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Biomedical subjects

S G Rostand

Publications and source records attributed to S G Rostand.

At least 37 records · Page 2Linked to original sources
PubMed1987

Metastatic calcification of the heart and lungs in end-stage renal disease: detection and quantification by dual-energy digital chest radiography.

Metastatic calcification of the lung and heart can cause severe cardiopulmonary compromise and death. Although it is found in most end-stage renal disease patients at autopsy, it is only rarely detected during life. Using a prototype dual-energy digital chest radiographic unit, we measured calcium content (mg/cm2) over the lung and heart in 32 hemodialysis patients. Pulmonary calcium content was significantly greater in these patients than in sex-matched control subjects (men, 230 +/- 43 [mean +/- standard error] vs 166 +/- 7, p less than .05; women, 168 +/- 19 vs 110 +/- 7.5, p less than .001). Abnormal values were detected by dual-energy radiography in 44% of patients (vs 9% of patients studied by conventional radiography). Cardiac calcium content was also significantly greater in the hemodialysis patients than in the control subjects (259 +/- 14 vs 184 +/- 8, p less than .05). Metastatic calcification was significantly correlated with elevated phosphate and calcium-phosphate product levels. Patients with significantly elevated pulmonary calcium content had evidence of restrictive lung disease by functional testing. There was an inverse correlation between elevated cardiac calcium content and ejection fraction. We conclude that dual-energy digital radiography allows premortem diagnosis of metastatic visceral calcification and is more sensitive than current techniques.

Adult↗
PubMed1986

Human complement protein D catabolism by the rat kidney.

Factor D (D) is an essential component of the alternative complement pathway. To determine whether D is catabolized by the kidney and, if so, at what site, we studied the renal handling of human D by in vivo nephron microperfusion and in vitro perfusion of rat kidneys. Human D was purified and labeled with 125I. Individual nephrons were perfused in vivo at varying rates with perfusate that contained 125I-D and [14C]inulin. When nephrons were perfused from proximal sites with perfusate 125I-D in a concentration of 3.0 micrograms/ml, urinary recovery of 125I-D increased (P less than 0.05) from 57.7 +/- 5.0 to 74.4 +/- 2.5% as tubule fluid flow rate was increased from 10 to 40 nl/min; recovery of 125I-D was less than (P less than 0.001) [14C]inulin recovery at all perfusion rates. At 20 nl/min, an increase in perfusate 125I-D concentration from 1.5 to 3.0 micrograms/ml was associated with an increase (P less than 0.001) in urinary 125I-D recovery (42.1 +/- 4.0 vs. 65.8 +/- 2.6%). Similarly, the addition of unlabeled D, 30 micrograms/ml, to 125I-D, 3.0 micrograms/ml, increased urinary 125I-D recovery (95.3 +/- 2.1%) at 20 nl/min. When nephrons were perfused from early distal segments at 10 nl/min, 125I-D recovery (91.2 +/- 4.3%) did not differ from [14C]inulin recovery (95.8 +/- 1.3%). In the isolated perfused filtering kidney, the concentration of intact 125I-D in the perfusate declined 60.3 +/- 14.6% over 1 h. 83.4 +/- 6.3% of the decrement in 125I-D was catabolized by the kidney; the remainder was excreted in the urine as intact D. When glomerular filtration was prevented by increasing perfusate albumin concentration to 16 g/dl, perfusate intact (125I-D) remained unchanged over 1 h. These data show that human D is catabolized by the kidney via glomerular filtration and reabsorption by the proximal nephron. Reabsorption of D appears to be a saturable process.

Animals↗
PubMed1986

Acute pancreatitis in patients with end-stage renal disease without transplantation.

Acute pancreatitis is infrequently described in patients with end-stage renal disease (ESRD) who have not undergone transplantation. We observed 35 attacks of acute pancreatitis in 23 of 1001 patients with ESRD and one additional patient with irreversible acute renal failure, during a ten-year period. Pancreatitis occurred more frequently in association with peritoneal dialysis than with hemodialysis. Four patients died of complications related to a pancreatic pseudocyst, and a fifth died from hemorrhagic pancreatitis. The ten-year incidence of pancreatitis was 2.3% and the overall mortality was 20.8% in patients with ESRD treated without transplantation. We conclude that clinically evident acute pancreatitis occurs more often than has been previously recognized in patients with ESRD who have not undergone transplantation and, particularly, in those patients managed with peritoneal dialysis.

Acute Disease↗
PubMed1985

Effect of reduced chloride reabsorption on renin release in the isolated rat kidney.

