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Solid Tumour and Glomerulopathy QJ Med 1996; 89:361-367 Solid tumour and glomerulopathy P. PAI, J.M. BONE, I. McDICKEN and CM. BELL From the Regional Renal Unit, Royal Liverpool University Hospital, Liverpool, UK Received 11 October 1995 and in revised form 31 January 1996 Downloaded from https://academic.oup.com/qjmed/article/89/5/361/1578010 by guest on 01 October 2021 Summary We retrospectively examined the prevalence of solid centic GN and one case of focal segmental GN. tumours in patients with glomerulonephritis (GN) Bronchogenic (6) and gastrointestinal carcinoma followed in our regional renal unit between 1977 (CA) (5) were the commonest tumours encountered. and 1994. We identified 17 cases of what was Other tumours included breast CA (1), renal cell thought to be solid-tumour-related glomerulo- CA (1), prostatic CA (1), an epithelial thymoma and nephritis. Tumours and GN were diagnosed together a leiomyosarcoma of the lung. All MGN and mesang- in six cases, and within a year of each other in ial proliferative GN cases developed nephrotic range another four. In addition, there were seven other proteinuria, whereas all patients with rapidly pro- cases with a weaker temporal relationship (median gressive crescentic GN presented with acute renal duration between GN and cancer diagnosis, two failure. Four cases had received immunosuppressive and a half years) but which nonetheless could be therapy prior to tumour diagnosis. We discuss the tumour-related. In total, there were seven membran- validity of each case as tumour-related glomerulo- ous GN, four mesangial proliferative GN, five cres- nephritis. Introduction Since the first clinicopathological study to present an University Hospital serves a population of 2 million association between cancer and nephrotic syndrome people in the Mersey region of the Northwest of (NS) was suggested by Lee et a\.? the subject of England. We have described in this paper our tumour-related nephropathy has remained a debatable experience of glomerulopathy associated with neo- issue. The prevalence of solid tumour in NS has been plasia in the period of 1977 to 1994. Haematological- reported to vary between 3% and 13%^~9 and preval- malignancy-associated glomerulonephritis has been ence as high as 20% has been described in patients excluded in this review, as the association is well over 60 year old.10'11 However, other case series have recognized. suggested a much lower incidence.12'13 Solid tumours have been most commonly associ- ated with membranous glomerulopathy (MGN); other Methods forms of paraneoplastic glomerulopathies are less well described. These include minimal change, extra- All cases have been referred to us from the northwest capillary crescentic, membranoproliferative, IgA, and region of England. The diagnoses of glomerulo- focal segmental glomerulonephritis. Gastrointestinal nephritis and carcinoma (between 1977 and 1994) (Gl)1'5'8'1^17 and lung tumours1'5'8'18'19 are most com- were identified through the renal departmental com- monly associated with MGN, but others have puter which stores all clinical data of our patient reported this renal lesion with other forms of solid population. All NS patients were routinely screened tumour such as breast, thyroid, kidney, skin, larynx, for tumours by a full clinical examination, full blood pharynx, pancreas, prostate, cervix, and mesenchy- count, full plasma chemistry including liver function mal as well as lymphoid tumour. test, full immunological test, chest X-ray and an The Regional Renal Unit at the Royal Liverpool abdominal ultrasound scan. Further investigations Address correspondence to Dr P. Pai, Link 6C, Royal Liverpool University Hospital, Prescot Street, Liverpool L7 8XP © Oxford University Press 1996 362 P. Pai etal. would be determined by any abnormalities in these no linear immunofluorescence was demonstrated. tests. For instance, iron-deficiency anaemia would He was given a short trial of plasma exchange and prompt further investigations of the upper and lower immunosuppressive therapy, but this was soon dis- gastrointestinal tract. continued when it became clear that he required chronic dialysis. Results Mesangial proliferative GN Between 1977 and 1994, we have seen from an Four patients (6-9) had neoplasia and NS as a result average of 120 renal biopsies performed yearly in of mesangial proliferative GN. The tumours were, our unit, 17 patients with glomerulonephritis (GN) respectively, renal cell CA, rectal CA, bronchogenic and neoplasia. None of the patients were known to CA and prostatic CA. have any secondary cause for their GN. The patient In patient 6, renal cell CA was detected in 1990 Downloaded from https://academic.oup.com/qjmed/article/89/5/361/1578010 by guest on 01 October 2021 characteristics are illustrated