Focal Segmental Glomerulosclerosis and Scheduled Pretransplant Plasmapheresis: A Timely Diagnosis of Nail-Patella Syndrome Avoided More Futile Immunosuppression.

Focal and segmental glomerulosclerosis (FSGS) is a histopathological pattern of injury. As such, it encompasses a wide variety of dissimilar entities with different pathophysiologic mechanisms. Although ultrastructural morphological characteristics can specifically diagnose certain diseases and genetic mutations can also be unravelled, this ideal situation is generally not available worldwide. In this respect, when proteinuria with or without nephrotic syndrome is encountered and FSGS is the histological lesion, patients start to be prescribed different regimes of immunosuppression, which should only be indicated in cases of primary FSGS, a rare entity that is elusive to response and can hardly be precisely diagnosed. We present a 35-year-old female patient with a life-long diagnosis of FSGS and a heavy burden of immunosuppressants, which had been unable to manage the persistent proteinuria that eventually led to end-stage kidney disease. She was referred to us to organize the kidney transplant. Plasmapheresis had been previously suggested to her to prevent the relapse of primary FSGS. A genetic test disclosed that the patient was heterozygous for LMX1B, and the diagnosis of nail-patella syndrome was made. In this entity, immunosuppression is not indicated, and there is no recurrence of the disease in the transplanted allograft.

Mucin-1 Gene Mutation and the Kidney: The Link between Autosomal Dominant Tubulointerstitial Kidney Disease and Focal and Segmental Glomerulosclerosis.

Glomerular diseases are one of the most frequent causes of chronic kidney disease, focal and segmental glomerulosclerosis being one of the commonest glomerulopathies. However, the etiology of this glomerular entity, which merely depicts a morphologic pattern of disease, is often not established and, in most of the patients, remains unknown. Nephrologists tend to assume focal and segmental glomerulosclerosis as a definitive diagnosis. However, despite the increasing knowledge developed in the field, genetic causes of glomerular diseases are currently identified in fewer than 10% of chronic kidney disease subjects. Moreover, unexplained familial clustering among dialysis patients suggests that genetic causes may be underrecognized. Secondary focal and segmental glomerulosclerosis due to genetic mutations mainly located in the podocyte and slit diaphragm can occur from childbirth to adulthood with different clinical presentations, ranging from mild proteinuria and normal renal function to nephrotic syndrome and renal failure. However, this histopathological pattern can also be due to primary defects outside the glomerulus. The present report illustrates an adult case of secondary focal and segmental glomerulosclerosis with a dominant tubulointerstitial damage that led to the pursue of its cause at the tubular level. In this patient with an undiagnosed family history of adult kidney disease, a genetic study unraveled a mutation in the mucin-1 gene and a final diagnosis of adult dominant tubular kidney disease-MUC1 was made.

In Acute IgA Nephropathy, Proteinuria and Creatinine Are in the Spot, but Podocyturia Operates in Silence: Any Place for Amiloride?

IgA nephropathy is the most frequent cause of primary glomerulonephritis, portends erratic patterns of clinical presentation, and lacks specific treatment. In general, it slowly progresses to end-stage renal disease. The clinical course and the response to therapy are usually assessed with proteinuria and serum creatinine. Validated biomarkers have not been identified yet. In this report, we present a case of acute renal injury with proteinuria and microscopic hematuria in a young male. A kidney biopsy disclosed IgA nephropathy. Podocyturia was significantly elevated compared to normal subjects. Proteinuria, renal function, and podocyturia improved promptly after steroids and these variables remained normal after one year of follow-up, when steroids had already been discontinued and patient continued on valsartan and amiloride. Our report demonstrates that podocyturia is critically elevated during an acute episode of IgA nephropathy, and its occurrence may explain the grim long-term prognosis of this entity. Whether podocyturia could be employed in IgA nephropathy as a trustable biomarker for treatment assessment or even for early diagnosis of IgA nephropathy relapses should be further investigated.

Increased urinary CD80 excretion and podocyturia in Fabry disease.

