While diarrheal illnesses are extremely common in communities and hospitals throughout the world, an etiologic diagnosis may be expensive and cost-ineffective. Although the presence of fecal leukocytes are helpful in the diagnosis and specific therapy of inflammatory diarrheas, this requires prompt microscopic examination of fecal specimens (preferably obtained in a cup rather than a swab or diaper) by a trained observer. We developed a simple, sensitive test for the detection of leukocytes in fecal specimens using antilactoferrin antibody. Whereas radial immunodiffusion detected 0.02 micrograms of lactoferrin (LF) per microliter or greater than or equal to 2,000 leukocytes per microliter, latex agglutination (LA) readily detected greater than or equal to 0.001 micrograms of LF per microliter or greater than or equal to 200 leukocytes per microliter added to stool specimens. Despite the destruction or loss of morphologic leukocytes on storage for 1 to 7 days at 4 degrees C or placement of specimens on swabs, measurable LF remained stable. Initial studies of stool specimens from six patients with Salmonella or Clostridium difficile enteritis were positive and those from three controls were negative for LF by LA. Of 17 children in Brazil with inflammatory diarrhea (greater than or equal to 1 leukocyte per high-power field), 16 (94%) had LF titers of greater than 1:50 by LA, whereas only 3 of 12 fecal specimens with less than 1 leukocyte per high-power field on methylene blue examination and none of 7 normal control specimens had an LF titer of greater than 1:50 by LA. Of 16 fecal specimens from patients with C. difficile diarrhea (cytotoxin titers, >/= 1:1,000), 95% (n = 15) had detectable LF by LA (in titers of 1:100 to 1: 800). Finally, of 48 fecal specimens from healthy adult U.S. volunteers before and after experimental shigellosis and of 29 fecal specimens from children with documented shigellosis and hospitalized controls in northeastern Brazil, fecal LF titers ranged from 1:200 to >/= 1:5,000 in 96% (25 of 26) samples from patients with shigellosis (and reported positive for fecal leukocytes), while 51 controls consistently had fecal LF titers of </= 1:200. We conclude that fecal LF is a useful marker for fecal leukocytes, even when they are morphologically lost swab specimens or when they are destroyed on transport or storage or by cytotoxic fecal specimens.

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Background: C3 glomerulopathy is a recently described entity classified as complementassociated glomerular disease. Case Presentation: We report a case of a 48-year-old man referred to the nephrology department for nephrotic syndrome with rapidly progressive kidney failure, acquired partial lipodystrophy and drusen in Bruch’s membrane of the retina. Blood tests showed low C3 and no evidence for autoimmune diseases, monoclonal gammopathy or infection. The renal biopsy revealed a proliferative endocapillary and crescentic glomerulonephritis with glomerular deposits exclusively of C3 and significant interstitial fibrosis. The electronic microscopy was consistent with dense deposit disease. The complement analysis revealed a pathogenic mutation of the complement factor B (CFB) gene not previously described in literature. Conclusions: The authors report a new mutation of CFB, in a dense deposit disease patient; this finding brings a new insight to the pathogenic pathway of C3 glomerulopathy and possibly to other complement dysregulation associated glomerular diseases. More clinical trials are needed to clarify both the pathogenicity and the optimal treatment for these entities.

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Vitamin B12 deficiency affects 10% to 15% of people over sixty years of age [1]. It is associated with haematological, neurological and psychiatric manifestations. It is a common cause of macrocytic anemia (megaloblastic) and, in more severe cases, pancytopenia. Neurological alterations include paraesthesias, peripheral neuropathy and demyelination of the corticospinal tract and spine. Vitamin B12 deficiency has also been associated with psychiatric disorders, including memory problems, irritability, depression, dementia and, rarely, psychosis [2]. A Vitamin B12 deficiency can have several causes, such as: pernicious anemia, inadequate diet, conditions that interfere with the absorption of Vitamin B12 namely gastrectomy, bariatric surgery, gastritis, pharmaceutical drugs, pancreatic insufficiency, short bowel syndrome. It can rarely be caused by genetic diseases. Its diagnosis is easy to make, by measuring serum levels of vitamin B12 or with a higher accuracy by measuring serum levels of methylmalonic acid and homocysteine, which will be high.We present an unexpected case of Vitamin B12 deficit. 85-year-old female patient, autonomous in her day to day activities, with the following personal background: severe aortic stenosis (proposed for surgery, which she refused), well-controlled

Background: Cardiac myxoma is the most frequent “benign” tumor of the heart and presents an important diagnostic challenge. Case presentation: A 51-year-old woman was admitted at the hospital for anorexia, fatigue, nausea, and vomiting for the last 10 days. Laboratory results showed hemoglobin 5.26 g/dl, platelets 83× 10^9 &#956;l, Lactate Dehydrogenase (LDH) 348 U/l, bilirubin 2.0 mg/dl, haptoglobin 100 mg/dl, negative Coombs test, blood smear with schistocytes and urea 327 mg/dl, creatinine 8.56 mg/dl. Non-autoimmune hemolytic anemia and acute kidney injury was assumed. After seven plasma exchange treatments, she went into acute pulmonary edema. Body tomography was performed, and revealed a mass in the left atrium. She underwent atriotomy and after surgery hemoglobin values stabilized but kidney function did not improve, and she became dialysis dependent. Conclusion: Myxomas can mimic other diseases which may delay diagnosis and compromise prognosis. In this particular case, the myxoma manifested with intravascular hemolytic anemia. This is an, especially, interesting case because a myxoma caused kidney failure without recovery.

Patients requiring renal replacement therapy remain a significant burden on the healthcare system. A substantial amount of hospitalization costs for these patients are related to vascular complications, especially catheter-related thrombosis, which is associated with a significant increase in morbidity and mortality.We report the case of a male patient with multiple myeloma (MM) and dialysis-dependent renal failure due to light-chain cast nephropathy, who presented recurrent early catheter dysfunction. A large thrombus was detected, extending from the superior vena cava (SVC) to the right atrium (RA) and later at the inferior vena cava (IVC), ultimately leading to exhaustion of vascular capital.To this date, there is limited evidence regarding the best approach to catheter-related thrombosis, which frequently leads to treatment dilemmas in clinical practice and demands careful evaluation and individualized decisions. In patients with a highly thrombotic profile, peritoneal dialysis may be considered earlier to prevent further vascular capital damage.