Tuberculosis prophylaxis for the chronically dialysed patient--yes or no?
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Biomedical subjects
Publications and source records attributed to A Korzets.
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Four patients with end-stage renal failure on intermittent hemodialysis in whom rhabdomyolysis developed after major surgery are described. This possibly underdiagnosed complication was manifested by extreme hyperphosphatemia, hypocalcemia, and elevated creatine phosphokinase levels. Serum myoglobin levels further supported the diagnosis. The metabolic abnormalities reached a peak on the fourth postoperative day. The possible precipitating factors included opiates used for anesthesia and postoperative pain control, anesthetic agents, and surgical position. The preferred treatment option is increasing dialysis to control hyperphosphatemia and hypocalcemia.
BACKGROUND: The use of the femoral vessels for permanent haemodialysis access has been neglected during the last two decades. Since 1981 femoral artery-vein loop polytetrafluoroethylene grafts have been constructed in our chronic haemodialysis patients. This study examines results obtained in patients with this particular graft over the last 14 years. METHODS: This clinical study is retrospective in nature. Overall 35 patients, with 37 femoral grafts, are included. Inclusion and exclusion criteria for this type of graft are given and the surgical procedure detailed. RESULTS: Seven patients had femoral grafts used as primary dialysis access. Twenty-eight patients had femoral grafts used after multiple access failures. There was no perioperative mortality. Immediate thrombotic non-function of the graft occurred in three patients. In the long term no patient death was related to the femoral grafts. Twenty-seven (73%) grafts had no long-term complications. The leading cause for graft 'loss' was patient death; in the first year 10 grafts were lost, eight because of patient death. All eight patients died with functioning grafts. Median graft survival was 21 months in all patients and 28 months in non-diabetic patients. Twenty-seven (73%) grafts were patent at the end of the first year, 33% of grafts were still patent after 5 years. Worsening claudication occurred in four patients; one diabetic required foot amputation. Four patients had late graft thrombosis; only two patients had bacteraemia originating from the femoral graft. Urea reduction ratio greater than 60% was measured in 87.5% of patients. CONCLUSION: The femoral artery vein graft is a good primary and secondary haemodialysis access. Both infection and thrombosis rates are low and graft survival is comparable, if not superior to, that of upper-limb grafts. The graft is easy to cannulate, can be used early, is easily protected, and is cosmetically acceptable.
Previous studies have reported that anemia is a frequent occurrence in patients with severe autonomic failure, that it can be corrected by exogenous erythropoietin and that upright blood pressure improves while on erythropoietin. The objective of this study was to determine the alteration of autonomic control during erythropoietin therapy in a patient with severe autonomic failure and severe symptomatic orthostatic hypotension, evaluated by spectral analysis of heart rate variability. The autonomic response to standing was evaluated before, after 1 month and after 6 months of erythropoietin therapy. The results were compared to an age- and sex-matched control adult. There was no improvement in the orthostatic hypotension during and at the end of the erythropoietin treatment despite an increase in hemoglobin from 9.6 g/dl before treatment to 12.5 g/dl during treatment. The spectral estimates of heart rate variability displayed a low variability at baseline, a paradoxical vagal enhancement and a lack of sympathetic increase on standing (before, during and at the end of the treatment). There was no improvement of baseline activity, nor of the response to standing during and at the end of the treatment with erythropoietin. We conclude that erythropoietin did not improve the autonomic response to standing, although it corrected anemia. Erythropoietin did not alter sympathetic activity, as reflected in the low frequency content of the power spectrum of heart rate fluctuations during and at the end of treatment.
