Raymond T. Krediet

Diagnosis and treatment of HIV-associated nephropathy

Human immunodeficiency virus-associated nephropathy (HIVAN) is a distinct clinico-pathological syndrome that occurs almost exclusively in black patients with an AIDS defining diagnosis. It is characterized by rapidly progressive renal failure with a severe nephrotic syndrome. The renal biopsy typically shows a collapsing glomerular sclerosis and variable tubulo-interstitial nephritis. The pathogenesis most likely involves infection of renal tubular and epithelial cells with HIV. The use of ACE-inhibitors and steroids may slow down the progression to end-stage renal failure. With the introduction of highly active anti-retroviral therapy, HIVAN may now be treated effectively although clinical data are so far limited to case-reports.

Predialytic Period and Baseline Peritoneal Membrane Status: Any Connection?

Editor: A 49-year-old African-American male with end-stage renal disease (ESRD) presented with cloudy effluent from his peritoneal dialysis. He had ESRD secondary to hypertensive nephrosclerosis and had been treated with continuous ambulatory peritoneal dialysis (CAPD) for about 31⁄2 years. He had no peritonitis for the first 21⁄2 years on dialysis. One year prior to the current episode, he had peritonitis caused by Klebsiella oxytoca (methicillin-sensitive Staphylococcus aureus was also cultured but was felt to be a contaminant). In his second episode, Micrococcus sp was cultured. The third episode was culture negative. In the current episode, the first fluid cell count was 2500 WBC/μL, with 86% segmented cells. He was treated empirically with intraperitoneal vancomycin and ceftazidime while cultures were pending. He had suboptimal clearing on this regimen. Initial cultures grew Acinetobacter lwoffii, sensitive to levofloxacin. Vancomycin and ceftazidime were discontinued and oral levofloxacin was started with the intention of 4 weeks of treatment. The patient discontinued therapy during the third week of treatment because of his improvement but did not report back to the dialysis center for follow-up for another 3 weeks. At that point, the peritoneal effluent had become cloudy again over the previous 2 days and the patient had abdominal pain and cramps. Peritoneal fluid cell count was 1583 WBC/μL, with 91% segmented cells. While new cultures were pending, treatment was resumed with oral levofloxacin and intraperitoneal vancomycin and ceftazidime. Culture results were delayed for about 1 week because of specialized growing requirements of the culprit organism, during which time the patient’s condition worsened. By the time the organism was identified, the peritoneal fluid cell count was 4850/μL. The organism was identified as Rothia mucilaginosa, sensitive to amoxicillin. The other antibiotics were discontinued and the patient was started on amoxicillin and rifampin. Within 48 hours he was asymptomatic, peritoneal fluid was clear, and cell count was 2 WBC/μL. Rothia mucilaginosa (formerly known as Stomatococcus mucilaginosus) is an encapsulated gram-positive CORRESPONDENCE