in Table 1. during an ultrasound scan as part of the investigations for proteinuria. A partial nephrectomy was carried Crescentic GN out with complete excision of the tumour. The renal tissue not involved by the tumour however also Patients 1-5 developed acute renal failure as a result demonstrated a mesangial proliferative GN. IF dem- of crescentic GN. Cancers were recognized at the onstrated strongly positive C3 granular deposits in same time of renal failure in two (2 and 3). All the glomerular mesangium and basement membrane. patients underwent a renal biopsy which showed Some 25% of the glomeruli were sclerosed. So far crescentic GN (100% crescent, in patients 1, 2, 4, this patient is stable with no clinical recurrence of 5; 25% crescent in patient 3). her cancer, although her proteinuria persists. Patient 1 gave a short history of dysphagia due to Renal biopsy of patient 7 demonstrated only very oesophageal CA. She underwent an oesophagogas- mild mesangial proliferation. IgA and C3 were seen trectomy but developed acute oliguric renal failure on immunofluorescence in the mesangium, and in two months later. Serology, including auto- smaller amount, in the GBM. This patient was known antibodies, ANCAs, anti-GBM antibodies and cryo- to have recurrent colonic adenomatous polyps for globulin, was all negative. Renal biopsy demon- which he required regular colonoscopy. Eight months strated florid crescent formation, with strong staining after his NS, he was found to have an inoperable of IgA and C3 deposits in the mesangium. There was adenocarcinoma of the rectum ('Duke' class B). His no demonstrable vasculitis. She died 1 month later. proteinuria improved 4-6 months after surgical A gastrograffin meal requested shortly before her debulking and radiotherapy to the tumour. death suggested tumour recurrence. Renal histology of patient 8 showed mild mesang- Patient 2 was found to have advanced breast CA ial proliferation. In 30% of the glomeruli, there was when she presented with acute renal failure. Renal mesangial proliferation with capsular adhesion. biopsy showed a florid extracapillary crescentic GN Immunofluorescence was negative. He was sub- with pauci-immune deposits in the GBM. Her sero- sequently found to have an incurable bronchogenic CA with metastases 9 months later. logy was positive for anti-neutrophil cytoplasmic antibody to proteinase 3 or c-ANCA (ELISA). There Patient 9 was diagnosed to have a well- was no renal response following pulse steroid, and differentiated prostatic CA 2 years before his NS. the patient was established on chronic haemodialysis Renal biopsy showed a mesangial proliferative GN. programme. She died 6 months later. IF data was unavailable. Following treatment with Patients 3 and 4 had crescentic GN associated stilboestrol and CS, his NS went into remission 2 months later. He died 2 years later from bronchopne- with a bronchogenic CA. Immunofluorescence (IF) umonia. data were unavailable. Patient 3 was given pulse steroid and cyclophosphamide (CPP) for his cres- centic GN. He died 2 weeks later from renal failure Membranous GN and cancer. Patient 4 received a course of radio- therapy 7 months prior to her renal failure. She died Seven patients (10-16) had MGN/NS and carcinoma. shortly afterwards from an intracerebral bleed. All membranous cases had typical IgG epimembran- In patient 5, the lung neoplasm was only disco- ous granular deposits. The neoplasia were CA of the. vered in a pre-transplant chest X-ray 18 months after bronchus (2), gastric CA (2), oesophageal CA (1), an his renal failure. Immunology, including anti-GBM epithelial thymoma and a leiomyosarcoma of the antibodies, was negative. Renal biopsy demonstrated lung. 100% crescents. Immunofluorescent microscopy Patient 10 presented with NS and bronchogenic showed intramembranous deposits of IgG and C3; CA together. Renal biopsy showed thickened base- Table 1 Summary of clinical data Patient Age Renal diagnosis Serum creatinine Proteinuria Tumour diagnosis Tumour therapy Renal therapy Renal outcome Follow-up (years)/Sex (with date) (Hmol/I) (g/24 h) (with date) Crescentic GN and malignancy 1 65/F ARF 8/93 441 - Oesophageal CA(T3) 6/93 Resection (incomplete) HD HD Died 9/93 2 69/F ARF 3/92 372 - Breast CA 3/92 Mastectomy (incomplete) CS, HD HD Died 9/92 62/M - 3 ARF 2/82 430 Bronchia! CA (met) 2/82 CPP PMP HD Died 2/82 IS) 4 75/F ARF 11/89 900 - Bronchial CA (met) 4/89 Radiotherapy HD HD Died 12/89 2. 5 54/M ARF 4/83 956 - Bronchial CA 10/84 Palliative PE, Aza, PMP HD Died 5/85 51 c Mesangioprol iterative GN and tumours )OLU i-. 6 72/F NS 10/90 230 4.0 Renal cell CA 10/90 Resection None Less proteinuria Alive -i &j 7 61/M NS 11/93 76 5.9 Rectal CA 7/94 Resection, radiotherapy None Partial remission Alive Q. 8 45/M NS 10/77 99 9.5
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