Doppler-detected tricuspid, mitral or aortic regurgitation in end-stage renal disease.
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Adult↗
Biomedical subjects
S D Migdal
Publications and source records attributed to S D Migdal.
Elevated plasma copper in chronic renal failure.
Hypercupremia has been described in patients undergoing chronic dialysis. To further characterize dialysis-associated hypercupremia, we studied plasma copper (PCu) and ceruloplasmin (Cp) in patients on hemodialysis (n = 20) and peritoneal dialysis (n = 25), in uremic patients (n = 10) not yet on dialysis, and in normal age-matched control subjects (n = 20). PCu was significantly elevated in all three patients groups (mean +/- SD) (20.6 +/- 4.1, 19.8 +/- 4.6, 19.8 +/- 4.9 mumol/L, respectively) vs control subjects (16.5 +/- 2.7 mumol/L). However, Cp levels were not significantly different among the four study groups (330 +/- 60, 320 +/- 70, 370 +/- 100, and 360 +/- 90 mg/L, respectively). Calculated nonceruloplasmin copper was significantly higher in all uremic groups. The measurement of chelatable Cu confirmed the presence of significantly higher extractable Cu in hemodialysis (2.7 +/- 0.6 mumol/L) and peritoneal dialysis patients (2.4 +/- 0.5 mumol/L) than control subjects (1.5 +/- 0.3 mumol/L). Cu is elevated in uremia regardless of dialysis status and this elevation is not accounted for by an increase in plasma ceruloplasmin.
Adult↗
Toxic nephropathies.
The general topic of kidney damage produced by drugs and toxins is introduced, emphasizing its clinical importance in critically ill patients. Specific toxins are then examined in detail with respect to the mechanisms of toxicity, clinical features, and management.
Anti-Bacterial Agents↗
Morphologic and immunohistochemical observations in granulomatous glomerulonephritis.
Eight renal biopsies of Wegener's granulomatosis and other vasculitic syndromes with periglomerular granulomatous reactions (granulomatous glomerulonephritis) are studied. Controls consist of 57 biopsies of crescentic and focal necrotizing glomerulonephritis (of various diseases, excluding systemic lupus erythematosus). Both groups have in common the morphologic alterations of inflammatory tuft necrosis, fibrin exudation into the urinary space, crescent formation, and breaks of Bowman's capsule. In the study group, the unique feature of glomeruli with surrounding granulomatous reactions was the presence, within the urinary space, of an exudate of fibrin mixed with immune reactants (immunoglobulins and usually complement) in association with gaps of Bowman's capsule. This contrasts with an exudate of fibrin alone in glomeruli of the control group and other glomeruli of the study group. The study group also had a significantly greater incidence of immune deposits in Bowman's capsule (P less than 0.001). Giant cells may result from the interaction of macrophages of the granuloma with Bowman's capsule that is permeated with immune reactants.
Fluorescent Antibody Technique↗
Zinc tolerance test in uremia. Effect of ferrous sulfate and aluminum hydroxide.
The effects of ferrous sulfate and aluminum hydroxide on the oral zinc tolerance test after administration of 25 mg of elemental zinc as sulfate were studied in six hemodialysis patients and six normal controls. Fasting plasma zinc levels, the 2-hour plasma zinc peak, and the area under the plasma zinc curve were significantly lower in patients compared with values in controls (plasma zinc, 92 +/- 4 compared with 108 +/- 3 micrograms/dL, p less than 0.025; 2-hour plasma zinc peak, 159 +/- 8 compared with 228 +/- 17 micrograms/dL, p less than 0.025; and area under the curve, 193 +/- 41 compared with 316 +/- 39 micrograms h/dL, p less than 0.025). Ferrous sulfate (300 mg orally), when administered along with zinc sulfate, decreased the area under the curve significantly (in patients by 28%, in controls by 40%) in comparison with the results obtained when zinc sulfate was given alone. When 30 mL of aluminum hydroxide was administered orally with zinc sulfate, the area under the curve decreased by 60% in controls and 75% in patients (p less than 0.005). These results confirm the presence of diminished zinc absorption in patients with renal failure and show that ferrous sulfate and aluminum hydroxide, which worsen this defect, also impair zinc absorption in normal subjects.
Administration, Oral↗
Effect of renal transplantation on zinc metabolism and taste acuity in uremia. A prospective study.