BACKGROUND: Certain glomerulopathies are associated with increased levels of CD80 (B7-1). We measured the urinary excretion of CD80, podocyturia and proteinuria in controls and in subjects with Fabry disease either untreated or on enzyme replacement therapy (ERT). METHODS: Cross-sectional study including 65 individuals: controls (n = 20) and Fabry patients (n = 45, 23 of them not on ERT and 22 on ERT). Variables included age, gender, urinary protein/creatinine ratio (UPCR), estimated glomerular filtration rate (eGFR), urinary uCD80/creatinine ratio (uCD80) and podocyturia. CD80 mRNA expression in response to lyso-Gb3, a bioactive glycolipid accumulated in Fabry disease, was studied in cultured human podocytes. RESULTS: Controls and Fabry patients did not differ in age, eGFR and gender. However, UPCR, uCD80 and podocyturia were significantly higher in Fabry patients than in controls. As expected, Fabry patients not on ERT were younger and a higher percentage were females. Non-ERT Fabry patients had less advanced kidney disease than ERT Fabry patients: UPCR was lower and eGFR higher, but uCD80 and podocyturia did not differ between non-ERT or ERT Fabry patients. There was a significant correlation between uCD80 and UPCR in the whole population (r 0.44, p 0.0005) and in Fabry patients (r 0.42, p 0.0046). Lyso-Gb3 at concentrations found in the circulation of Fabry patients increased uCD80 expression in cultured podocytes. CONCLUSIONS: Fabry disease is characterized by early occurrence of increased uCD80 excretion that appears to be a consequence of glycolipid accumulation. The potential for uCD80 excretion to reflect early, subclinical renal Fabry involvement should be further studied.

Podocyturia: A Clue for the Rational Use of Amiloride in Alport Renal Disease.

No specific or efficient treatment exists for Alport syndrome, an X-linked hereditary disease caused by mutations in collagen type IV, a crucial component of the glomerular basement membrane. Kidney failure is usually a major complication of the disease, and patients require renal replacement therapy early in life. Microhematuria and subsequently proteinuria are hallmarks of kidney involvement, which are due to primary basement membrane alterations that mainly cause endothelial thrombosis and podocyte contraction and ulterior irreversible detachment. Commonly drug-based approaches include angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, which are employed to reduce proteinuria and thus retard kidney disease progression and cardiovascular morbidity and mortality. However, as any hereditary disease, it is expressed as early as in the intrauterine life, and usually an index case is helpful to detect family-related cases. As no specific treatment exists, pathophysiologically based approaches are useful. The present case illustrates the reduction rate of urinary podocyte loss and proteinuria after amiloride administration and suggests the molecular pathways involved in Alport renal disease. Finally, podocyturia rather than proteinuria should be considered as an earlier biomarker of kidney involvement and disease progression in Alport disease.

Copious Podocyturia without Proteinuria and with Normal Renal Function in a Young Adult with Fabry Disease.

The time for starting a patient with Fabry disease on enzyme replacement therapy is still a matter of debate, particularly when no overt classical clinical signs or symptoms are present. With respect to Fabry nephropathy, a dual problem coexists: the reluctance of many nephrologists to start enzyme replacement infusion until signs of renal disease appear as the appearance of proteinuria or an elevation in serum creatinine and the lack of validated biomarkers of early renal damage. In this regard, proteinuria is nowadays considered as an early and appropriate marker of kidney disease and of cardiovascular morbidity and mortality. However, in this report we demonstrate that podocyturia antedates the classical appearance of proteinuria and could be considered as an even earlier biomarker of kidney damage. Podocyturia may be a novel indication for the initiation of therapy in Fabry disease.

Amiloride as an Alternate Adjuvant Antiproteinuric Agent in Fabry Disease: The Potential Roles of Plasmin and uPAR.

Patients with Fabry disease present a higher risk of cardiovascular and kidney morbidity. We present a patient with a past history of biopsy-proven Fabry disease and stage 3 chronic kidney disease. Proteinuria partially dropped from 6.8 g/day to 2.1 g/day despite an aggressive regime which consisted of low-salt diet, agalsidase beta infusions, dual blockade of the renin-angiotensin system, and low-dose maintenance of steroids. As proteinuria is considered a risk marker of cardiovascular disease and of progression of kidney disease, we added amiloride 5 mg/day, a drug with proven effects in podocyte stabilization and proteinuria actions at the distal convoluted tubule. Proteinuria finally decreased to 0.8 g/day. This report highlights the relevance of intervening on proteinuria in a multitarget approach in order to reduce it as much as possible. Due to this pharmacological response, we suggest that although agalsidase beta specific treatment protects the endothelium, the podocyte, and the tubule in Fabry disease and secondary haemodynamic and immunologic pathways are treated with inhibition of the renin-angiotensin system and steroids, amiloride may act as a complementary tool in podocyte stabilization and in proteinuria effects at the distal tubule.

