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AimsIn individuals with chronic kidney disease (CKD), including those undergoing maintenance hemodialysis (MHD), coronary artery calcification (CAC) is common. We hypothesized that, in MHD patients, intake of the calcium-free phosphate binder sevelamer is associated with lower CAC compared to calcium-based phosphate binders (CBPB).Material and methodsThis is a cross-sectional study of MHD patients, who underwent computerized tomography to assess coronary artery calcium scores (CACS). Patients were stratified into two mutually exclusive groups based on taking only a CBPB vs. sevelamer. Logistic regression was used to calculate adjusted odds ratio (OR) of CACS > or = 400, CACS 100 < or =; CACS < 400, 10 < or =; CACS < 100 vs. CACS < 10.Results117 MHD patients were either on a CBPB alone (n = 60) or sevelamer alone (n = 57). Despite increased prevalence of DM in the sevelamer group (58%) as compared to the CBPB group (35%), CACS was significantly lower with sevelamer use (283 + or - 83 vs. 494 + or - 94, p = 0.02). The OR of significant CACS > or =; 400 vs. CAC < 10 was 4.35 (95% confidence interval: 1.5 - 9.9, p = 0.008) for CBPB compared with sevelamer, after controlling for case-mix, cholesterol-lowering medication, DM, and inflammatory markers.ConclusionIn our cohort, significant CAC was significantly more prevalent among MHD patients taking CBPB as compared to sevelamer monotherapy.

Background: Diabetic nephropathy (DN) is one of the major complications of diabetes. Hyperglycemia, inflammation and oxidative stress as well as advanced glycation end products (AGEs) are reported as the risk factors for DN. Sevelamer has shown promising results in reducing inflammation and even HbA1c levels in DN. Objectives: We aim to evaluate the therapeutic effects of sevelamer on blood sugar, HbA1c level, lipid profile, and high sensitivity CRP (hs-CRP) in patients with diabetic nephropathy. Patients and Methods: In this clinical trial, 18 patients (13 female with mean age of 61.22±9.32 years) with stages 2-4 of diabetic nephropathy were recruited. Patients were administered with 800 mg of sevelamer twice a day for three months. Blood sugar, HbA1C, hs-CRP, lipid profile and other laboratory findings were measured before and 1, 2 and three months after initiation of the treatment. Results: There was significant decline in HbA1c (p=0.001), postprandial blood sugar (p=0.02) and phosphorus (p

End-stage renal disease (ESRD) is a common disease encountered in clinical practice and is associated with increasing metabolic derangements through disease progression. Phosphate retention is one of the most common derangements and is associated with increased mortality. Hyperphosphatemia becomes increasingly prevalent as glomerular filtration rate decreases. Non-calcium phosphate-binding resins and dietary phosphate restriction are the mainstays for managing hyperphosphatemia in patients with ESRD. Sevelamer carbonate is the most frequently used non-calcium phosphate binder in the US due to ease of administration and an excellent safety profile. However, there is increasing recognition of gastrointestinal injury associated with medication use. Here we report a case of an 81-year-old male with biopsy-proven gastrointestinal mucosal injury secondary to sevelamer carbonate administration.

Many traditional and nontraditional risk factors contribute to vascular calcification among maintenance hemodialysis (MHD) patients. It is not clear whether coronary artery calcification (CAC) delineates a higher mortality risk independent of known risk factors. We examined 6-year (10/2001-9/2007) survival of 166 MHD patients, aged 53 +/- 13 years, with baseline CAC scores. Patients were grouped into four CAC groups: 0, 1-100, 101-400, and 400+. The 101-400 and 400+ groups were associated with a significantly higher adjusted risk of death than CAC 0 with hazard ratios (HR) 8.5 (95% CI: 1.1-48.1, p = 0.02) and 13.3 (95% CI: 1.3-65.1, p = 0.01), respectively, independent of demographics, comorbidity, lipids and other cardiovascular risks, surrogates of bone disease, nutritional and inflammatory markers and dialysis dose. Total CAC [HR 6.7 (1.1-21.5, p = 0.03)] followed by the presence of CAC in the left main [4.6 (2.2-9.8, p = 0.001)] and left anterior descending artery [4.3 (2.1-14.2, p = 0.001)] were strong independent predictors of mortality even after adjusting for above covariates. Total and vessel-specific CAC predict mortality in MHD patients independent of traditional and nontraditional risk factors.