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Oral pulse therapy with vitamin D is effective in suppressing parathyroid hormone (PTH) secretion in continuous ambulatory peritoneal dialysis patients with secondary hyperparathyroidism (2'hpt). However, this treatment often leads to hypercalcemia. The goals of the study were: (1) to examine whether the incidence of hypercalcemia decreases when dialysate calcium is reduced from 1.25 to 1.0 mmol/L; (2) to determine the relative role of the factors involved in the pathogenesis of hypercalcemia; and (3) to study the efficacy of a low oral pulse dose of alfacalcidol in preventing the recurrence of 2'hpt. Fourteen continuous ambulatory peritoneal dialysis patients with 2'hpt were treated with pulse oral alfacalcidol and calcium carbonate and dialyzed with a 1.0-mmol (n = 7) or a 1.25-mmol (n = 7) dialysate calcium. The response rate (87%) and the incidence (71%) and severity of hypercalcemia were similar in both groups. In the early response stage, PTH decreased by 70% in both groups, and serum ionized calcium (iCa) increased from 1.18 +/- 0.02 to 1.27 +/- 0.04 mmol/L (P < 0.005) in the 1.0 group and from 1.19 +/- 0.02 to 1.29 +/- 0.02 mmol/L in the 1.25 group (P < 0.005). Nine of the 12 responders had a further decrease in serum PTH, which was associated with an additional increase in iCa from 1.28 +/- 0.02 to 1.47 +/- 0.04 (P < 0.005). Multivariate analysis showed that the early increase in iCa was positively correlated with alfacalcidol dosage (r = 0.69). In contrast, the late increase in iCa was mostly accounted for by the decrease in serum PTH (r = -0.93). This occurred while calcium carbonate, alfacalcidol dosage, and serum 1,25 hydroxy D3 remained unchanged compared with the early response stage. Finally, an alfacalcidol dose of 1 microg twice weekly was unable to maintain serum PTH at an adequate level in the long term. These data show that a reduction in dialysate calcium from 1.25 to 1.0 mmol does not reduce the occurrence of hypercalcemia and suggest that lowering serum PTH reduces the ability of the bone to handle a calcium load within a few weeks, thus causing hypercalcemia.
In chronic renal failure, epidermal growth factor (EGF) excretion is decreased. In this study, asymptomatic adult polycystic kidney disease (APKD) patients with a relatively preserved glomerular filtration rate were examined. Excretion of EGF was studied in 6 patients with APKD (median age 42 years; serum creatinine [median] 95 [range-80-133] mumol/l) and compared with that of 28 healthy controls. EGF was determined in a spot morning urine by using a specific radioimmunoassay, and expressed in relation to creatinine excretion. Excretion of EGF in APKD was (median) 157 (range-13-359) and in the controls (median) 546 (range-238-1199) pmol/mmol creatinine (p < 0.001). Low excretion of EGF in APKD patients with preserved kidney function suggests a distal abnormality at an early stage of the disease, prior to the development of renal failure.
A 28-year-old woman, treated for schizophrenia, developed severe hypotonic hyponatremia (serum Na: 109 mEq/L) after several days of compulsive water drinking. The patient was admitted in a coma and required intensive supportive therapy. Rhabdomyolysis quickly followed with high serum creatine phosphokinase levels and myoglobinuria. A high volume alkaline diuresis was initiated. Renal failure or compartment syndrome did not complicate the clinical picture. The mechanisms causing water intoxication and hyponatremia are discussed as are the possible pathogenetic explanations behind acute hyponatremia and rhabdomyolysis.
BACKGROUND: Factors affecting cardiac function in dialysis patients include arterial blood pressure, anaemia, intravascular volume, and the arteriovenous (a-v) access. Cardiac failure has been directly attributed to dialysis a-v access in several cases. The contribution of the a-v access to cardiac performance has been tested, in the past, by a short manual compression on the fistula, but this technique has obvious limitations. METHODS: The present study examined prospectively the effect of dialysis a-v access on both cardiac function and various hormonal responses. Ten patients (age, mean +/- SD, 59.6 +/- 12.3) with end-stage renal failure being prepared for chronic dialysis therapy were included. All patients underwent an echocardiographic study before and 2 weeks after the creation of the a-v access. Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA), and plasma aldosterone were measured at the same time periods. RESULTS: Following the creation of the a-v fistula or graft, shortening fraction increased by 15.8 +/- 6.3% (P < 0.01), stroke volume increased by 21.9 +/- 5.3% (P < 0.01), ejection fraction increased by 10.6 +/- 4.5% (P < 0.02), cardiac output increased by 19.0 +/- 6.9% (P < 0.02), and cardiac index increased by 18.3 +/- 7.1% (P = 0.05). Systemic vascular resistance decreased by 23.5 +/- 7.1% (P < 0.01). There was no change in blood pressure, heart rate, weight, haemoglobin or serum creatinine. ANP increased by 83.7 +/- 17.0% following the a-v access operation (P < 0.001), PRA decreased by 41.2 +/- 10.0% (P < 0.05), and plasma aldosterone did not change. None of the patients developed overt high-output cardiac failure. CONCLUSIONS: This study shows that at least in the short term following the creation of a dialysis a-v access, a mild state of volume overload develops, which is offset by the ¿unloading' effect of the decreased peripheral vascular resistance; the latter is probably mediated by secretion of ANP in response to atrial stretching.
