Oxalosis 1

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Bernard Stallenberg - One of the best experts on this subject based on the ideXlab platform.

  • Late diagnosis of Oxalosis in an adult patient: findings on bone radiography.
    AJR. American journal of roentgenology, 1998
    Co-Authors: Niloufar Sadeghi, L De Pauw, Anne Vienne, M Dhaene, Julien Struyven, Bernard Stallenberg
    Abstract:

    P nmary hyperoxaluria type 1 (PH!) is a hereditary metabolic disease caused by a deficiency of the hepatic-specific peroxisomal enzyme, alanine-glyoxalate aminotransferase, and is characterized by an overproduction of oxalate. Renal deposition of insoluble calcium oxalate leads to urolithiasis or nephrocalcinosis and finally to chronic renal failure. At this stage of chronic renal failure, oxalate starts to accumulate in other tissues such as bone, constituting SyStemiC Oxalosis [1]. Clinically, PH! is an cxtremely heterogeneous disease. Most commonly, symptoms and renal failure occur in childhood and early adulthood. Infrequently, the patient remains asymptomatic until late in adult life [1, 2]. Radiographic bone lesions of Oxalosis in children and young patients have been extensively described [3, 4]. In older patients, radiographic bone lesions are less specific and can mimic those of renal osteodystrophy. The diagnosis is then difficult to make, and the symptoms can be attributed to secondary hyperparathyroidism, which may also complicate the course of the disease after long-term hemodialysis, superimposing radiographic abnormalities. Furthermore, it is important to distinguish patients with PH! and no associated secondary hyperparathyroidism from those with associated hyperparathyroidism, to avoid useless and harmful parathyroidectomy. In the present case, we report some radiographic features suggesting the diagnosis of oxalate osteopathy late in adult life.

Niloufar Sadeghi - One of the best experts on this subject based on the ideXlab platform.

  • Late diagnosis of Oxalosis in an adult patient: findings on bone radiography.
    AJR. American journal of roentgenology, 1998
    Co-Authors: Niloufar Sadeghi, L De Pauw, Anne Vienne, M Dhaene, Julien Struyven, Bernard Stallenberg
    Abstract:

    P nmary hyperoxaluria type 1 (PH!) is a hereditary metabolic disease caused by a deficiency of the hepatic-specific peroxisomal enzyme, alanine-glyoxalate aminotransferase, and is characterized by an overproduction of oxalate. Renal deposition of insoluble calcium oxalate leads to urolithiasis or nephrocalcinosis and finally to chronic renal failure. At this stage of chronic renal failure, oxalate starts to accumulate in other tissues such as bone, constituting SyStemiC Oxalosis [1]. Clinically, PH! is an cxtremely heterogeneous disease. Most commonly, symptoms and renal failure occur in childhood and early adulthood. Infrequently, the patient remains asymptomatic until late in adult life [1, 2]. Radiographic bone lesions of Oxalosis in children and young patients have been extensively described [3, 4]. In older patients, radiographic bone lesions are less specific and can mimic those of renal osteodystrophy. The diagnosis is then difficult to make, and the symptoms can be attributed to secondary hyperparathyroidism, which may also complicate the course of the disease after long-term hemodialysis, superimposing radiographic abnormalities. Furthermore, it is important to distinguish patients with PH! and no associated secondary hyperparathyroidism from those with associated hyperparathyroidism, to avoid useless and harmful parathyroidectomy. In the present case, we report some radiographic features suggesting the diagnosis of oxalate osteopathy late in adult life.

Md Osman Dönmez - One of the best experts on this subject based on the ideXlab platform.

  • Adv2003601
    2020
    Co-Authors: Michel Fischbach, Börje Haraldsson, Pauline Helms, Stéphanie Danner, Vincent Laugel, Joëlle Terzic, Md, Pédiatrie Michel Fischbach, Md Osman Dönmez
    Abstract:

