Outcome of percutaneous endoscopic gastrostomy feeding in patients on peritoneal dialysis.

Protein malnutrition is now well established as an important contributory factor to the high mortality in peritoneal dialysis (PD) patients. Low dietary protein calorie intake is one of the factors leading to protein malnutrition. If PD patients develop difficulty eating, percutaneous endoscopic gastrostomy (PEG) feeding may prove beneficial in providing adequate nutrition. Studies on the effectiveness of PEG feeding in PD patients are limited to pediatric patients. The objective of the present study was to assess the outcome of PEG feeding in adult patients with end-stage renal disease (ESRD) on PD. We retrospectively reviewed charts from May 1992 to February 2000 of 10 consecutive patients in our center who had had feeding tubes inserted. The patients' ages ranged from 37 to 81 years, with mean age of 65. Of the 10 patients, 7 were male, 5 were diabetic, and 1 was infected with the human immunodeficiency virus. Two patients had cerebrovascular accident (CVA) with dysphagia, 3 had multi-infarct dementia, 2 had anoxic encephalopathy, 2 had dementia, and 1 had calciphylaxis with anorexia. Of the 10 patients, 9 failed to eat because of neurologic disorders. Two patients who had functioning PEG feedings before starting PD had no complications. Only 2 of 8 patients already on PD continued with long-term PD after a PEG was inserted. Both patients whose PD was not interrupted at the time of PEG placement immediately developed peritonitis. Of the 6 patients who were maintained on hemodialysis (HD), 2 developed peritonitis within one week of starting PEG feedings. The other 4 had no complications from PEG feedings while being maintained on HD, but 1 developed peritonitis when PD was resumed. Of the 5 patients who developed peritonitis, 3 experienced fungal peritonitis. In PD patients, PEG feeding is associated with frequent complications. However, PEG placement prior to PD initiation appears to be safe. Maintaining patients on HD for at least 6 weeks appears to decrease the incidence of peritonitis, but does not eliminate it. Use of anti-fungal prophylaxis and maintenance of the patient on HD for longer than 6 weeks may produce better results.

Severe necrotizing mastopathy caused by calciphylaxis alleviated by total parathyroidectomy.

Calciphylaxis is a complication caused by secondary hyperparathyroidism in patients with chronic renal failure. These patients may present with clinical findings of ischemic necrosis involving the skin and muscle resulting in subsequent gangrene and vascular calcifications. We report a rare case of necrotizing mastopathy caused by calciphylaxis in a 70-year-old female with end-stage renal disease whose symptoms resolved with a total parathyroidectomy.

Reticulocyte hemoglobin content predicts functional iron deficiency in hemodialysis patients receiving rHuEPO.

Early detection of iron sufficiency at the level of the erythropoietic cell is necessary to optimize management of uremic anemia with recombinant human erythropoietin (rHuEPO). "Absolute" and "functional" iron deficiency are the most important factors causing resistance to administered rHuEPO. Transferrin saturation and serum ferritin measurements have been noted to be insensitive and inaccurate measures to detect functional iron deficiency. Recently, the reticulocyte hemoglobin content (CHr) has been shown to be a sensitive and specific indicator of functional iron deficiency in nondialysis patients treated with rHuEPO. The purpose of this study is to compare CHr with currently used indices of iron sufficiency in rHuEPO-treated hemodialysis (HD) patients. In study 1, 364 stable HD patients were studied at two outpatient dialysis centers. CHr was normally distributed, with a mean value of 28.3 pg, and was consistent over two consecutive monthly samples in each center. CHr was weakly but consistently correlated with transferrin saturation and serum ferritin. CHr and reticulocyte number were inversely correlated with red blood cell (RBC) number, suggesting that the erythropoietic stimulus of routinely administered rHuEPO may have resulted in functional iron deficiency. Month-to-month changes in CHr correlated weakly with changes in serum iron and percent transferrin saturation, but not at all with changes in serum ferritin. When we analyzed those patients with baseline CHr less than 26 pg, a level strongly suggestive of functional iron deficiency, these correlations strengthened, and in addition, month-to-month changes in CHr correlated strongly and directly with concomitant changes in RBC count, hemoglobin, and hematocrit, suggesting that rising CHr was indicative of an erythropoietic response. In study 2, 79 patients received a single-dose infusion of 500 mg iron dextran. After intravenous iron, CHr rose within 48 hours, peaked at 96 hours, and then fell toward baseline. Patients who were iron deficient by standard measures (serum ferritin < 100 ng/mL or transferrin saturation less than 20%) had a greater and a sustained CHr response to intravenous iron dextran. A CHr less than 28 pg at baseline predicted functional iron deficiency, defined as a corrected reticulocyte increase of greater than 1% to iron dextran, more accurately than transferrin saturation, ferritin, or their combination. Eighty-two percent of individuals who were iron deficient at baseline responded to intravenous iron with an increase in CHr of greater than 2 pg. Sixty percent of patients who were iron sufficient by usual iron indices also responded to intravenous iron with a CHr rise of greater than 2 pg, suggesting that they were, in fact, functionally iron deficient despite "normal" conventional iron parameters. We conclude that CHr may be a more sensitive marker of functional iron deficiency in rHuEPO-treated hemodialysis patients than percent transferrin saturation and ferritin, particularly in those with "normal" conventional iron parameters.