Initially Nondiagnosed Fabry's Disease when Electron Microscopy Is Lacking: The Continuing Story of Focal and Segmental Glomerulosclerosis.

Focal and segmental glomerulosclerosis is classified as either primary or secondary. We present a patient with a past history of biopsy-proven focal and segmental glomerulosclerosis. Despite initial response to dual blockade and steroids, proteinuria raised when steroids were decreased. After the patient was restarted on steroids, proteinuria did not improve. Another biopsy confirmed the previous diagnosis but suggested Fabry's disease, later confirmed by electron microscopy, α-galactosidase A serum and leukocyte deficiency as well as genetic studies. Proteinuria decreased when agalsidase ß was prescribed in parallel with steroid tapering, increased with steroid discontinuation and improved with meprednisone administration. This report highlights the relevance of electron microscopy in kidney biopsy. In glomerulosclerosis, despite specific treatment, secondary hemodynamic and immunologic pathways may contribute to the development of proteinuria and accelerate the renal disease progression due to the primary disease. We discuss possible pathophysiologic pathways involved in proteinuria in Fabry's disease according to the biopsy and the therapeutic response.

Esclerosis focal y segmentaria glomerular primaria: ubi sumus et quo eamus? / Primary focal segmental glomerulosclerosis: ubi sumus et quo eamus?

La esclerosis focal y segmentaria glomerular primaria es una causa frecuente de sindrome nefrótico con alta morbilidad que con frecuencia lleva a la insuficiencia renal terminal debido a que sus esquemas terapeúticos no son exitosos, ya que sus mecanismos fisiopatológicos a la actualidad han sido parcialmente descifrados. Éstos son heterogéneos, complejos de integrar, y además el término agrupa bajo la misma denominación -la cual evoca una descripción histológica- a un variado número de causas moleculares con distinta fisiopatogenia. En esta revisión se describen los últimos adelantos respecto a la fisiopatología de esta compleja entidad y los últimos adelantos en su terapéutica.

Primary focal and segmental glomerulosclerosis is a common cause of nephrotic syndrome with high morbidity that often leads to end-stage renal failure as the different available therapeutic approaches are unsuccessful, due in part to the fact that the pathophysiological mechanisms have not been fully deciphered, are heterogeneous and complex to integrate, and more important, the denomination employed evokes a histological description shared by a number of different causes with different molecular pathogenesis. This review describes the latest developments regarding the pathophysiology of this complexentity and describes recent advances in therapy.

Results of the conversion to everolimus in renal transplant recipients with posttransplantation malignancies.

Management of posttransplantation malignancies should include control of the neoplasia and preservation of renal function. Conversion to everolimus (EVL) would potentially have both effects. Twenty-one patients were converted to EVL due to posttransplantation neoplasms. We have presented herein descriptive data and postconversion (PC) outcomes among subjects of mean age 53.6 +/- 10.1 years (range, 36-69), 57.1% were males, undergoing conversion at 108.2 +/- 74.7 (range, 5-316) months after transplantation. All patients received standard immunosuppressive therapy and 9.5% had been induced with thymoglobulin. Malignant neoplasms were as follows: skin (n = 7), gynecological (n = 3), gastrointestinal (n = 3), PTLD (n = 2), renal (n = 2), CNS (n = 1), seminoma (n = 1), Kaposi's sarcoma (n = 1), and prostate cancer (n = 1). PC to EVL, calcineurin inhibitors (CNIs) were discontinued in 18 of 19 patients, mycophenolate in 9/12, and azathioprine in 5/7; all patients continued to receive steroids. In 16 patients (79%) tumors were removed. Chemotherapy was performed in 2 patients with PTLD and radiotherapy was performed in 1 patient with prostate cancer. Mean follow-up was 505 days (range, 59-1151); baseline glomerular filtration rate (GFR) was 53.5 +/- 21.6 mL/min versus 48.5 +/- 25.7 mL/min (P = not significant [NS]) at the last control. One patient experienced graft loss at day 744 after conversion due to chronic rejection. Adverse events were observed in 57% of patients and 28% displayed infections; no patient discontinued EVL. There were 2 deaths: 1 due to an infection and the other due to postsurgical complication. No deaths due to cancer progression were observed. The results observed in this series suggested that conversion to EVL for a posttransplantation neoplasm is a valid therapeutic alternative to preserve graft function and control disease progression.