    Peritoneal dialysis prescription in children should be individualized-based not only on numerical targets (Kt/V urea , K creat ), but also on consideration of the peritoneal membrane, a dynamic dialysis membrane. In fact, the effective peritoneal surface area is at least a triple entity: an anatomic area, a contact area, and an exchange area. The anatomic area appears to be twice as large in infants as in adults if expressed per kilogram of body weight (BW), although the area is independent of age if expressed per square meter of body surface area (BSA). Therefore, scaling of the intraperitoneal fill volume (IPV) by BSA in square meters is necessary to avoid a low IPV/area ratio, which results in a functionally "hyperpermeable" peritoneal exchange. The contact area (the wetted membrane) is only a fraction of the anatomic area-that is, 30% -60% in humans (by computed tomography). Contact area depends on a variety of factors, such as posture and fill volume, that affect the degree of recruitment of membrane contact area. The exchange area is influenced by both the anatomic are and the contact area. However, it is mainly governed by the specific vascular area as determined by the peritoneal vascular perfusion and the capillaries available for exchange. Vascular area is dynamically affected by a variety of factors, such as the composition of the peritoneal dialysis fluid, the fill volume, and possible inflammatory agents. Key words Children, peritoneal membrane, anatomic, contact, exchange Introduction To be optimal, peritoneal dialysis (PD) should be individualized and adapted to the requirements of the patient. In that respect, various parameters are important: for example, intraperitoneal fill volume (IPV), renal residual function, and the properties of the peritoneal membrane. But, in contrast to a standard hemodialysis prescription, a PD prescription cannot choose the dialyzer. Thus, the PD prescription is not primarily selected based on the peritoneal membrane area recruited for the dialysis exchange (a dynamic process). During the last decade, we have learned that, in children, the peritoneal membrane is a dynamic dialysis membrane. In fact, the effective surface area of the peritoneal membrane involved in dialysis exchange should be considered in bedside practice to be at least a triple entity: an anatomic area (SA), a contact area (SC), and an exchange area (SE). Anatomic surface area The peritoneum is a large, intricately arranged serous membrane that lines the abdominal wall [parietal peritoneum (PP)] and the visceral organs of the abdominal cavity [visceral peritoneum (PV)]. The PV accounts for approximately 90% of the total anatomic surface of the peritoneal membrane; the PP accounts for only 10%. Nevertheless, the relative contributions of the PV and the PP in peritoneal dialysis may not necessarily correlate to anatomic surface. In fact, studies using eviscerated rats suggest that the contribution of the PP to peritoneal exchange is much less than would be predicted from the relative surface areas of PP and PV. Only a few measurements of anatomic surface area have been performed. Putiloff (1), who assessed, post mortem, the PP and PV surface areas of an infant (weight: 2.9 kg) and an adult (weight: 70 kg), found that the anatomic surface per unit body weight was about twice as large in the infant (522 cm 2 /kg) as in the adult (284 cm 2 /kg). On the other hand, a constant, age-independent relationship is noted between anatomic surface area and body surface area (BSA) in square meters. In fact, the anatomic surface area approximates the surface area of the skin (1,2). 266 From the aforementioned data, it appears that young people with a low body weight will receive less dialysate in proportion to the anatomic surface area of their peritoneal membrane if weight is used as the determinant of IPV. They may therefore appear to be high transporters during a peritoneal equilibration test (2). To avoid this functional state of "hyperpermeability" in infants and children as compared with adults, scaling of the fill volume by BSA in square meters was proposed (3,4). Indeed, the prescribed fill volume directly modifies the ratio IPV/SA (2,3). Therefore, scaling the IPV by BSA (mL/m 2 ), particularly in infants and small children, is good clinical practice (3,4). It avoids certain potential clinical consequences-for example, loss of ultrafiltration capacity (5) owing to the functional hyperpermeability induced by a too-low IPV that has been scaled simply to weight (4). Contact surface area In a PD exchange, it is the contact surface area that is important, not the anatomic surface area. The mass transfer area coefficient [MTAC (4)] or the permeability surface area product (PS) provides information about the effective SC, the "wetted membrane" in contact with the dialysis solution. The mass transfer coefficient (MTC) of the effective membrane surface area is a solute characteristic factor. The area factor (A) depends on the SC, a dynamic area influenced in humans by the fill volume (6,7) and patient position (7), and in animals by mechanical factors [for example, agitation (8)] and by pharmacologic factors [for example, surfactant (8)]. Studies in rodents by Flessner and colleagues (8) demonstrated that, during a dialysis exchange, SC is significantly less than SA. Only approximately 25% -40% of SA is in contact with dialysate after instillation of a quantity of dialysis solution scaled to approximate a 2-L to 3-L exchange in a 70-kg human subject. Those authors also demonstrated that the contact area could be increased with agitation or administration of surfactant, leading to increased peritoneal transport (9). In fact, the mean SC/SA ratio of mouse peritoneum increased by a factor of 4 when surfactant was added to the PD fluid (8). In humans, Chagnac (10) developed a method that applies stereologic techniques to a computed tomography scan, imaging the peritoneal membrane to estimate SC. The contact area during a 2-L dialysis exchange was only approximately 0.55 m 2 , a value lower than previous estimates suggested. Thus, in animals and in humans, only a fraction of SA is used for dialysis exchange. The data confirm the theoretic estimate proposed in 1973 by Henderson (11), who reasoned that the functional surface area of the peritoneum must be substantially less than the SA. It could also be hypothesized that, in humans, the SC is a dynamic dialysis membrane affected by various parameters, some mechanical (such as agitation), others pharmacologic (such as surfactant), and still others related to the prescription (such as an optimized fill volume). In fact, Chagnac (6) was able to demonstrate the effect of increased IPV on membrane surface in PD patients: increasing the IPV by 50% (to 3 L from 2 L) results in a significant increase in SC to 0.67 ± 0.04 m 2 from 0.57 ± 0.03 m 2 (18% ± 2.3%), and a significant increase in MTAC creat to 13.6 ± 1.2 mL/min from 10.6 ± 0.7 mL/min (28% ± 2.4%). Altogether, the PD prescription-and especially the fill volume-has a direct impact on SC, allowing for optimized dialysis exchanges. Exchange surface area The peritoneal membrane is not only an anatomic area and a contact