Objectives: Raltegravir (RAL) that can form chelates with multivalent metal cations shows lateral interactions with multivalent metal cation and polycationic polymer. We investigated the interactions of RAL with multivalent metal cation preparations, Al(OH)3 and LaCO3, and polycationic polymer preparations, bixalomer (Bxl) and sevelamer (Svl). Methods: Immediately before the oral administration of 40 mg/kg RAL, the rats were administered orally with the vehicle, Al(OH)3, LaCO3, Bxl, or Svl, and the time course of RAL serum concentration was followed. The in vitro binding affinity of RAL with multivalent metal cation and polycationic polymer was also evaluated using isothermal titration calorimetry (ITC). Results: When Al(OH)3, LaCO3, Bxl, or Svl was concomitantly administered with RAL, the maximum concentration and area under the curve were significantly lower than those when RAL was administered alone. ITC showed the interaction of RAL with Al(OH)3 as an enthalpy‐driven reaction and its interactions with LaCO3 and Bxl as entropy–enthalpy mixed reactions. Conclusions: The interaction of RAL with Al(OH)3, LaCO3, Bxl, or Svl can inhibit RAL absorption into the gastrointestinal tract, and thus, the multivalent metal cation and polycationic polymer are the modifying factors that can affect RAL pharmacokinetics. [ABSTRACT FROM AUTHOR]

Amino-terminally truncated parathyroid hormone (PTH) fragments are detected to differing degrees by first- and second-generation immunometric PTH assays (PTH-IMAs), and acute changes in serum calcium affect the proportion of these fragments in circulation. However, the effect of chronic calcium changes and different vitamin D doses on these PTH measurements remains to be defined. In this study, 60 pediatric dialysis patients, aged 13.9 ± 0.7 years, with secondary hyperparathyroidism were randomized to 8 months of therapy with oral vitamin D combined with either calcium carbonate (CaCO3) or sevelamer. Serum phosphorus levels did not differ between groups. Serum calcium levels rose from 9.3 ± 0.1 to 9.7 ± 0.1 mg/dl during CaCO3 therapy (p

IntroductionCardiovascular disease accounts for almost half of all deaths in individuals with chronic kidney disease stage 5 despite advances in both dialysis treatment and cardiology. A combination of lipid-lowering and anti-inflammatory effects along with avoidance of hypercalcemia should be taken into account when choosing phosphorus binders for maintenance hemodialysis (MHD) patients.MethodsWe examined the association of sevelamer versus calcium-based phosphorus binders with lipid profile, inflammatory markers including C-reactive protein (CRP), and mineral metabolism in MHD patients who participated in the Nutritional and Inflammatory Evaluation of Dialysis Patients (NIED) study from October 2001 to July 2005.ResultsOf the 787 MHD patients in the NIED study, 697 were on either sevelamer, a calcium-based binder, or both and eligible for this study. We compared the groups based on taking sevelamer monotherapy (n = 283) or calcium binder monotherapy (n = 266) for serum phosphate control. There were no differences between the groups on dialysis vintage. There were significant differences in age, serum calcium and phosphorus levels, as well as intact parathyroid hormone levels. Using a logistic regression models, the sevelamer group had a higher odds of serum CRP

P-cresyl sulfate and indoxyl sulfate are strongly associated with cardiovascular events and all-cause mortality in chronic kidney disease (CKD). This randomized controlled trial was conducted to compare the effects between sevelamer and calcium carbonate on protein-bound uremic toxins in pre-dialysis CKD patients with hyperphosphatemia. Forty pre-dialysis CKD patients with persistent hyperphosphatemia were randomly assigned to receive either 2400 mg of sevelamer daily or 1500 mg of calcium carbonate daily for 24 weeks. A significant decrease of total serum p-cresyl sulfate was observed in sevelamer therapy compared to calcium carbonate therapy (mean difference between two groups −5.61 mg/L; 95% CI −11.01 to −0.27 mg/L; p = 0.04). There was no significant difference in serum indoxyl sulfate levels (p = 0.36). Sevelamer had effects in terms of lowering fibroblast growth factor 23 (p = 0.01) and low-density lipoprotein cholesterol levels (p = 0.04). Sevelamer showed benefits in terms of retarding CKD progression. Changes in vascular stiffness were not found in this study.