The effect of successful renal transplantation on zinc metabolism and taste acuity was determined prospectively in 15 adult uremic patients. Before transplantation all patients had subnormal concentrations of zinc in plasma and hair, as well as abnormal taste detection and recognition thresholds for sodium (salty), sucrose (sweet), hydrochloric acid (sour), and urea (bitter). Following renal transplantation, abnormalities of taste acuity and zinc metabolism persisted and were accompanied by increased urinary zinc excretion in all patients. Normalization of zinc concentration in plasma and hair as well as taste acuity did not occur until one year after transplantation and was associated with a concomitant decrease in urinary zinc excretion. The plasma zinc levels and daily urinary zinc excretion were inversely related (r = 0.62, P less than .001) in all patients with normal allograft function. None of the zinc parameters was significantly related to azathioprine or corticosteroid dosage. The results of this study suggest that zinc deficiency and taste abnormalities of uremia persist up to one year posttransplant and may be related to increased urinary zinc losses. The mechanisms underlying post-transplant hyperzincuria as well as clinical significance of zinc deficiency following transplantation remain to be determined.
Adult↗
Zinc metabolism and taste acuity in renal transplant recipients.
To determine the effect of renal transplantation on taste acuity and zinc metabolism, we tested 43 patients with functioning allografts for 2.5 to 96 months. They were tested for taste by the 3-drop stimulus technique. In 30 of them, we determined zinc levels in plasma, hair, and urine. Subnormal plasma and hair zinc, as well as hyperzincuria, was present in all of the 15 patients less than 12 months posttransplant. In contrast, 10 patients who were more than 12 months posttransplant had plasma zinc levels, hair zinc, and urinary zinc excretions in the normal range. Zinc concentrations in plasma and hair of 5 patients who were more than 12 months posttransplant with renal failure, were subnormal and were similar to those in hemodialysis patients. Similarly, taste detection and recognition thresholds for sodium chloride, sucrose, urea, and hydrochloric acid were normal only in patients more than 12 months posttransplant with normal renal function. Plasma zinc, hair zinc, and urinary zinc were not related to prednisone or azathioprine dosage. These results suggest that abnormalities of zinc and taste persist up to 12 months posttransplant and may be related to increased urinary zinc losses.
Adult↗
Glucose tolerance, insulin release, and insulin binding to monocytes in kidney transplant recipients.
In order to evaluate glucose tolerance following renal transplantation, intravenous glucose tolerance tests (IVGTT), with evaluation of hormonal responses to the intravenous glucose load and percent specific 125I-insulin binding to peripheral blood monocytes, were studied in eight clinically stable kidney transplant recipients. For comparison purposes, identical studies were done in eight control subjects and seven clinically stable hemodialysis patients. One transplant recipient was glucose intolerant, with fasting hyperglycemia, elevated HbA1C, and abnormal glucose decay constant. Impaired pancreatic insulin release appeared to be the major factor accounting for his glucose intolerance. The seven glucose-tolerant transplant recipients had significantly increased insulin release during IVGTT compared to control subjects, and significant correlations were found among insulin release, glucose decay constant, and fasting blood sugar in those patients. Insulin binding to monocytes was significantly greater in transplant recipients than control subjects due to an increase in insulin binding capacity per cell. A significant correlation was found between percent specific 125I-insulin binding and steroid dose, expressed as mg/kg body weight/day, in those patients. Thus, chronic steroid administration does not cause glucose intolerance in transplant recipients who manifest steroid-associated increases in pancreatic insulin release and cellular insulin binding capacity.
Adolescent↗
Epidemic methanol poisoning: clinical and biochemical analysis of a recent episode.
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Adult↗
Renal handling of zinc: effect of cysteine infusion.
Zinc clearance studies in anesthetized dogs were performed during hydropenia, mannitol infusion, and infusion of mannitol plus ZnSO4, ZnCL2, or cysteine. Mannitol expansion caused no significant change in Zn clearance. ZnSO4 infusion increased filtered Zn 13-fold without changing clearance. Zn excretion increased only sixfold, indicating increased net Zn reabsorption. Cysteine infusion increased urinary Zn excretion 86-fold, indicating net tubular Zn secretion, some of which derived from nonplasma sources. Stop-flow studies localized Zn reabsorption to the distal nephron during infusion of mannitol and mannitol plus ZnSO4 or ZnCl2. Net Zn secretion was shown to occur in the proximal tubule during cysteine infusion with reversal of the distal reabsorption pattern seen during ZnSO4 and ZnCl2 infusion. Despite increased urinary Zn excretion during ZnSO4 infusion, calcium excretion was unaltered. During cysteine infusion dissociation of tubular handling of CA2+ and Zn occurred in both the proximal and distal tubule. These experiments demonstrate that the nephron under these experimental conditions is capable of both proximal secretion and distal reabsorption of Zn.
Animals↗
Noninflammatory renal microangiopathy of systemic lupus erythematosus ('lupus vasculitis').