area, it is also of course an exchange area. Those areas together result in a patient-specific "effective peritoneal surface area" (3,6). The SE is a complex structure. It might be simplified this way: on the one hand, it has an anatomic part (capillaries, extracellular matrix, and mesothelial cells); on the other hand, it has a functional part (the peritoneal microvasculature). The degree of microvascular perfusion has a direct impact on the exchange (6,7). For example, in the case of reduced SA secondary to old infections or prior abdominal surgery, or in the case of reduced SC secondary to a small fill volume prescription (4,5), the direct effect is a reduction in the exchange area (3). In the past decade, our knowledge of the transport processes across the peritoneal membrane has expanded considerably. In particular, the three-pore model introduced by Rippe and co-workers (12) has been most successful in predicting the transperitoneal exchange of fluid and solutes. (The model seems to be universal for microvascular beds in general.) According to the theory, the peritoneal membrane contains three populations of functional pores: the water-exclusive aquaporins, the small-pore pathways, Fischbach et al. 267 and the large-pore pathways. The frequency of the pores is inversely related to their size. Those physiologic concepts have been used to estimate the PD capacity of individual patients (7,12). The most important parameter describing exchange across the peritoneal membrane is the "area parameter" (total pore area / diffusion). It determines the rate of diffusion (the MTAC) for any hydrophilic solute, and it seems mainly to reflect the number of capillaries available for exchange (the density of the functional pores of the perfused capillaries). Using the three-pore model Our results support the view of Keshaviah (13) that IPV indeed affects the area available for exchange until functional recruitment reaches a plateau. They also agree with findings from a study of iohexol uptake from the abdominal cavity (14). The results of a calculated exchange area based on capillary pores varying with IPV can be confirmed by measurements of contact surface area from computed tomography imaging of the peritoneal membrane (6; However, factors other than membrane area may affect the increased transport associated with an increase in IVP. One of those factors might be the differential increase in the contact area of PV and PP. In fact, the low efficiency of the PV might be attributable to the presence of unmixed or poorly mixed fluid trapped in the many pouches formed by the complex shape of the peritoneal space (8,6). Increasing IPV or applying agitation or vibration to the abdomen of experimental animals improved SC (8) and solute clearance (9), suggesting that a lack of mixing is a main factor limiting solute transport by the PV. In the same way, Flessner (8) demonstrated that surfactant enhanced SC in mice and rats, probably by increasing the surface tension between PP and PV surfaces. An increase in IPV increases SE. However, the associated increase in intraperitoneal pressure would be expected to increase fluid absorption by peritoneal tissues and lymphatic vessels, thus reducing net ultrafiltration (9) and, consequently, solute removal. The use of surfactants in human subjects (if such treatment is proved to be nontoxic) might provide an alternative or combined approach for enhancing SC without increasing intraperitoneal pressure (8,6). Effective surface area The effective surface area of the peritoneal membrane is related to the SA, the SC, and SE [mainly the capillaries recruited for dialysis exchange: density of and the more constant functional pores of the capillaries (7,12)]. Peritoneal vascular perfusion affects the number of perfused capillaries (15). The composition of the PD fluid (15,16) also directly affects capillary recruitment. Altogether, the PD fluid-in terms of both composition and fill volume-appears to be a main determinant of the dynamic changes of the peritoneal membrane as a dialysis membrane. Key words Causes of end-stage renal disease, children, complications Introduction End-stage renal disease (ESRD) occurs in all age groups. Children with ESRD differ from adults with respect to the causes of renal failure (1-3). The introduction of continuous ambulatory peritoneal dialysis (CAPD) to the pediatric ESRD population occurred in the late 1970s. The advantages of CAPD are simple application in infants and young children, ability to attend school for school-age children, and ability of adolescents to perform their own therapy. The CAPD procedure is relatively simple to learn, and home dialytic therapy can therefore be started quickly. Unlike hemodialysis (HD), CAPD requires no specialized, complex equipment. Also, the therapy results in continuous steady-state biochemical and fluid states, avoiding seesaw fluctuations that occur with intermittent HD (2,4). Continuous ambulatory peritoneal dialysis is better suited to children than is HD. However, the main disadvantages of chronic peritoneal dialysis (PD) are infections and mechanical and metabolic complications (1,2,5). The aim of the present retrospective study was to evaluate the causative factors, outcomes, and complications of therapy in children treated with chronic PD. Patients and methods Between July 1997 and August 2002, 35 children (16 girls, 19 boys) diagnosed with ESRD at the department of Pediatric Nephrology, Medical Faculty of Uludag University, were dialyzed with chronic PD. The average age at initiation was 9.3 ± 4.4 years (range: 3 days -16 years). We determined the causative factors leading to ESRD. At the start of PD, 6 patients received double-cuff Tenckhoff catheters and 29 patients received doublecuff, swan-neck coiled catheters. Catheter insertion was performed by percutaneous trocar (n = 5), laparotomy (n = 19), or laparoscopy (n = 11). In 29 of our patients (82.9%), the catheter exit-site orientation was downward; in the others, it was lateral. All patients started on CAPD. Nine patients switched to automated peritoneal dialysis (APD) during the follow-up period. The follow-up period was 15.1 ± 5.1 months (range: 7 -23 months). The dialysate exchange volumes used by our patients were determined as 30 -50 mL/kg. All CAPD patients used the UltraBag twin-bag system (Baxter Healthcare Corporation, McGaw Park, IL, U.S.A. Pac-Xtra, HomeChoice (Baxter Healthcare). Patients on chronic PD were evaluated at 5 stages during follow-up (start, <12 months, 13 -24 months, 25 -36 months, >36 months). Serum biochemical and hematologic parameters were measured monthly from blood samples. The measured values included sodium, potassium, chloride, urea, creatinine, uric acid, calcium, phosphorus, alkaline phosphatase, triglycerides, total cholesterol, glucose, albumin, and hematocrit. Body weight, blood pressure, and height were recorded at each control visit. Dialysate, exit-site, and nasal cultures were performed each month. The frequency of infectious and noninfectious complications was analyzed. The criteria for peritonitis was cloudy peritoneal fluid and increased dialysate white cell count (>100 cells/mL) with >50% polymorphonuclear cells. Facultative