Metabolic acidosis, a common condition in patients with renal failure, may be linked to protein-energy malnutrition (PEM) and inflammation, together also known as malnutrition-inflammation complex syndrome (MICS). Methods of serum bicarbonate measurement may misrepresent the true bicarbonate level, since the total serum carbon dioxide measurement usually overestimates the serum bicarbonate concentration. Moreover, the air transportation of blood samples to distant laboratories may lead to erroneous readings. In patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD), a significant number of endocrine, musculoskeletal, and metabolic abnormalities are believed to result from acidemia. Metabolic acidosis may be related to PEM and MICS due to an increased protein catabolism, decreased protein synthesis, endocrine abnormalities including insulin resistance, decreased serum leptin level, and inflammation among individuals with renal failure. Evidence suggests that the catabolic effects of metabolic acidosis may result from an increased activity of the adenosine triphosphate (ATP)-dependent ubiquitin-proteasome and branched-chain keto acid dehydrogenase. In contrast to the metabolic studies, many epidemiologic studies in maintenance dialysis patients have indicated a paradoxically inverse association between mildly decreased serum bicarbonate and improved markers of protein-energy nutritional state. Hence metabolic acidosis may be considered as yet another element of the reverse epidemiology in ESRD patients. Interventional studies have yielded inconsistent results in CKD and ESRD patients, although in peritoneal dialysis patients, mitigating acidemia appears to more consistently improve nutritional status and reduce hospitalizations. Large-scale, prospective randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in malnourished and/or inflamed CKD and maintenance hemodialysis patients. Until then, all attempts should be made to adhere to the National Kidney Foundation Kidney Disease and Dialysis Outcome Quality Initiative guidelines to maintain a serum bicarbonate level in ESRD patients of at least 22 mEq/L.

Metabolic acidosis, a common condition in patients with renal failure, may be linked to protein-energy malnutrition (PEM) and inflammation, together also known as malnutrition-inflammation complex syndrome (MICS). Methods of serum bicarbonate measurement may misrepresent the true bicarbonate level, since the total serum carbon dioxide measurement usually overestimates the serum bicarbonate concentration. Moreover, the air transportation of blood samples to distant laboratories may lead to erroneous readings. In patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD), a significant number of endocrine, musculoskeletal, and metabolic abnormalities are believed to result from acidemia. Metabolic acidosis may be related to PEM and MICS due to an increased protein catabolism, decreased protein synthesis, endocrine abnormalities including insulin resistance, decreased serum leptin level, and inflammation among individuals with renal failure. Evidence suggests that the catabolic effects of metabolic acidosis may result from an increased activity of the adenosine triphosphate (ATP)-dependent ubiquitin-proteasome and branched-chain keto acid dehydrogenase. In contrast to the metabolic studies, many epidemiologic studies in maintenance dialysis patients have indicated a paradoxically inverse association between mildly decreased serum bicarbonate and improved markers of protein-energy nutritional state. Hence metabolic acidosis may be considered as yet another element of the reverse epidemiology in ESRD patients. Interventional studies have yielded inconsistent results in CKD and ESRD patients, although in peritoneal dialysis patients, mitigating acidemia appears to more consistently improve nutritional status and reduce hospitalizations. Large-scale, prospective randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in malnourished and/or inflamed CKD and maintenance hemodialysis patients. Until then, all attempts should be made to adhere to the National Kidney Foundation Kidney Disease and Dialysis Outcome Quality Initiative guidelines to maintain a serum bicarbonate level in ESRD patients of at least 22 mEq/L.

Changes in phosphate-calcium metabolism commonly occurred in patients with chronic kidney disease and are a major pathogenetic factor in the development of secondary hyperparathyroidism and mineral and bone disorder in this group of patients. This article is mainly devoted to a review of basic drugs for CKD-MBD therapy, in particular, Sevelamer and Cinacalcet.