A hemodialysed patient with abdominal pain, severe lactic acidosis and prolonged hypoglycemia is described. The diagnosis of acute necrotizing pancreatitis was delayed and the patient died from both systemic and peripancreatic complications of the acute pancreatitis. The article deals with the problem of diagnosing acute pancreatitis in an end-stage renal failure (ESRF) patient; on the possible surgical options open to the physician in the management of acute pancreatitis and on a pathophysiological explanation behind both the lactic acidosis and hypoglycemia in this patient.
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BACKGROUND: Bullous dermatosis (BD) is becoming increasingly recognized in patients with end-stage renal disease (ESRD). It is clinically reminiscent of porphyria cutanea tarda, but its detailed pathogenesis remains unclear. Studies have shown increased porphyrin levels in dialysis patients, and this may partly explain the skin lesions and photosensitivity evident in these patients. In experimental studies, aluminum can induce various abnormalities in porphyrin and haem metabolism. This study investigated a possible involvement of porphyrin metabolism and aluminum in the development of bullous dermatosis in chronically dialysed patients. METHODS: Three groups were studied (12 healthy controls; 12 patients on chronic dialysis without BD and six patients on chronic dialysis with BD). Clinical characteristics of these patients were evaluated and the levels of plasma porphyrins, erythrocyte porphyrins and enzymes involved in the porphyrin chain were determined. RESULTS: The patients with BD were predominantly male, 50% had ADPKD, all had been on dialysis for a long period of time (7.8 +/- 2.1 years) and all were anuric. CAPD and haemodialysis were used equally in the affected patients. Aminolaevulinic dehydratase activity was significantly reduced in all ESRD patients (892 +/- 47 versus 302 +/- 36 versus 408 +/- 37 nmol/ml RBC/h). Plasma uroporphyrins as well as RBC protoporphyrin were significantly elevated in ESRD patients (1.7 +/- 0.6 versus 21.6 +/- 4.7 versus 43.4 +/- 12.0 nmol/L) and (1.43 +/- 0.14 versus 2.4 +/- 0.42 versus 4.19 +/- 2.44 mumol/l) respectively. Serum A1 levels were markedly elevated in patients with BD (28.3 +/- 10.0 micrograms/l). Both uroporphyrin and protoporphyrin were significantly more elevated in ESRD patients with BD compared to ESRD patients without BD. CONCLUSIONS: Elevated plasma porphyrin levels in ESRD patients are caused by lack of urinary excretion and the inability of haemodialysis and CAPD therapy to remove them. These elevated porphyrin levels may lead to the development of porphyria cutanea tarda symptoms. Elevations in plasma uroporphyrin, red blood cell protoporphyrin, and elevated A1 levels suggest a possible relationship between an A1 'load' and abnormal porphyrin metabolism in the development of overt skin disease in the dialysed patient.
Glomerular pathology in liver cirrhosis is common in autopsies but is underdiagnosed antemortem. The most common pathologic findings are mesangial disease with immunoglobulin A deposits, and membranoproliferative glomerulonephritis. The latter is associated, most frequently, with hepatitis C infection and cryoglobulinemia. We describe a patient with longstanding liver cirrhosis who presented with a nephritic and nephrotic syndrome. Membranoproliferative glomerulonephritis was diagnosed on kidney biopsy. There was no clinical, laboratory or histologic evidence of hepatitis C infection or cryoglobulinemia. The different aspects of "cirrhotic glomerulonephritis" are discussed and the need for searching for this underdiagnosed condition in patients with chronic liver disease is emphasized.
This study describes a previously undescribed cause of reflex sympathetic dystrophy involving both patellae. This syndrome developed following burns inflicted over both knees in a male industrial worker. The report highlights physical examination findings, investigation results, socioeconomic and psychological evaluation, and rehabilitation treatments involved in patients suffering from reflex sympathetic dystrophy.