findings were abdominal pain or fever. Every 3 months or 6 months, daily urine output and drained dialysate volume were obtained to estimate creatinine clearance (CCr) and Kt/V urea. Creatinine and urea levels were measured in serum, urine, and peritoneal dialysate. The PD Adequest program (Baxter Healthcare) was used for calculations of adequacy (6). Statistical analysis The data are given as mean ± standard deviation. The differences in the various parameters during dialysis treatment were compared using analysis of variance. Values of p less than 0.05 were accepted as significant. Results The average follow-up period was 21.1 ± 17.1 months. The average duration of CAPD was 17.1 ± 14.5 months (range: 1 -62 months) and of APD, 15.7 ± 15.0 months (range: 1 -47 months). The causes of ESRD were reflux nephropathy [n = 8 (22.9%)], chronic interstitial nephritis [n = 3 (8.6%)], chronic glomerulonephritis [n = 2 (5.7%)], membranoproliferative glomerulonephritis [n = 3 (8.6%)], focal segmental glomerulosclerosis [n = 6 (17.1%)], hemolytic uremic syndrome [n = 2 (5.7%)], Alport syndrome [n = 2 (5.7%)], renal tubular acidosis [n = 1 (2.9%)], nephronophthisis [n = 1 (2.9%)], primary hyperoxaluria type I [n = 1 (2.9%)], polycystic kidney disease [n = 1 (2.9%)], and unknown [n = 5 (14.3%)]. Five children had hereditary familial nephropathy (14.1%) as the underlying cause for ESRD, 2 of whom had Alport syndrome; 1, Oxalosis; 1, polycystic kidney disease; and 1, nephronophthisis. The major complication during therapy was peritonitis. During the study, 41 episodes of peritonitis occurred in 17 patients. The overall frequency of peritonitis was 1 episode per 18 patient-months. Of the children on APD, 7 developed 17 peritonitis attacks (1 episode per 8.3 patient-months), including 1 child who developed peritonitis 10 times. Of the patients on CAPD, 10 developed 24 peritonitis attacks (1 episode per 24.9 patient-months). During the study, 51% of the patients had no episodes of peritonitis. No tunnel or exit-site infections occurred. Of all peritonitis episodes, 43.9% were caused by gram-positive bacteria, 24.4% by gram-negative bacteria, and 2.3% by Candida albicans. In 29.3% of the episodes, cultures were negative. All patients received human recombinant erythropoietin (rHuEPO). The rHuEPO dosage was individually adjusted according to hemoglobin values. We also recorded noninfectious complications during follow-up. The overall rate of subcutaneous leak was 11.4% (n = 4). In those cases, conservative management did not help the leaks to regress, and the catheters had to be replaced. The overall rate of dialysate leak was 5.7% (n = 2). In those 2 patients, conservative management did not stop the leakage, and the catheters had to be replaced. A hydrothorax and a pericardial effusion regressed with conservative management. Inguinal hernia developed in 3 patients (8.6%) and umbilical hernia in 1 patient (2.9%). Those complications were treated surgically. Two patients (5.7%) experienced drainage problems. In 1 of those patients, the catheter had to be replaced. Three paDönmez et al. 271 tients (8.6%) had problems with catheter cuff protrusion. Medical treatment for hypertension was given to 22 patients (62.9%) at some time during the study. Hypertension was controlled with 1 antihypertensive drug in 8 patients, with 2 drugs in 10 patients, and with 3 or more drugs in 4 patients. By the end of the follow-up, 4 patients had died of sepsis or cardiopulmonary complications. One case was transferred to HD because of resistant Candida peritonitis. Discussion and conclusions In our study, reflux nephropathy was the most common primary renal disease, and focal segmental glomerulosclerosis was the second most common. Among the preventable causes of chronic renal failure, reflux nephropathy was reported at 22.9% among our patients, as compared with 12.5% in France (7), 0% in Sweden (8), 16.7% in Chile (9), and 32.4% in Turkey (10). The differences may be attributable to early detection of renal disease. The high incidence of reflux nephropathy in our patients was similar to that reported by Sirin et al. (10). We think that reflux nephropathy is one of the most important causative factors of chronic renal failure in children. The incidence of peritonitis still has a significant impact on the success of chronic PD. The overall peritonitis rate of 1 episode per 18 patient-months in our patients compares with a frequency of 1 episode per 7.1 -28.6 patient-months in recent reports (5,(11)(12)(13). The frequency of peritonitis in our CAPD patients was found to be 1 episode per 24.9 patient-months. That result is similar to the findings of Honda et al. (13). The incidence of peritonitis in our APD patients was higher than that in our CAPD patients. In the literature, the peritonitis incidence with APD is reported to be lower than the incidence with CAPD (14). On the other hand, some authors reported that the incidences were not different between the modalities (15,16). In our patients on CAPD, the peritonitis incidence was similar to those reported in the literature; but, in our patients on APD, the incidence was higher. We think that the 10 recurrent peritonitis episodes in 1 patient on APD affected the result. Swan-neck double-cuff catheters and a downward exit-site orientation are reported to reduce peritonitis and tunnel and exit-site infections (5). The lack of tunnel or exit-site infections and the low incidence of peritonitis seen in our CAPD patients may be the result of our use of swan-neck double-cuff catheters and a downward orientation in 82.9% of our patients. In our patients, the most common exit-site orientation was downward; we therefore think that choosing that orientation reduced the peritonitis attacks in our study. A literature review revealed that, during chronic PD, gram-positive bacteria cause peritonitis more frequently than do gram-negative bacteria (1). In our study, we found that gram-positive bacteria caused peritonitis 43.9% of the time. That result is similar to results reported in the literature. The incidence of Candida albicans observed in our study (2.3%) was slightly lower than in other reports (12,17). We targeted weekly Kt/V urea clearances of >2.0 and CCr > 60 L/week/1.73 m 2 . The guideline for the Peritoneal Dialysis in Children Complications related to the catheter are an important cause of morbidity (1,5). The most common problems are subcutaneous leaks, dialysate leaks, cuff protrusion, inguinal hernia, and obstruction. The frequency of those complications reported in the literature ranges from 12% to 73% (19). We observed such problems in 17 of our 35 patients (48.6%). Those results are similar to the results reported in the literature. According to the 1995 annual report of the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS), 49% of PD patients were given antihypertensive drugs (11). The overall incidence of hypertension in our patients was 62.9%. Hypertension was an important complication in our patients. Four (11.4%) patients died. That mortality rate is similar to the rates given in previous reports (5,11,12). One patient was transferred to HD because of resistant Candida peritonitis.