To investigate the relationship between tubular reabsorption of chloride and renal renin release in the isolated perfused rat kidney, perfusate renin activity was measured during substitution of either nitrate or thiocyanate for varying amounts of perfusate chloride but with maintained perfusate sodium concentration. Renin rose significantly as perfusate chloride fell; there was a sevenfold increase between perfusion with normal chloride and almost complete substitution of chloride by nitrate. With a normal perfusate chloride the addition of furosemide 10(-4) M to the perfusate also led to an increase in renin and a reduction in tubule chloride reabsorption. For all these experiments there was a significant negative correlation between renin and absolute tubular reabsorption of chloride (r = -0.68, P less than 0.001), but no such relationship with absolute sodium reabsorption. Renin release in a nonfiltering kidney, produced by elevating perfusate albumin concentration, increased approximately 40-fold. Thus increasing plasma oncotic pressure elevates renin by mechanisms additional to cessation of tubular chloride absorption. However, substitution of chloride in the perfusate by nitrate in this nonfiltering kidney did not further elevate renin release. We conclude that renin release is influenced by a signal dependent on, and inversely proportional to, chloride reabsorption in the thick ascending limb of the Loop of Henle.

Absorption↗
PubMed1985

Staphylococcus aureus bacteremia in patients on chronic hemodialysis.

Staphylococcus aureus bacteremia occurred 96 times in 58 of 671 patients on chronic hemodialysis during a nine-year period. Seventy-one instances of bacteremia originated in the vascular access site and resulted in the loss of the access device in 45 episodes. The overall mortality was 8%, and the incidence of infective endocarditis was 4%. Death occurred more often when bacteremia arose from an identifiable site other than the vascular access device (P less than .02). Patients who developed one or more metastatic foci of infection had a higher incidence of primary treatment failure (P less than .001) and a higher mortality (P less than .001) than did those with no metastatic infection. Although meaningful comparisons of differing antibiotic regimens could not be made, patients receiving antibiotic therapy for 28 days or longer relapsed less frequently (P less than .05). These data suggest that chronic hemodialysis patients with S aureus bacteremia have a relatively low mortality and a low risk of infective endocarditis. Antibiotic treatment, however, should be given for at least 28 days in order to minimize the risk of relapse.

Adolescent↗
PubMed1985

Effect of 6-aminonicotinamide on renin release in isolated rat kidney: possible role for the pentose pathway.

To study the association between renal renin release and the pentose pathway, we perfused nonfiltering kidneys from Sprague-Dawley rats with Krebs-Ringer bicarbonate buffer containing 5 mM glucose and 14 g/100 ml bovine serum albumin in the presence or in the absence of 0.25 mM 6-aminonicotinamide (6AN), an inhibitor of glucose-6-phosphate dehydrogenase, the rate-limiting step of the pentose pathway. Eleven kidneys perfused in the absence of 6AN had a renin secretion rate of 7.4 +/- 2.2 ng ANG I X min-1 X ml-1. In six kidneys perfused in the presence of 6AN, renin release was depressed to 0.56 +/- 0.24 ng ANG I X min-1 X ml-1. The renal renin content for four control kidneys was 56 +/- 3.3 ng ANG I X mg-1 X h-1 while in four kidneys perfused with 6AN renal renin content was lower, 35 +/- 2.9 ng ANG I X mg-1 X h-1. In the presence of 5 mM lactate, the renin release of eight nonfiltering kidneys was 0.31 +/- 0.06 ng ANG I X min-1 X ml-1. The addition of 6AN did not further depress renin secretion in the presence of lactate. 6-Aminonicotinamide also completely blocked furosemide-stimulated renin release without having any effect on glomerular filtration rate or furosemide-induced natriuresis. However, 6AN did not inhibit stimulation of renin secretion by isoproterenol. We conclude that 6-aminonicotinamide interferes with renin release by nonfiltering kidneys and also inhibits furosemide-stimulated renin release but does not affect beta-adrenergic-stimulated renin secretion. Glucose but not lactate is important for maintaining augmented rates of renin secretion in nonfiltering kidneys. 6-Aminonicotinamide significantly reduced renal renin content in the presence of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Aminonicotinamide↗
PubMed1984

Dialysis-associated ischemic heart disease: insights from coronary angiography.

We reviewed the records of 44 dialysis patients who had undergone one or more coronary angiograms to determine the frequency with which symptomatic ischemic heart disease (IHD) and significant coronary artery narrowing coincided and to determine those factors which were associated with the coronary atherosclerotic process. Thirty-four patients were catheterized for angina pectoris or myocardial infarction. Of this group, 53% were found to have significant narrowing of coronary arteries. This group was older than the group with trivial or no coronary artery occlusion and their duration of dialysis was shorter. All the patients with significant coronary occlusion were white and the majority were adult males. Discriminant function analysis revealed that the presence of significant coronary artery occlusion could be predicted with high sensitivity and specificity by the following variables: older age, white race, male sex, the presence of symptomatic IHD prior to the onset of dialysis, increased total serum cholesterol, abnormal left ventricular wall motion, and reduced alkaline phosphatase. We also found that the occurrence of symptomatic IHD far exceeded the presence of significant atherosclerotic coronary artery narrowing. We suggest that this may result from several dialysis-associated alterations in oxygen delivery and myocardial oxygen consumption.

