Sheldon Greenberg

Superior vena cava and right atrium wall infective endocarditis in patients receiving hemodialysis

Infective endocarditis is significantly more common and causes greater morbidity and mortality in patients receiving hemodialysis than in the general population. Episodes of bacteremia during hemodialysis are primarily the result of frequent vascular access through an arteriovenous fistula, a vascular graft, or an indwelling vascular catheter. This leads to dialysis access infection and secondary bacteremia. We describe 4 cases of patients receiving hemodialysis, with an indwelling intravascular dialysis catheter, who developed right-sided endocarditis with vegetations located exclusively on the superior vena cava and right atrium wall. All patients had persistent bacteremia with Staphylococcus, secondary to an indwelling intravascular hemodialysis catheter, which led to seeding of the right-sided cardiac wall, causing infective endocarditis. The rates of acceptance for hemodialysis are increasing, along with improved survival in this group of patients. This will probably lead to an increase in the incidence of infective endocarditis, with atypical presentations such as superior vena cava and right-sided cardiac wall endocarditis.

A case of peritoneal TB causing renal failure in a patient with rheumatoid arthritis and initial negative PPD after treatment with infliximab

Abstract Opportunistic infection and reactivation of latent infection has been reported with use of monoclonal TNF alpha antibodies used for treatment of severe rheumatoid arthritis. We present a case of peritoneal tuberculosis (TB) causing renal failure secondary to ureteral constriction in a patient who had been treated with infliximab for rheumatoid arthritis. We suggest that physicians should be aware of the increased risk of false negative and false positive TST and IGRA among patients treated with monoclonal TNF alpha antibodies and should regularly look for usual and unusual symptoms of TB in this patient population.

Rare Association of Immunoglobulin A Nephropathy and Lymphedema-Distichiasis Syndrome

Immunoglobulin A nephropathy is the most common primary glomerulonephritis worldwide. The pathogenesis is still unknown and newer treatments are being researched. Rarely, it can be associated with other disorders. Its association with hereditary lymphedema has been reported on one occasion but never with lymphedema-distichiasis syndrome. We report a patient with hereditary lymphedema-distichiasis syndrome and immunoglobulin A nephropathy occurring simultaneously.

Nontraumatic Exertional Rhabdomyolysis Leading to Acute Kidney Injury in a Sickle Trait Positive Individual on Renal Biopsy

A 26-year-old African American male with a history of congenital cerebral palsy, sickle cell trait, and intellectual disability presented with abdominal pain that started four hours prior to the hospital visit. The patient denied fever, chills, diarrhea, or any localized trauma. The patient was at a party at his community center last evening and danced for 2 hours, physically exerting himself more than usual. Labs revealed blood urea nitrogen (BUN) level of 41 mg/dL and creatinine (Cr) of 2.8 mg/dL which later increased to 4.2 mg/dL while still in the emergency room. Urinalysis revealed hematuria with RBC > 50 on high power field. Imaging of the abdomen revealed no acute findings for abdominal pain. With fractional excretion of sodium (FeNa) > 3%, findings suggested nonoliguric acute tubular necrosis. Over the next couple of days, symptoms of dyspepsia resolved; however, BUN/Cr continued to rise to a maximum of 122/14 mg/dL. With these findings, along with stable electrolytes, urine output matching the intake, and prior use of proton pump inhibitors, medical decision was altered for the possibility of acute interstitial nephritis. Steroids were subsequently started and biopsy was taken. Biopsy revealed heavy deposits of myoglobin. Creatinine phosphokinase (CPK) levels drawn ten days later after the admission were found to be elevated at 334 U/dl, presuming the levels would have been much higher during admission. This favored a diagnosis of acute kidney injury (AKI) secondary to exertional rhabdomyolysis. We here describe a case of nontraumatic exertional rhabdomyolysis in a sickle cell trait (SCT) individual that was missed due to findings of microscopic hematuria masking underlying myoglobinuria and fractional excretion of sodium > 3%. As opposed to other causes of ATN, rhabdomyolysis often causes FeNa < 1%. The elevated fractional excretion of sodium in this patient was possibly due to the underlying inability of SCT positive individuals to reabsorb sodium/water and concentrate their urine. Additionally, because of their inability to concentrate urine, SCT positive individuals are prone to intravascular depletion leading to renal failure as seen in this patient. Disease was managed with continuing hydration and tapering steroids. Kidney function improved and the patient was discharged with a creatinine of 3 mg/dL. A month later, renal indices were completely normal with persistence of microscopic hematuria from SCT.

Elevated Amylase in Clostridium difficile–Associated Diarrhea: A Case Report and Follow-Up Retrospective Study

BackgroundClostridium difficile–associated diarrhea (CDAD) is associated with high morbidity and mortality. There are several risk factors that have been identified that are linked to worsening outcomes including age of the patient, length of hospitalization, comorbidities, use of certain high-risk antibiotics, and more recently renal insufficiency. At our institution, we recently identified a patient with recurrent CDAD with elevated amylase level. More impressively, his level of amylase followed the course of his infection and returned to normal during his remission state. We proposed an association between C. difficile infection and amylase level. MethodsWe enrolled 726 patients who were 18 years or older, who had a history of CDAD and positive C. difficile toxin at time of diagnosis and had a measurement of amylase level within 3 days of toxin positivity. Patients were excluded if amylase levels were measured 3 days before or 3 days after C. difficile toxin positivity or were younger than 18 years. This study was retrospective in design. We also gathered other laboratory data such as basic metabolic panel, complete blood count, liver function test, lipase, length of hospital stay, and patient outcome of those who met the inclusion criteria. The primary outcome was death during hospitalization, and secondary outcome was length of stay. We also did a subset analysis looking at variables such as age, sex, albumin, renal insufficiency, anemia, amylase level, and leukocytosis and its association with C. difficile. ResultsA total of 726 cases of CDAD were identified. Overall hospital mortality was 26.6%, and mean length of stay was 25.3 days. When analyzing with logistic regression, only increasing age (odds ratio, 1.08; P < 0.001), increased creatinine (odds ratio, 1.50; P = 0.003), and decreased albumin (odds ratio, 0.19; P = 0.001) were associated with increased in-hospital mortality. All other factors including sex, white blood count, hemoglobin, and amylase did not show any change in mortality. ConclusionsBased on this retrospective study, we were unable to identify any relationship between amylase level and CDAD. Secondary outcomes from the analysis revealed that whereas increasing age, decreased albumin, and renal insufficiency put one at risk for C. difficile infection, other factors such as sex, anemia, leukocytosis, and amylase level cannot be used to risk stratify patients.