Plasminogen activator inhibitor-1 activity and 4G/5G polymorphism in hemodialysis.

INTRODUCTION: Chronic insufficiency alters homeostasis, in part due to endothelial inflammation. Plasminogen activator inhibitor-1 (PAI-1) is increased in renal disease, contributing to vascular damage. We assessed PAI-1 activity and PAI-1 4G/5G polymorphism in hemodialysis (HD) subjects and any association between thrombotic vascular access (VA) events and PAI-1 polymorphism. METHODS: Prospective, observational study in 36 HD patients: mean age: 66.6 +/- 12.5 yr, males n=26 (72%), time on HD: 28.71 +/- 22.45 months. Vascular accesses: 10 polytetrafluoroethylene grafts (PTFEG), 22 arteriovenous fistulae (AVF), four dual lumen catheters (CAT). Control group (CG): 40 subjects; mean age: 60.0 +/- 15 yrs, males n=30 (75%). Group A (GA): thrombotic events (n=12), and group B (GB): No events (n=24). Groups were no different according to age (69.2 +/- 9.12 vs. 65.3 +/- 14.5 yrs), gender (males: 7; 58.3% vs. 18; 81.8%), time on HD (26.1 +/- 14.7 vs. 30.1 +/- 38.7 months), causes of renal failure. Time to follow-up for access thrombosis: 12 months. RESULTS: PAI-1 levels in HD: 7.21 +/- 2.13 vs. CG: 0.42 +/- 0.27 U/ml (p<0.0001). PAI-1 4G/5G polymorphic variant distribution in HD: 5G/5G: 6 (17%), 4G/5G: 23 (64%); 4G/4G: 7 (19%) and in CG: 5G/5G: 14 (35%); 4G/5G: 18 (45%); 4G/4G: 8 (20%). C-reactive protein (CRP) in HD: 24.5 +/- 15.2 mg/L vs. in CG 2.3 +/- 0.2 mg/L (p<0.0001). PAI-1 4G/5G variants: GA: 5G/5G: 3; 4G/5G: 8; 4G/4G: 1; GB: 5G/5G: 3; 4G/5G: 15; 4G/4G: 6. Thrombosis occurred in 8/10 patients (80%) with PTFEG, 3/22 (9%) in AVF, and 1/4 (25%) in CAT. Among the eight PTFEG patients with thrombosis, seven were PAI 4G/5G. CONCLUSIONS: PAI-1 levels were elevated in HD patients, independent of their polymorphic variants, 4G/5G being the most prevalent variant. Our data suggest that in patients with PTFEG the 4G/5G variant might be associated with an increased thrombosis risk.

[Myelomatous ascites]. / Ascitis mielomatosa: reporte de un caso y revisión de la literatura.

Ascites is rare in patients with multiple myeloma (MM). It may be due to diverse mechanisms, most frequently because of an increased permeability of the peritoneum or because of portal hypertension due to liver infiltration. Myelomatous ascites occurs more frequently in patients having Ig-G or Ig-A paraprotein and their prognosis is poor. It is submitted the case of a female patient aged 50 years with IgA-kappa MM, who evolved with cardiac failure (CF), plasma cells leukemia and ascites of mixed cause, because of peritoneal infiltrate of myelomatous cells, hepatic compromise and CF. A review of the different causes of ascites in patients with MM is performed. There are also summarized all myelomatous ascites cases published in the literature. Our report presents the first case of myelomatous ascites in a patient with plasma cells leukemia.

[Gastroesophageal reflux as a cause of night sweating]. / Sudoración nocturna secundaria a reflujo gastroesofágico.

Night sweats has been defined as drenching sweats that require the patient to change bed clothes. In current studies night sweats appear in 30% of non-obstetric patients and affects approximately 60% of pregnant women. Differential diagnoses include infections, malignancy, medications, hot flashes and panic attacks, making of each patient a challenge. We present two patients with night sweating. After excluding systemic diseases the diagnosis of gastroesophageal reflux was made, with excellent response to anti-reflux treatment. The presentation of our two patients coupled with a deep literature review, underscores the importance of gastroesophageal reflux as a cause of night sweating.