Enarodustat is an orally available hypoxia-inducible factor-prolyl hydroxylase inhibitor which can correct the erythropoietic capacity and improve anemia in chronic kidney disease. Sevelamer carbonate, a non-calcium-based polymeric resin, is one of the commonly prescribed agents for the management of hyperphosphatemia in patients undergoing hemodialysis. This was an open-label, crossover study in healthy male subjects (N = 12) that evaluated the effect of sevelamer carbonate (2400 mg) on the bioavailability of enarodustat (25 mg) when the 2 drugs were administered together (Treatment B) or when enarodustat was administered 3 hours after (Treatment C) or 1 hour before (Treatment D) sevelamer carbonate compared to enarodustat alone (Treatment A). With coadministration of the 2 drugs (Treatment B), enarodustat C max and AUC inf reductions were 53% and 45%, respectively. For Treatment C, C max and AUC inf reductions were 11% and 6%, respectively, and for Treatment D the corresponding values were 8% and 20%. Thus, coadministration of enarodustat and sevelamer carbonate resulted in a substantial reduction (≈50%) in the oral bioavailability of enarodustat. However, the interaction was substantially mitigated by staggering the administration of enarodustat and sevelamer carbonate. Administration of 4 single oral doses of enarodustat 25 mg, with or without sevelamer carbonate, were safe and well tolerated in this study., (© 2023, The American College of Clinical Pharmacology.)

Introduction: Calciphylaxis is a lethal and rare disease characterized by ischemic and necrotic skin lesions caused by vascular calcification of adipose tissue. There have been many risk factors analyzed in the literature; however, the pathogenesis of calciphylaxis is still not well understood and treatment options are limited due to the lack of interventional studies. Our objectives were to describe risk factors, prevalence, incidence, and outcomes for calciphylaxis in hemodialysis patients within the Fraser Health Renal Program. Methods: This was a retrospective matched case-control study of hemodialysis patients within the Fraser Health Renal Program. Hemodialysis patients with calciphylaxis were matched to hemodialysis patients without calciphylaxis in a 1:2 ratio for age and sex from September 2, 2017 to July 3, 2020. Findings: There was a total of 40 calciphylaxis cases matched to 80 controls. In the univariate analysis, peritoneal dialysis, higher body mass index, lower serum iron, lower transferrin saturation, sevelamer, cinacalcet, warfarin, iron (PO), and insulin were associated with increased risk of calciphylaxis. In the multivariate analysis, only peritoneal dialysis, serum iron, sevelamer, and warfarin were identified as significant and strong risk factors associated with calciphylaxis. A low prevalence of 1.9% and high mortality rate of 57.5% at 12 months was found for calciphylaxis cases. Discussion: Significant risk factors associated with calciphylaxis were peritoneal dialysis, serum iron, sevelamer, and warfarin. Future studies should further investigate the impact of minimizing exposure to these risk factors to reduce calciphylaxis development., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Few clinical studies have investigated the value of phosphate (P)-lowering therapies in early chronic kidney disease (CKD) patients in whom hyperphosphataemia has not yet clearly developed and they report conflicting and even unexpected results. In this issue of Clinical Kidney Journal , de Krijger et al. found that sevelamer carbonate (4.8 g/day for 8 weeks) did not induce a significant reduction of pulse wave velocity (PWV) and that fibroblast growth factor 23 (FGF23) did not decrease despite a decline in 24-h urine P excretion. To some extent these findings challenge the concept that 'preventive' P binder therapy to lower FGF23 is a useful approach, at least over this short period of time. Interestingly, in a subgroup of patients with absent or limited abdominal vascular calcification, treatment did result in a statistically significant reduction in adjusted PWV, suggesting that PWV is amenable to improvement in this subset. Interpretation of the scarce and heterogeneous observations described in early CKD remains difficult and causality and/or the possibility of 'preventive' treatment may not yet be completely disregarded. Moreover, de Krijger et al. contribute to the identification of new sources of bias and methodological issues that may lead to more personalized treatments, always bearing in mind that not all patients and not all P binders are equal. [ABSTRACT FROM AUTHOR]

