Vaughn W. Folkert

Continuous Arteriovenous Hemofiltration: A Report of Six Months' Experience

Continuous arteriovenous hemofiltration using small hollow-fiber hemofilters, without pumps, was used as an alternative to conventional methods of acute dialytic therapy. During a 6-month period, 15 patients had 17 treatments. Mean treatment duration was 98.5 +/- 101.1 (SD) hours (range, 4 to 300 hours), for a total of 1673 hours. Mean output per treatment was 9.5 +/- 4.4 mL/min, which was found to be adequate to control uremia despite a considerable protein intake. Six patients had a significant hemorrhage; however, all 6 had active bleeding and existing coagulopathies before beginning treatment. Overall, continuous arteriovenous hemofiltration was found to be a convenient and safe method for providing continuous fluid, electrolyte, and acid-base balance in patients with inadequate renal function. The treatment was particularly useful in patients with vascular instability or severe fluid overload.

Prostaglandin synthesis in isolated glomeruli

Prostaglandins are thought to play an important role in the local regulation of glomerular blood flow and in the release of renin from the juxtaglomerular apparatus. We therefore examined prostaglandin synthesis by isolated rat glomeruli. Isolated glomeruli were either prelabeled with [14C] arachidonic acid or were incubated with [14C] arachidonic acid for the entire experimental incubation in Krebs buffer. Prostaglandin synthesis was determined by thin layer radio-chromatography of acid extracts of the supernatant solutions. Indomethacin inhibitable synthesis of small amounts of 6-keto-PGF1 alpha, the metabolite of prostacyclin (PGI2,) and larger amounts of PGF2 alpha, and PGE2, and possibly thromboxane B2 (TXB2) by isolated glomeruli could be demonstrated with either prelabeling or direct incubation. These findings support the hypothesis that prostaglandins are produced within the glomerulus where they may affect local glomerular blood flow and function.

Renal vein thrombosis treated with thrombolytic therapy: Case report and brief review

Renal vein thrombosis (RVT) can occur as a complication of the nephrotic syndrome. We present the case of a young woman with systemic lupus erythematosus with nephrotic syndrome and bilateral RVT with extension of the thrombus into the vena cava to the level of the right atrium and multiple pulmonary emboli. She was treated acutely with streptokinase, with complete resolution of the thrombi. In general, anticoagulation is the mainstay of therapy for RVT. Review of the literature reveals that thrombolytic therapy can be used safely and appears to have been reserved for those patients with the most severe disease or the more grave prognosis. we feel that thrombolytic therapy is warranted in the presence of bilateral RVT with acute renal failure, massive clot size with high risk of acute embolic events, or recurrent pulmonary emboli, in the absence of overriding contraindications.

Sequential occurrence of IgA nephropathy and Henoch-Schönlein purpura : support for common pathogenesis

We report a patient who developed Henoch-Schönlein purpura (HSP) 13 years after he presented with IgA nephropathy (IgAN). In both HSP and IgAN renal biopsy most commonly reveals focal proliferative glomerulonephritis on light microscopy and immunofluorescence displays mesangial IgA deposits. In addition, patients with HSP or IgAN have elevated serum IgA levels, circulating IgA immune complexes, IgA-bearing lymphocytes, immunoglobulin-producing cells, and binding of IgG to glomerular components of similar molecular weight. The occurrence of both diseases in the same patient or the same families and the presence of immune abnormalities compatible with HSP or IgAN in relatives of patients with these diseases suggest a common pathogenesis.

Prostaglandin synthesis linked to phosphatidylinositol turnover in isolated rat glomeruli

Prostaglandins produced by the glomerulus are important factors in controlling glomerular function. The controlling step, i.e., the release of arachidonic acid from the phospholipids by either phospholipase A2 and/or C, remains poorly defined. The present studies were designed to determine which factors control arachidonic acid turnover and prostaglandin synthesis in glomeruli. As tools we used the calcium ionophore A23187, mepacrine, a phospholipase inhibitor, trifluoperazine, a calmodulin antagonist, and angiotensin II. A23187 (2 microM) caused a significant stimulation of both prostaglandin E2 and prostaglandin F2 alpha synthesis (measured by radioimmunoassay), which was associated with increased phosphatidylinositol turnover (measured by [14C]arachidonic acid and [32P]orthophosphate incorporation). Surprisingly, trifluoperazine (10-100 microM) also progressively increased synthesis of both prostaglandins, which was accompanied by increased phosphatidic acid/phosphatidylinositol turnover and decreased phosphatidylinositol content. In contrast, phosphatidylcholine and phosphatidylethanolamine turnover were significantly inhibited by trifluoperazine and their total content remained unaffected. Mepacrine (1 mM) decreased prostaglandin synthesis and both phosphatidylcholine and phosphatidylethanolamine turnover, and had no consistent effect on phosphatidylinositol turnover in control glomeruli. Mepacrine did, however, inhibit both A23187 or trifluoperazine-induced increase in phosphatidylinositol turnover. Angiotensin II increased turnover of phosphatidylinositol and also phosphatidylcholine, as determined by incorporation of [14C]arachidonic acid. Thus, all agents that increased prostaglandin synthesis also enhanced phosphatidylinositol turnover. The exact pathway of arachidonic acid release remains to be determined.

Renal function recovery in chronic dialysis patients.

Renal function recovery (RFR) from acute kidney injury requiring dialysis occurs at a high frequency. RFR from chronic dialysis, on the other hand, is an uncommon but well‐recognized phenomenon, occurring at a rate of 1.0–2.4% according to data from large observational studies. The underlying etiology of renal failure is the single most important predicting factor of RFR in chronic dialysis patients. The disease types with the highest RFR rates are atheroembolic renal disease, systemic autoimmune disease, renovascular diseases, and scleroderma. The disease types with the lowest RFR rates are diabetic nephropathy and cystic kidney disease. Initial dialysis modality does not appear to influence RFR. Careful observation and history taking are needed to recognize the often nonspecific clinical and laboratory signs of RFR. When RFR is suspected in a chronic dialysis patient, a 24‐hour urine urea and creatinine clearance should be measured. Based on the renal clearance, along with other clinical factors, the dialysis prescription may be gradually reduced until a complete discontinuation of dialysis. After RFR from maintenance dialysis, patients require close follow‐up in an office setting for chronic kidney disease management.

Acute Sterile Peritonitis

We have encountered a sporadic form of aseptic peritonitis, not previously described, that we refer to as acute sterile peritonitis (ASP). This syndrome, which occurs with a frequency of 0.1% of dialyses, begins abruptly during peritoneal dialysis with abdominal pain, fever, and occasionally chills and vomiting. Coincident with the onset of symptoms, the dialysate return becomes cloudy with many white blood cells. Cultures are negative and resolution occurs within hours with continued dialysis. In this report we detail the clinical features of this new syndrome.

Hidden Obesity in Dialysis Patients: Clinical Implications

While body‐mass index (BMI) is used to diagnose obesity in the general population, its application in the end‐stage renal disease (ESRD) population is fraught with difficulty. A major limitation is its inability to distinguish muscle mass from fat mass, thereby leading to misclassification of individuals with poor muscle mass but excess adipose tissue as non‐obese (i.e. BMI <30 kg/m2). As muscle wasting is common among ESRD patients, this is an important problem. A substantial proportion of ESRD patients have levels of BMI in the normal range, yet excess adiposity based on other measures. The importance of this “hidden” obesity remains to be determined, but it must be recognized in order for obesity interventions to be appropriately targeted and tested in the ESRD population.