Armando Lindner

Synergism of Dopamine and Furosemide in Diuretic-Resistant, Oliguric Acute Renal Failure

This paper describes our initial clinical findings in a small group of patients with acute oliguric renal failure, who were resistant to extracellular volume expansion and furosemide in large doses. Based on our experience in an experimental model of acute renal failure in the dog, we administered a combination of low-dose dopamine (1-3 micrograms/kg/min i.v.) and furosemide (100-200 mg every 6-8 h). This combination was uniformly effective in inducing a brisk, lasting diuresis and was associated with either stable or reduced serum creatinine levels in two-thirds of the patients. No toxicity was found. These findings would warrant extensive study of this drug combination in a larger, well-controlled, randomized group with oliguric renal failure.

Effects of Verapamil and Nifedipine on Renal Function and Hemodynamics in the Dog

This study evaluates the direct effects of verapamil (5 micrograms/kg/min) or nifedipine (0.32 micrograms/kg/min) when infused into one renal artery for 2 h. The role of calcium in the systemic and renal vascular effects of angiotensin II (1 microgram/i.v. bolus) was examined in each period. Renal blood flow was increased 11% by verapamil and 29% by nifedipine. Unlike other vasodilators, these drugs markedly increased GFR (by 75% with verapamil and 50% with nifedipine), and both caused a profound natriuresis, which outlasted the renal hemodynamic changes. Further, they abolished the renal vascular responses to angiotensin II. These major direct effects on renal function and hemodynamics suggest that: (a) calcium blockers may affect the determinants of GFR differently from other vasodilators, and (b) they may interfere with proximal tubular Na+ transport.

Albuminuria in Hematopoietic Cell Transplantation Patients: Prevalence, Clinical Associations, and Impact on Survival

Chronic kidney disease (CKD) is common after hematopoietic cell transplantation (HCT). We prospectively measured the urinary albumin:creatinine ratio (ACR) in 142 patients. Total (intact) monomeric albumin was determined by liquid chromatography of untreated urine samples collected weekly to day 100 after HCT. Albuminuria was defined as ACR (mg/g creatinine) > 30; proteinuria, as ACR >300. Cox and logistic regression analyses evaluated ACR as a risk factor for clinical events. The prevalence of albuminuria was 37% at baseline, 64% at day 100, and 50% at 1 year. Proteinuria occurred in 4% of patients at baseline, in 15% at day 100, and in 4% at 1 year. Characteristics associated with albuminuria include age, sex, donor type, hypertension, and sinusoidal obstruction syndrome (SOS). Albuminuria was associated with an increased risk of acute graft-versus-host disease (aGVHD) and bacteremia, but not acute kidney injury (AKI). Albuminuria at day 100 was associated with CKD at 1 year (odds ratio = 4.0; 95% confidence interval [CI] = 1.1 to 14.6). Nonrelapse mortality (NRM) risk was elevated (hazard ratio = 6.8; 95% CI = 1.1 to 41.5) in patients with overt proteinuria at day 100. Albuminuria occurs frequently after HCT and is correlated with aGVHD, bacteremia, hypertension, and progression of renal disease. Proteinuria at day 100 is associated with an 6-fold increased risk of NRM by 1 year after HCT.

111In-Oxine Platelet Imaging in Hemodialysis Patients: Detection of Platelet Deposition at Vascular Access Sites

The value of 111In-oxine platelet imaging to assess abnormal platelet deposition at different vascular access sites was studied in 19 hemodialysis patients. Platelets were labelled immediately following dialysis and imaging was performed 2 and 48 h later; abnormal platelet deposition was defined as a localized increase in activity over time when compared to the opposite, control extremity. 10 patients had bovine grafts, 4 had arteriovenous fistulae, and 5 had Gore-Tex grafts. 111In-oxine platelet imaging demonstrated abnormal platelet deposition in 13 out of 19 patients. Positive images were obtained in some patients with each type of vascular access. Preliminary evaluation showed no clear relationship between image positivity and the history of prior graft occlusion. The imaging method provided in vivo evidence of the efficacy of treatment with the antiplatelet agent sulfinpyrazone in half of the treated patients. Following 1 week of sulfinpyrazone, 200 mg t.i.d., in 6 patients, 3 showed a definite decrease in platelet deposition, 2 showed a probable decrease, and 1 showed no change following therapy. We conclude that platelet imaging may provide organ-specific, in vivo evidence for abnormal platelet deposition in several types of vascular access sites, and may be useful in assessing the thrombogenicity of prosthetic materials and the efficacy of antithrombotic drugs.

Influence of Anabolic Steroids on Nitrogen Balance in Chronic Peritoneal Dialysis

Nitrogen balance was studied in 6 patients on maintenance peritoneal dialysis by classical metabolic balance techniques. Protein losses were compensated in all cases by administration of a high protei

Morbidity and Mortality Associated with Long-Term Hemodialysis

Now that problems of circulatory access, infection, osteodystrophy, and neuropathies seem under control, the major concerns today are the acceleration of atherosclerosis in patients in long-term treatment and the rehabilitation of those with psychosocial problems arising from dependence on a machine. Patients who previously faced only rapid, usually painful death are in some instances surviving for a decade or more.

Hemodynamics of a Renal Arteriovenous Fistula in Oliguric Renal Failure

A woman with oliguric post partum renal failure was studied by means of the xenon-133 washout technique, renal biopsy, and selective renal arteriogram. An arteriovenous fistula was found in the lower

Free Calcium in Red Blood Cells of Human Hypertensives is Elevated: How Can This be?

Abnormal regulation of calcium transport has been proposed as one mechanism by which increased levels of intracellular free Ca2+ may occur and could be a factor in essential hypertension (Bohr and Webb, 1984). Since vascular smooth muscle cells from human subjects are not readily available for studies of ion transport, circulating blood cells have frequently been used as a model for such measurements in hypertension (Erne et al., 1984a; Lindner et al., 1987; Postnov et al., 1977). While several abnormal Na+ transport pathways have been described in human red blood cells (RBCs) in hypertension (Postnov et al., 1977; Diez et al., 1987), little is known concerning intracellular free Ca2+ in these cells.