Objective: Medication resins such as Kayexalate and Sevelamer used in the setting of chronic kidney disease for the correction of hyperkalemia and hyperphosphatemia are associated with gastrointestinal mucosal injury. In this study we describe the clinico-pathological features of Resin-induced gastrointestinal mucosal injury highlighting the histo-morphological appearances and differential diagnoses. The aim of this study is to increase the awareness of pathologists and clinicians alike to an under-reported etiology and pattern of intestinal mucosal injury related to medical resin therapy which may at times pose a clinical emergency. Material and Method: The archives of the Department of Histopathology, Mubarak Al Kabir hospital were analyzed for cases of resin-induced gastrointestinal mucosal injury between 2013 and 2018. Results: Of the 15 cases, Kayexalate crystals were identified in 7 cases, Sevelamer in 5 cases and both together were seen in 3 cases. Resin crystals were identified in the gastric antrum&duodenum (3 cases), colon (9 cases in the left colon, 2 cases in the right colon) and anal canal (1 case). The histological tissue reactions included mucosal necrosis (1 case), inflammatory polyps (2 cases), mucosal ulcerations with granulation tissue formation (10 cases), perforation (1 case) , and luminal crystals (1 case). Conclusion: Accurate and timely recognition of the resin crystals in biopsy samples with clinical correlation is mandatory to avoid serious complications. [ABSTRACT FROM AUTHOR]

Hyperphosphatemia in the absence of renal failure is an unusual occurrence, particularly in children, but is a common primary feature of familial hyperphosphatemic tumor calcinosis. We report a child with hyperphosphatemia who presented with multiple episodes of neurologic dysfunction involving lower motor neuron facial nerve palsy along with sequential visual loss. He also had an episode of stroke. There was an extensive metastatic calcification of soft tissue and vasculature. Hyperphosphatemia with normal serum alkaline phosphatase, calcium, parathyroid hormone, and renal function was noted. He was managed with hemodialysis and sevelamer (3 months) without much success in reducing serum phosphate level, requiring continuous ambulatory peritoneal dialysis (3 years). Intact fibroblast growth factor 23 (FGF23) was undetectable, with C-terminal FGF23 fragments significantly elevated (2575 RU/ml, normal <180 RU/ml). Sequencing demonstrated homozygous c.486C >A (p.N162K) mutation in FGF23 exon 3, confirming the diagnoses of primary FGF23 deficiency, the first case to be reported from India. [ABSTRACT FROM AUTHOR]

Introduction: End-stage renal disease is associated with significant comorbidity and mortality. Among its implications, hyperphosphatemia constitutes a consistent and independent risk factor. The use of benchmark treatment, low-cost calcium-based binders declined due to a potential calcification effect on coronary arteries.Areas Covered: Given the increasing prevalence of end-stage renal disease and the high cost of hyperphosphatemia's new primary modality, the non-calcium based phosphate binders, we set-off to systematically assess the economic evaluations of non-calcium containing phosphate binders, sevelamer and lanthanum. The study was performed based on a systematic review of the economic evaluations of sevelamer and lanthanum. The cost-effectiveness profile of the two non-calcium-containing Phosphate Binders compared to calcium-based phosphate binders depends on several factors such as future dialysis costs, utility values, age, survival, and phosphorus levels.Expert Opinion: The comparison between the two agents is rather inconclusive; nevertheless, current review suggests that non-calcium-based phosphate binders may yield a positive cost-effectiveness ratio in patients with inadequate phosphorus management and patient with longer life-expectancy. It is crucial that the literature is endowed with more data, specifically on survival, future dialysis costs, and calcification. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) is a life-threatening disease with numerous complications. Hemodialysis (HD) patients are prone to magnesium deficiency due to malnutrition, which can cause cardiovascular complications and increase mortality. The present study aimed to investigate the effects of sevelamer and calcium carbonate, as phosphate binders, on serum levels of magnesium, calcium, and phosphorus in HD patients. Methods: A parallel clinical trial was conducted on 54 patients undergoing HD at Kosar Hospital of Semnan. The inclusion criteria were end-stage renal disease (ESRD), alternative HD treatment for at least 3 months 3 times a week, and serum phosphate levels greater than 4.5 mg/dL. The participants were randomly assigned to two groups of sevelamer (n = 27) and calcium carbonate (n = 27). If the participants were taking a phosphate binder, they were asked to stop it for 3 weeks. Participants in the sevelamer group received 800 mg of sevelamer at most three times a day and those in the calcium carbonate group were treated with 500 mg of calcium carbonate at most 3 times a day. Before and 3 months after the intervention, the serum levels of calcium, magnesium, and phosphorus were measured through the Arsenazo method using the Pars Azmun kit in the Selectra auto-analyzer. Twenty-one patients in the sevelamer group and 22 patients in the calcium carbonate group finished the study. Results: The results showed that calcium carbonate and sevelamer increased serum magnesium level by 0.20 (P = 0.028) and 0.26 (P = 0.002), on average, which were statistically significant. The administration of calcium carbonate did not significantly change serum calcium levels (P = 0.53), whereas sevelamer reduced serum calcium levels by 0.23 (P = 0.017), on average. This reduction was statistically significant. The results also indicated that none of the calcium carbonate (P = 0.099) and sevelamer (P = 0.543) caused significant changes in serum phosphorus levels. The study findings showed no significant difference between the two groups in terms of changes in the serum levels of magnesium (0.590), calcium (0.116), and phosphorus (0.113). Conclusions: Both drugs (Sevelamer and calcium carbonate) prevented hypomagnesemia and increased serum magnesium levels, but no significant differences were found in blood levels of calcium, phosphorus, and magnesium compared to the two drugs. Considering the effect of magnesium on cardiovascular diseases, increasing the serum magnesium levels through the administration of calcium carbonate and sevelamer can prevent the likelihood of cardiovascular diseases. However, none of the studied drugs was superior to the other in this regard.