5 (group 1) of 9 patients with systemic lupus erythematosus (SLE) who underwent a kidney biopsy during a 1-year period had a noninflammatory renal microangiopathy which significantly narrowed or occluded the lumens of arterioles and terminal segments of interlobular arteries. Though these lesions resemble those of malignant hypertension and the thrombotic microangiopathies, their distinctive features, revealed by light, immunofluorescence and electron microscopy, differentiate them from the others. 4 of these 5 (group 1) patients developed hypertension; in 3 the microangiopathy predated the hypertension. None of the remaining 4 (group 2) patients without these lesions has become hypertensive. One group-1 patient with extensive lesions involving 40% of intrarenal arterioles at biopsy developed renal failure shortly thereafter with increasing arteriolar involvement but unchanged glomerular histology.
Adult↗
Recovery following prolonged postoperative renal failure.
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Acute Kidney Injury↗
Influenza vaccination in kidney transplant recipients: cellular and humoral immune responses.
Influenza infection in renal transplant recipients may cause either morbidity and mortality or acute allograft rejection; thus, routine annual influenza vaccination should be considered. We have studied the humoral and cellular immune responses to influenza virus antigens before and after trivalent vaccine administration in 13 patients and 16 control subjects. The patients, nine of whom were either on alternate-day or low-dose daily steroid therapy, showed highly significant serum hemagglutination-inhibition antibody responses to each influenza virus strain, There was no significant change in mean lymphocyte stimulation index to any influenza virus strain after vaccination in either group. There was no correlation in the patient group between hemagglutination-inhibition antibody titer or response, or lymphocyte stimulation index or response, and the degree of allograft function or dose or duration of immunosuppressive therapy. The vigorous antibody response and the evidence of cellular immunity support the efficacy of influenza vaccination in these patients.
Adult↗
Phenytoin, renal function and renin release.
Phenytoin (DPH), a widely used anticonvulsant, has been shown to effect membrane transport in a wide variety of tissues. After injection, DPH is known to accumulate in high concentration in the kidney, however the renal effects of this drug have not been investigated. Therefore, these studies were designed to elucidate the effect of DPH on renal function and renin release. Dogs were anesthetized and had renal venous, aortic, brachial and ureteral catheters placed. During each of three successive experimental clearance periods, either saline, propylene glycol vehicle (V) or V + DPH (0.18 mg/kg/min) was infused via a 23-gauge needle in the left renal artery. In five dogs (Group I), the sequences of infusion was saline, (V) and (V). Five animals (Group II) differed only in that V was infused during all three periods. Seven animals (Group III) underwent sequential infusions of V, V + DPH, and V. Infusion of V alone resulted in a significant increase in systemic blood pressure from 120 to 135 mm Hg (P < .05). Significant increases after V infusion were found in urine volume (0.45 to 0.87 ml/min) (P < .05) and osmolar clearance (1.23 to 1.83 ml/min). Infusion of DPH produced a 22% increase in renal blood flow from 238 to 291 ml/min (P < .05) and a fall in renal vascular resistance from 0.51 to 0.41 mm Hg/ml/min (P < .05). Significant increases were also seen in urine volume from 0.87 to 1.58 ml/min (P < .05), urine sodium excretion (157 to 269 microEq/min) (P < .05) and osmolar clearance (1.54 to 2.62 ml/min) (P < .05). Renal renin secretion rate was unchanged in Group I and II animals but DPH infusion resulted in a 7-fold increase in renin secretion from 21 to 151 ng A-I/hr x min (P < .05). We conclude that intrarenal arterial infusion of DPH results in renal vasodilation, diuresis and natriuresis. Furthermore, this agent also stimulates renin release which may be the result of its effect on membrane transport.
Animals↗
Successful renal transplantation in focal glomerular sclerosis: report of two cases.
The fate of renal allografts has provided much useful information about the pathogenesis of certain glomerular diseases. Idiopathic nephrotic syndrome with focal glomerular sclerosis (FGS) has been reported to recur in transplants. Two patients are reported with idiopathic nephrotic syndrome who progressed to renal failure. Immunopathologic and ultrastructural studies appeared to exclude immune pathogenic mechanisms in both patients, and light microscopic findings were characteristics of FGS. The nephrotic syndrome in one patient was initially steroid-dependent. Both patients underwent bilateral nephrectomy prior to renal transplantation. Graft function and urine protein excretion were normal in both patients 2 and 4 years respectively after transplantation, and transplant biopsies revealed no evidence of recurrent FGS. These results indicate that renal transplantation in patients with idiopathic nephrotic syndrome and FGS is not invariably followed by recurrent glomerular disease and suggest that the responsible pathogenetic mechanism(s) may not always persist.
Adult↗