Nephrol Dial Transplant (1991) 6: 227-228 © 1991 European Dialysis and Transplant Association-European Renal Association

Nephrology Dialysis Transplantation

Letters Nephrotic Syndrome in Ulcerative Colitis

Renal Unit Royal Victoria Infirmary Newcastle upon Tyrie

N. Nand M. K. Ward

Department of Pathology Royal Victoria Infirmary Newcastle upon Tyne

A. R. Morley

1. Stokke KT, Teisberg PA, Myhre E, Hovig T, Flatmark A , Gjone E. Nephrotic syndrome in ulcerative colitis. Scand J Gastroenterol 1976; 11: 571-576 2. Hellwege HH, Blaker F, Gebbers JO. Hypocomplementeric membrano-proliferative glomerulonephritis in a child with ulcerative colitis. Monatschr KinderheUk 1976; 124: 706-711 3. Hurbert D , Beaufils M, Meyrier A. IgA glomerulonephritis and inflammatory colitis - two cases. Presse Medicate 1984; 13 (17): 1083-1085 4. Thomas DM, Nicholls AJ, Feest TG. Ulcerative colitis and glomerulonephritis: Is there an association? Nephrol Dial Transplant 1990; 5(8): 628-629 5. Bendixen G, Goltermann N, Jarnum S, Jensen KB, Weeke B, Westergaard H. Immunoglobulin and albumin turnover in ulcerative colitis. Scand J Gastroenterol 1970, 5: 433-441 6. Teisberg P, Gjone E. Humoral immune system activity in inflammatory bowel disease. Scand J Gastroenterol 1975, 10: 545-549

Downloaded from http://ndt.oxfordjournals.org/ at Dalhousie University on November 9, 2014

Sir, Ulcerative colitis is frequently associated with hepatic disease, arthritis, uveitis, and cutaneous manifestations that these have been characterised as complications. Renal involvement may be in the form of increased frequency of renal stones. However, parenchymatous renal disease or nephrotic syndrome in association with ulcerative colitis is not described in standard textbooks of gastroenterology or nephrology, and on review of the literature we could find only a few case reports of such an association [1-4]. The purpose of this report is to highlight this association. In 1956 a 49-year-old woman was diagnosed ulcerative colitis and was treated with Salazopyrin. She remained well until 1975 when she developed nephrotic syndrome and renal biopsy revealed evidence of mild inactive glomerulitis. She was treated with prednisone without much response, and therefore, her renal biopsy was repeated in 1978; this showed histopathological changes consistent with inactive focal-segmental proliferative glomerulonephritis with C3 deposits in mesangium and capillary wall, and another course of steroid therapy was given without any significant change. In 1982 she had activation of her ulcerative colitis, which was confirmed by a barium enema, sigmoidoscopy, and rectal biopsy. Interestingly, her glomerular changes were activated and showed evidence of chronic but still active mesangial-proliferative glomerulonephritis. In 1986 she presented with anuria and was treated with pulse steroid therapy and cyclophosphamide and dialysed for three months. In February 1987 cyclophosphamide was substituted for azathioprine and she continued on a small maintenance dose of 10 mg prednisone. In October 1987 the patient's renal function further deteriorated (serum creatinine of 561 fonol/1) and she required haemodialysis. Her eosinophil count was also found to be elevated (20%), for which no cause could be found. For the last two years she has had established end-stage renal failure, inactive ulcerative colitis and eosinophilia. Chronic ulcerative colitis is rarely known to cause glomerulonephritis and nephrotic syndrome. Stokke et al described two cases of chronic ulcerative colitis who developed nephrotic syndrome. In one case a kidney biopsy was done, showing evidence of mild nephritis in the first instance and later focal glomerular sclerosis at the corticomedullary junction. This patient was given prednisone therapy to which he responsed. In the second case, the biopsy was unsuccessful, but there was a positive test for in-vivo activation of C3. The observation of mild glomerulitis in the first instance in our patient and then progression to focal segmental glomerulonephritis is in line with the case described by Stokke et al

[1]. There are also similarities to the cases described by Thomas et al [4], although C3 was confined to the glomerulus in two of these. However, the exact pathophysiological mechanism for causation of glomerulonephritis is a matter for speculation. Several studies suggest that humoral immune mechanisms are of pathogenetic significance in ulcerative colitis. There is a large increase in mucosal IgG concentrations and fractional catabolic rate of IgG and IgM is also increased [5]. The complement system is also known to be active as a result of a humoral immune reaction taking place in the wall of the bowel and/or in the circulation [6] and circulating immune complexes are present in the majority of cases. But why extraintestinal organs are so often affected in ulcerative colitis, and kidneys relatively spared, still remains to be answered. Some studies suggest that these complications may be caused by circulating immune complexes. Multiple organ involvement with deposition of complement in the mesangium and capillary wall of glomeruli in these cases would further suggest an immune deposit pathogenesis. However, the role of cellular immune mechanism in these cases is still unclear. In conclusion, we think that nephrotic syndrome and renal failure in this patient is most probably related to ulcerative colitis. However, longitudinal multi-center studies of ulcerative colitis for evidence of renal involvement would be desirable to confirm such an association.

Nephrotic syndrome in ulcerative colitis.

Nephrol Dial Transplant (1991) 6: 227-228 © 1991 European Dialysis and Transplant Association-European Renal Association Nephrology Dialysis Transpla...
115KB Sizes 0 Downloads 0 Views