Clopidogrel diminishes hemodialysis access graft thrombosis.

BACKGROUND: The most common complication of hemodialysis access graft is thrombosis. Clopidogrel, an inhibitor of platelet aggregation, was assessed to prevent this serious complication. METHODS: Nineteen patients on chronic hemodialysis whose vascular accesses were grafts were divided into two groups: Group A (n=11, 58%) consisted of patients who did not receive anti-thrombotic therapy after graft placement; Group B (n=8, 42%) received clopidogrel 75 mg/day from two days after surgery onwards. Both groups were well matched with respect to age, gender, cause of renal failure, hematocrit, platelet count and Kt/V. All patients' thrombotic episodes were followed up from the day of graft surgery until thrombosis was diagnosed. Finally, the survival difference between both groups was determined. RESULTS: Ten thrombotic episodes were diagnosed in Group A while no events were reported in Group B (p<0.001). Graft access days of patency were significantly more in Group B than in Group A (350.8+/-166 vs 86.8+/-69, p<0.001). The time elapsed from dialysis initiation to graft placement was not different (Group A: 18+/-12 days; Group B: 20+/-10 days). Days in hemodialysis were different between both groups (Group A: 195.9+/-96; Group B: 545.5+/-291, p<0.001) and all patients of Group A (n=11, 57.9%) and two patients of Group B (25%) died (p=0.001). No major bleeding events were reported. CONCLUSIONS: Clopidogrel significantly decreased thrombotic graft episodes. Patients on clopidogrel had a prolonged vascular access patency, longer time on hemodialysis and longer survival.

La hiperhomocisteinemia como factor de riesgo vascular en hemodializados crónicos / Hyperhomocysteinemia as a vascular risk factor in chronic hemodialysis patients

La homocisteína es un factor de riesgo independiente de enfermedad cardiovascular en la población general, y juega un rol protagónico en el desarrollo de la aterogénesis y las trombosis vasculares, sobre todo en pacientes con insuficiencia renal. Así pues, los pacientes en hemodiálisis están bajo los efectos tóxicos de la hiperhomocisteinemia, presente en cerca del 90% de estos pacientes. En nuestra experiencia hemos encontrado que el ácido fólico es un tratamiento eficaz para disminuir los niveles de homocisteína, y el agregado de metilcobalamina intravenosa potencia este efecto; sin embargo, la metilcobalamina por sí sola fue insuficiente para normalizar la homocisteinemia. A lo largo del tiempo, un grupo de pacientes requirió dosis más elevadas de ácido fólico para corregir la hiperhomocisteinemia. Los pacientes homocigotas y, en menor medida hete-rocigotas para la variante termolábil C677T de la enzima metilentetrahidrofolato reductasa (MTHFR), presentaron una actividad catalítica reducida reflejada en la necesidad de una mayor dosis de ácido fólico para normalizar los niveles de homocisteína. Los efectos trombóticos vasculares fueron similares en todos los pacientes respecto a las variantes genéticas de la enzima metilentetrahidrofolato reductasa, sugiriendo que el tratamiento de la hiperhomocisteinemia es importante para disminuir el riesgo de trombosis. Sin embargo, también la hipoho-mocisteinemia, asociada generalmente a estados de desnutrición, se asocia a mayor mortalidad. Si bien se considera a la hiperhomocisteinemia como un factor de riesgo vascular en los pacientes con insuficiencia renal, aún no se determinó en esta población si su corrección se asocia a una disminución de la tasa de enfermedad vascular y de trombosis. No obstante...

Homocysteine is an independent risk factor for cardiovascular disease in the general population. In addition, it plays a main role in the development of atherogenesis and thrombosis, particularly in end-stage renal disease patients. Therefore, hemodialysis patients are under the burden of homocysteine toxic effects, present in nearly 90% of dialysis patients. Our group found that folic acid is an efficient therapeutic approach to decrease homocysteine levels, and the addition of intravenous methylcobalamin potentiates this effect; however, methylcobalamin alone was unsuccessful to normalize homocysteine levels. With time a group of patients required a higher dose of folic acid to reduce hyperhomocysteinemia. Patients homozygous and, to a lesser extent heterozygous, to the C677T thermolabile variant of methylenetetrahydrofolate reductase (MTHFR) presented a reduced catalytic activity and required a higher folic acid dose. Vascular-access thrombotic events were similar in all patients according to the variants of the enzyme, suggesting that treating hyperhomocysteinemia was the key to lower the risk of thromboses. Noteworthy, hypohomocysteinemia, generally acompanying malnourishment, is associated to higher mortality. Albeit hyper-homocysteinemia is considered a vascular risk factor in renal failure patients, it has not yet been established in this population if its correction is associated with a decrease in the rate of vascular disease and thrombosis. However, given the mentioned evidence about the low risk and good tolerance of vitamin therapy, we believe it useful to know folate, cobalamin and homocysteine blood levels in chronic renal patients and start a prompt treatment, which may proof adequate to maintain homocysteine levels of 10 +/- 5 micromol/l.

