Inflammatory Bowel Diseases Accompanied by Renal Impairment

Inflammatory bowel disease (IBD) is a chronic systemic disorder, which mainly affects the bowel. However, both ulcerative colitis (UC) and Crohn’s disease (CD) are often associated with extra intestinal manifestations, complications, and other autoimmune disorders. These manifestations can involve almost any organ system, including the musculoskeletal, dermatologic, hepatopancreatobiliary, ocular, renal, and pulmonary systems, and can provoke an interesting challenge to physicians managing IBD patients [1]. In our days, an increasing number of kidney manifestations and complications in patients suffering IBD are mentioned, profoundly due to therapists’ vigilance. Many pathophysiological pathways have been accused for renal involvement. Kidney damage can be provoked by the disease itself, from secondary extra intestinal complications of the disease (malnutrition), or side effects of therapy. Aim of this paper is to review the renal involvement in IBD so that it can be easily recognized and rapidly treated. Severe long-standing disease consists a predisposing factor for renal complications that answer in 4-23% of patients [2]. Uric acid and oxalate stones are met in a number 10-100 times greater than for the general population. Glomerulonephritis is mentioned in several reports on patients with IBD at least 27 patients; of these 7 had CD, 17 had UC and 3 were indeterminate. Tubular abnormalities were seen in 31% of CD and in 23% of UC patients who were not on ASA. Furthermore, IBD is an uncommon cause of secondary amyloidosis. Lastly, there are drugs used to treat IBD (amino salicylates, cyclosporine) with significant possibility of renal toxicity [3,4]. The hazard of nephrolithiasis is 10-100 times greater than the general population it patients with IBD, specifically those with ileocolic CD who undergo surgery. Kidney stones consist mostly of calcium oxalate or uric acid and occur more often in the right urinary tract. Urate stones are caused by increased acidic urine due to intestinal fluid and bicarbonate losses. Furthermore, the loss of electrolytes (potassium, magnesium) with diarrhea impedes crystallization. Thus, treatment of urate stones includes treatment of diarrhea, alkalinizing the urine and increasing fluid intake. Increased intestinal absorption of oxalate (enteric hyperoxaluria) leads to the production of calcium oxalate stones. Bile salt mal absorption in a dysfunctional terminal ileum (diseased or resected) results in fat mal absorption, that bind intraluminal calcium, decreasing the amount of calcium bound to oxalate (this last complex is poorly absorbed) resulting in increased oxalate absorption. Enteric hyperoxaluria is infrequent in patients with colectomy, ileostomy or jejunostomy, since the majority of oxalate is absorbed in the colon but can be met in parenteral nutrition, minimal oral intake, even in patients with colectomies [5,6]. A good strategy for preventing the recurrence of calcium oxalate stones includes hydration, oral urinary alkalization, low fat and oxalate diet, increasing the dietary intake of calcium and restricting the intake of salt. The gold standard imaging technique for the detection kidney stones in asymptomatic population is ultrasound [7]. Different histological patterns of glomerulonephritis, as a form of renal involvement in patients with IBD, have been reported: immunoglobulin IgA nephropathy, IgM nephropathy and membranous, mesangiocapillary, focal segmental and anti-glomerular basement membrane glomerulonephritis. There is no association with duration of disease and IBD can present with or after the GN. There is a male predominance and association with the active inflammation in the bowel or biliary system. Glomerulonephritis is directly associated with intestinal or biliary disease activity, and it has been indicated that remission of bowel inflammation improves renal function. There is no connection with duration of disease and there is a male predominance. Histological lesions may vary from minimal change nephropathy and IgA nephropathy to rapidly progressive crescentic GN with or without tubulointerstitial nephritis. The genetic connection of IBD and IgA nephropathy could be the base of the explanation in their correlation. Hematuria, nephritic syndrome oliguria, proteinuria, elevated serum creatinine and edema are the usual symptoms, signs and laboratory findings in patient’s clinical presentations. Treatment includes steroid administration and bowel resection if there is no response [2,8]. Although tubulointerstitial nephritis has been reported in patients with IBD and ASA therapy, it is also considered an extra intestinal manifestation. This admission was supported by counting the urinary enzymes beta-N-acetylglucosaminidase (bNAG), dipeptidylpeptidase 4 (DPP4) and alanine amino peptidase (AAP) before initiating therapy in patients with active UC and after an effective treatment. In particular, enzymuria (elevated B-NAG levels) changed to normal values, pointing out Editorial