Urinary red cell size: diagnostic value and determinants.

Urinary red blood cells (RBC) are usually small and morphologically abnormal in glomerular (GN) hematuria, and slightly enlarged and morphologically normal in nonglomerular (NG) hematuria. This study was performed to evaluate the diagnostic value of urinary red cell size and morphology and to investigate the mechanism of the alteration in cell size. In 34 consecutive patients with hematuria we examined the urinary RBC size distribution and mean corpuscular volume (MCV) by electronic sizing of suspensions of RBC in an isotonic medium and, in 28 cases, compared it with the presence of 50% or greater dysmorphia. In 15 consecutive cases, we correlated MCV values with urine chemistries. In two GN cases we recorded the urine MCV serially during a furosemide-induced diuresis. In vitro incubations of peripheral or urinary RBC in various electrolyte solutions prior to sizing were also performed. The MCVs were significantly lower in GN (p less than 10(-6)) and probable GN (p less than 10(-4)) than NG hematuria. A cutoff of 72 fl completely separated GN and probable GN from NG cases. Fifty percent or more 'dysmorphic' RBC were seen in 12 of 13 GN, 3 of 4 probable GN but in no NG sediments. In patients with NG hematuria, the ratio of urinary to peripheral MCV tended to be greater than unity and correlated strongly with pH (r = -0.97; p less than 0.002). The effect of pH was confirmed in vitro. Furosemide diuresis induced a partial correction of the microcytosis of GN RBC, which correlated with the changes in urine composition. Furosemide had no effect on GN cells in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol and lipid disturbances in renal disease: the natural history of uremic dyslipidemia and the impact of hemodialysis and continuous ambulatory peritoneal dialysis.

Lipid abnormalities have been postulated to contribute to renal insufficiency by a mechanism that is analogous to atherogenesis. The majority of patients treated for chronic renal failure die of cardiovascular complications. Lipid abnormalities in this group are thought to contribute to this high mortality. Proving a causal association between dyslipidemia and accelerated atherosclerosis in the end-stage renal disease population has been confounded by the presence of other pro-atherogenic conditions in this population. The current study compiles the lipid data we have accumulated from our renal population for the years 1987 to 1989. The report is divided into three main parts: The first is a survey of lipid levels and atherogenicity indicators in groups with different types of renal disease or modalities of treatment. The second is a multivariate analysis of the relationship of clinical and biochemical variables (and their interactions) to the serum lipid and apolipoprotein levels and their ratios and their change over time in a large dialysis population. In the third study, we quantitate the peritoneal clearances of apolipoproteins A-I and B in patients undergoing continuous ambulatory peritoneal dialysis and assess the relationship of these clearances to serum lipid and lipoprotein levels and risk ratios.

Lipids in diabetic and nondiabetic hemodialysis and CAPD patients.

To examine the question of "accelerated atherogenesis" in ESRD patients, the authors conducted a lipid survey among their hemodialysis and CAPD populations and evaluated data relevant to the lipid and diabetic status of these groups. Interestingly, longer duration of hemodialysis in nondiabetic patients was associated with lower cholesterol but not HDL, which may reflect diminished cardiac risk and mortality in the long-term survivors. Diabetic patients showed lower HDL but no cholesterol change with longer duration on hemodialysis. Type I diabetics showed the highest HDL and lowest risk ratio and a strong inverse correlation between PTH and HDL. This study highlights the role of lipids in the atherogenesis of uremia and serves as a baseline for a longitudinal study.