Ion-exchange resins are commonly used to manage complications of chronic kidney disease, such as hyperphosphatemia, hyperkalemia, and hypercholesterolemia. Occasionally, these drugs can irritate the gastrointestinal lining and cause life-threatening intestinal necrosis. Currently, the pathophysiology of drug crystal-induced intestinal necrosis is not well understood. We hypothesized that crystals of ion-exchange resins like sevelamer, polystyrene sulfonate, and cholestyramine can trigger the formation of neutrophil and monocyte extracellular traps by contributing to intestinal barrier dysfunction. Light and fluorescence microscopy of the colonic resection specimen from a patient with chronic kidney disease revealed severe intestinal necrosis, ulceration, sevelamer crystals, and inflammation upon oral intake of sevelamer, as well as the formation of neutrophil extracellular traps in proximity to small sevelamer crystals. Indeed, drug crystals reduced metabolic activity and induced barrier dysfunction and cell death in human intestinal epithelial cells in vitro. In addition, drug crystals triggered the release of neutrophil and monocyte extracellular traps. Taken together, these data raise the possibility that besides other factors including chronic kidney disease, diabetes mellitus, and hypertension, drug crystals may further amplify a pre-existing barrier dysfunction and necroinflammation in a crescendo of local intestinal necrosis and systemic inflammation/infection, as occasionally observed in patients on ion-exchange resin therapy.

Lower GI bleeding is a common cause for hospitalization in adults. Medication-associated mucosal injury is an important clinical entity that can result in significant morbidity and mortality. We present the case of a 45-year-old woman with a 3-month history of intermittent abdominal cramping and rectal bleeding. Her medical history was extensive and included end-stage renal disease and a remote history of endometrial carcinoma that was treated with radiation. Initial workup was concerning for ischemic and radiation colitis, however, histology was most consistent with acute inflammation and ulceration associated with crystal fragments. Sevelamer and cholestyramine are commonly used ion-exchange resins that have been associated with mucosal damage. Both medications were discontinued and her symptoms resolved. Our case highlights an underrecognized but important cause of hematochezia.

Background: Kayexalate and sevelamer are resin medications commonly used in the setting of chronic renal failure for the treatment of hyperkalemia and hyperphosphatemia respectively, are known to cause bowel ischemia, ulcerations, necrosis, pseudotumors and perforations and the incidence is higher after post-transplant. Herein we report its presence on the surface of a graft nephrectomy following a masked intestinal perforation. Case Presentation: A 30-year-old male, a renal transplant recipient for dysplastic kidney underwent graft nephrectomy due to wound infection, peri-graft collection and risk of hemorrhage from the vascular anastomotic site. Histological evaluation showed extensive acute tubular necrosis and peri-renal abscess with vegetable matter and numerous colored crystals morphologically consistent with kayexalate and sevelamer. The possibility of an underlying resin induced intestinal perforation was rendered. Conclusions: Kayexalate or sevelamer induced mucosal injury in the gastrointestinal tract could be a clinical emergency and a high index of suspicion particularly in a post-transplant setting may allow prompt recognition and surgical cure. From the pathologists’ view familiarity with the morphological appearances of these non-systemic resin medications and its histologic mimics enables accurate diagnosis and timely clinical intervention.