L De Pauw - One of the best experts on this subject based on the ideXlab platform.

  • Late diagnosis of Oxalosis in an adult patient: findings on bone radiography.
    AJR. American journal of roentgenology, 1998
    Co-Authors: Niloufar Sadeghi, L De Pauw, Anne Vienne, M Dhaene, Julien Struyven, Bernard Stallenberg
    Abstract:

    P nmary hyperoxaluria type 1 (PH!) is a hereditary metabolic disease caused by a deficiency of the hepatic-specific peroxisomal enzyme, alanine-glyoxalate aminotransferase, and is characterized by an overproduction of oxalate. Renal deposition of insoluble calcium oxalate leads to urolithiasis or nephrocalcinosis and finally to chronic renal failure. At this stage of chronic renal failure, oxalate starts to accumulate in other tissues such as bone, constituting SyStemiC Oxalosis [1]. Clinically, PH! is an cxtremely heterogeneous disease. Most commonly, symptoms and renal failure occur in childhood and early adulthood. Infrequently, the patient remains asymptomatic until late in adult life [1, 2]. Radiographic bone lesions of Oxalosis in children and young patients have been extensively described [3, 4]. In older patients, radiographic bone lesions are less specific and can mimic those of renal osteodystrophy. The diagnosis is then difficult to make, and the symptoms can be attributed to secondary hyperparathyroidism, which may also complicate the course of the disease after long-term hemodialysis, superimposing radiographic abnormalities. Furthermore, it is important to distinguish patients with PH! and no associated secondary hyperparathyroidism from those with associated hyperparathyroidism, to avoid useless and harmful parathyroidectomy. In the present case, we report some radiographic features suggesting the diagnosis of oxalate osteopathy late in adult life.

