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Serum biochemical measures suggestive of undernutrition have been reported to correlate with 1-yr mortality risk in prevalent groups of hemodialysis patients. The predictive power of these variables has not been reported in newly diagnosed patients or in patients whose dialysis prescription is guided by urea kinetics. The relationship of these predictors to mortality over periods of longer than 1 yr is also unreported. Therefore, the survival of 184 hemodialysis patients was examined for up to 44 months (1987 to 1991) with the Cox proportional hazards model. Baseline demographic, clinical, and biochemical parameters were used as independent variables. To adjust for bias in patient selection, the survival of patients with 12 months or less of prior dialysis at the time of enrollment ("new cases") was analyzed separately from that of patients with more than 1 yr of prior treatment ("long-standing cases"). Serum albumin was less than 3.5 g/dL in 31% of new cases and in 12% of long-standing cases. Adjusting for the other variables, low serum albumin was the strongest mortality risk predictor in both new and long-standing cases. Low serum cholesterol was an independent risk predictor in both groups. Diabetes and race were not significant predictors. Mean age at enrollment was nearly a decade higher for nonsurvivors than for survivors, in both new and long-standing groups. Yet, age was not an independent risk predictor in the Cox model for the new group because of an unexpectedly high death rate among young black men. Female gender, which was confounded by increased age, took the place of age in the model for the new group. For each model, there was good agreement between observed and predicted mortality for up to 24 months. To assess the influence of dialysis treatment time and dose (measured as pre-to-post treatment urea ratio) on risk, survival was examined in a subset of 139 patients monitored for up to 22 months, from 1989 to 1991, a period when the urea ratio was used routinely. Adjusting for the other variables, low serum albumin and cholesterol again independently increased risk. The urea ratio was also a significant independent predictor. The pattern of mortality by urea ratio was U shaped, with minimum risk for values between 2.5 and 3.4 Treatment time did not influence risk. It was concluded that baseline serum values of albumin and cholesterol strongly influence survival for up to 2 yr in new and long-standing hemodialysis patients.(ABSTRACT TRUNCATED AT 400 WORDS)

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A 60‐year‐old African‐American man was admitted to the hospital in October 1991 with seizures and right hemiparesis. He had end‐stage renal disease (ESRD), presumed due to hypertension and/or analgesic nephropathy, and had been on maintenance hemodialysis since July 1987. Noncontrast CAT of the brain revealed mild cortical atrophy and non‐specific while matter ischemic changes. Contrast CAT showed a right hemisphere CVA, and magnetic resonance imaging (MRI) suggested a right frontal meningioma. Cerebral arteriogram was confirmatory, and he underwent resection of the fronto‐parietal tumor in early November 1991. Past medical history included over 20 years of hypertension, angina for five years, gout, and peptic ulcer disease. Cardiovascular evaluation of exertional dyspnea and bilateral calf weakness included a negative thallium stress test and minimal to moderate flow impairment of tibial‐peroneal vessels by Doppler. Low iron stores led to upper and lower endoscopy and a colonic polypectomy. There was a question of an allergic reaction to intravenous iron administration (the patient reported lip swelling), and erythropoietin therapy was started in December 1990 (starting hematocrit was 23%). Hemodialysis access was achieved via a Brescia‐Cimino arteriovenous fistula in his left arm, which developed extensive upper arm and shoulder collaterals, leading to a fistulogram and a diagnosis of subclavian stenosis in January 1989. Angioplasty was successful, and repeat fistulogram was unremarkable in February 1991. Blood pressure control was usually adequate, ranging from 140–180/80–100 on diltiazem, clonidine, and captopril. Occasional elevation to 210/120 were seen. In the months prior to the seizure, his treatments were adjusted because of low Kt/V (by increased dialyzer surface area and increased time). Hematocrit had risen to 30%‐33% with erythropoietin therapy (2000 Units thrice weekly). Hemodialysis was accomplished without heparin use, due to his gastrointestinal bleeding history. He was felt to be gaining “flesh” weight. In late March 1992, he had a tonic‐clonic seizure. Repeat CAT scan of the brain was unchanged. He was started on phenytoin thrice daily, but he discontinued therapy and had two more seizures (with negligible serum levels of phenytoin) in April 1992. In May, he was readmitted after another tonic‐clonic seizure. Phenytoin levels were in the therapeutic range, and CAT scan was again unchanged. Phenobarbital was added to his regimen. Drowsiness limited his compliance, and he had several additional seizures. In late July, he suffered a respiratory arrest shortly after a seizure.

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