Prevalencia de hipertension arterial en una comunidad aborigen del norte argentino / Prevalence of hypertension in an Indian community in the North of Argentina

El objetivo fue establecer la prevalencia de hipertensión arterial (HTA) en adultos de ambos sexos en la comunidad aborigen Wichi-Chorote de Santa Victoria Este, Provincia de Salta, Argentina. Se midió la presión arterial a personas mayores de 18 años de ambos sexos, en posición sentada luego de 5 minutos de reposo con esfingomanómetro calibrado. La población evaluada fue de 522 adultos, 318 mujeres y 204 hombres, con una media de edad de 43.5 años (DS 16.31). La presión arterial sistólica (PAS) media fue de 125.21 mm Hg (DS 22.74) y la presión arterial diastólica (PAD) media de 76.34 mm Hg (DS 12.57). El 35% de las personas evaluadas presentaron valores de normotensión (<120/80), el 37% de pre-hipertensión (PAS 120-139 o PAD 80-89) y el 28% de HTA (>140/90). Treinta y un porciento de los hombres (media de edad: 43.93 ± 17.11, PAS media: 126.81 ± 22.61 y PAD media: 77.80 ± 13.33) y 27% de las mujeres (media de edad: 42.93 ± 16.3, PAS media: 124.92 ± 24.02 y PAD media: 75.28 ± 12.57) presentaron cifras de HTA así como el 59% de los mayores de 65 años (58 gerontes evaluados, media de edad de 73.15 ± 6.36, PAS media 144.81 ± 28.72 y PAD media 79.68 ± 13.17). La prevalencia de hipertensión arterial en esta comunidad aborigen inmersa en un ámbito rural y con condiciones geográficas y socioeconómicas desfavorables es muy similar a la descripta para una sociedad desarrollada y urbanizada como EE.UU., pero inferior a la descripta para habitantes de áreas rurales como capitales provinciales de nuestro país.

Low initial vitamin B12 levels in Helicobacter pylori--positive patients on chronic hemodialysis.

BACKGROUND: Helicobacter pylori has been identified as a possible cause of vitamin B12 deficiency in the general population. We assessed any potential relationship between low cyanocobalamin serum levels and Helicobacter pylori status in hemodialysis patients and subsequently correlated these results with the existence of anemia (a common complication in hemodialysis patients), and macrocytosis. METHODS: In 29 chronic hemodialysis patients, active H. pylori infection was diagnosed using two different methods regardless of digestive symptoms: by searching for bacterial antigens in stools and by the detection of urea breakdown through breath testing. If these results were non-coincident, gastroscopy was performed and antral biopsies obtained. Patients were subsequently divided into group A (H. pylori-positive, n = 8, 28%) and group B (H. pylori-negative, n = 21, 72%). The corresponding initial values of erythrocytic folic acid, vitamin B12 and homocysteine prior to the first hemodialysis session of each patient were retrospectively collected. RESULTS: Vitamin B12 levels (normal 200- 900 pg/ml) were significantly lower in group A compared to group B (225.4 +/- 111.9 vs. 707.9 +/- 258.3 pg/ml, p < 0.011). In group A, 5 patients (63%) had vitamin B12 deficiency (154 +/- 24.6 pg/ml). Baseline hematocrits, erythrocyte folic acid and serum homocysteine levels were not different between the groups, but mean corpuscular volumes were significantly higher in group A compared to group B (109.7 +/-14.1 vs. 91.8 +/- 8.8 fl, p = 0.002). CONCLUSIONS: H. pylori-positive chronic hemodialysis patients may present with lower vitamin B12 blood levels and macrocytosis. H. pylori infection should be suspected in this population when low or low-normal vitamin B12 levels or macrocytosis exist.