medicine , adenocarcinoma , pathology , complement system , cancer , renal cell carcinoma , nephropathy , renal biopsy , antibody , biopsy , immunology , endocrinology , diabetes mellitus
C1q is a key intermediary in the classical complement pathway. It is known to be activated by several factors including immunoglobulins and charged molecules and is an initiator of the complement cascade. C1q nephropathy (C1qN) is a rare idiopathic glomerulonephritis characterized by predominant presence of glomerular deposits of C1q fraction of complement. Although few uncommon associations of C1qN have been seen with various disorders, we present the first case of C1qN diagnosed in an elderly male with gastric adenocarcinoma. Few months after the onset of symptoms related to gastric-outlet obstruction, the patient presented with oliguria and anasarca. A gastric biopsy revealed a well-differentiated gastric adenocarcinoma, while a renal biopsy showed mesangial hypercellularity with C1q dominant immunofluorescence deposits. The development of C1qN in this case may be a result of the activation of C1q by necrotic or apoptotic cancer cell debris. C1q has been shown to induce apoptosis experimentally in other cancers. The findings suggest a complex role for C1q in initiating tumor apoptosis and subsequent linkage with apoptotic cell products and immunoglobulins to initiate renal damage.