Anne Vienne - One of the best experts on this subject based on the ideXlab platform.

  • Late diagnosis of Oxalosis in an adult patient: findings on bone radiography.
    AJR. American journal of roentgenology, 1998
    Co-Authors: Niloufar Sadeghi, L De Pauw, Anne Vienne, M Dhaene, Julien Struyven, Bernard Stallenberg
    Abstract:

    P nmary hyperoxaluria type 1 (PH!) is a hereditary metabolic disease caused by a deficiency of the hepatic-specific peroxisomal enzyme, alanine-glyoxalate aminotransferase, and is characterized by an overproduction of oxalate. Renal deposition of insoluble calcium oxalate leads to urolithiasis or nephrocalcinosis and finally to chronic renal failure. At this stage of chronic renal failure, oxalate starts to accumulate in other tissues such as bone, constituting SyStemiC Oxalosis [1]. Clinically, PH! is an cxtremely heterogeneous disease. Most commonly, symptoms and renal failure occur in childhood and early adulthood. Infrequently, the patient remains asymptomatic until late in adult life [1, 2]. Radiographic bone lesions of Oxalosis in children and young patients have been extensively described [3, 4]. In older patients, radiographic bone lesions are less specific and can mimic those of renal osteodystrophy. The diagnosis is then difficult to make, and the symptoms can be attributed to secondary hyperparathyroidism, which may also complicate the course of the disease after long-term hemodialysis, superimposing radiographic abnormalities. Furthermore, it is important to distinguish patients with PH! and no associated secondary hyperparathyroidism from those with associated hyperparathyroidism, to avoid useless and harmful parathyroidectomy. In the present case, we report some radiographic features suggesting the diagnosis of oxalate osteopathy late in adult life.