Adult↗
PubMed1984

Attenuated pressure natriuresis in the early phases of two-kidney Goldblatt hypertension.

We studied the effect of changing perfusion pressure on the excretory function of isolated perfused nonclipped kidneys from the two-kidney Goldblatt hypertensive rat ( GHR ). Kidneys were studied from newly hypertensive rats about 8 days after contralateral renal artery clipping [blood pressure (BP) 138 +/- 4.3 mmHg] and before onset of hypertension 3 days following surgery (BP 111 +/- 1.9 mmHg). In addition, nonclipped kidneys from adrenalectomized Goldblatt rats were also examined approximately 9 days following surgery (BP 114 +/- 4.7 mmHg). Kidneys from sham-operated rats served as controls. We noted no differences in GFR in kidneys from newly hypertensive rats and sham controls above a perfusion pressure of 120 mmHg. In response to increasing perfusing pressure, perfusate flow and fractional sodium excretion were significantly lower in newly hypertensive rats than in sham-operated controls. No differences in glomerular filtration rate, perfusate flow, or sodium excretion were noted in kidneys from sham-operated rats or Goldblatt rats 3 days following surgery. After clipping, adrenalectomized (ADX) Goldblatt rats had less of a rise in blood pressure than did rats with intact adrenal glands. No attenuation of natriuresis was noted in the ADX-clipped group in response to increasing perfusion pressure. Isolated perfused kidneys from ADX rats had greater sodium excretion at all levels of pressure than kidneys from rats with intact adrenal glands. Deoxycorticosterone acetate replacement returned sodium excretion to that approaching intact rats. We conclude that nonclipped kidneys of newly hypertensive Goldblatt rats exhibit blunted pressure natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1983

Profound hypokalemia in continuous ambulatory peritoneal dialysis.

Symptomatic hypokalemia is not known to complicate continuous ambulatory peritoneal dialysis (CAPD), although this treatment is associated with continuous peritoneal potassium losses. Severe hypokalemia and muscular abnormalities associated with potassium loss developed in a patient undergoing CAPD, illustrating that oral supplementation and/or intraperitoneal potassium administration may be needed to treat patients with chronically poor nutritional intake or increased gastrointestinal potassium losses. Intraperitoneal potassium administration may be indicated in patients who cannot tolerate oral potassium supplements.

Diabetic Nephropathies↗
PubMed1982

Relationship of coronary risk factors to hemodialysis-associated ischemic heart disease.

The records of 320 hemodialysis patients at risk for developing ischemic heart disease (IHD) were examined to determine the influence of the established risk factors of blood pressure, smoking, serum triglycerides, and age on the incidence of IHD and to develop coronary risk profiles for the hemodialysis population. The role of packed red blood cell volume, race, sex, and cause of renal failure on the development of IHD were also examined. None of these risk factors alone, with the exception of age and chronic pyelonephritis, were found to contribute significantly to the incidence of dialysis-acquired IHD. When the joint contribution of these variables was analyzed using Cox regression analysis, race and diastolic hypertension also were discovered to contribute significantly to IHD. However, smoking and serum triglycerides were not found to be significant risk factors. From these data, it is concluded that older patients are a greater risk than younger patients, that white patients are at a greater risk than black patients, that patients with elevated diastolic blood pressure are at an increased risk and that patients with chronic pyelonephritis as the underlying renal disease are at an increased risk.

Adolescent↗
PubMed1982

Attenuated pressure natriuresis in hypertensive rats.

We studied the isolated blood-free perfused nonclipped kidneys from the 2-kidney Goldblatt hypertensive rat model (GHR) to evaluate intrinsic excretory responses to changes in perfusion pressure. We examined kidneys from 10 control rats (in vivo systolic BP 110 +/- 3.6 mm Hg), from 9 rats with nonmalignant hypertension (HBP) (in vivo systolic BP 158 +/- 6.5 mm Hg), and from 5 rats with malignant HBP (in vivo systolic BP 183 +/- 6.4 mm Hg). We found that at all levels of perfusion pressure, the renal vascular resistances were significantly higher and glomerular filtration rate (GFR) lower in kidneys from hypertensive rats than in kidneys from control rats. Kidneys from hypertensive rats had lower urinary excretion of sodium (UNaV) and urine flow than kidneys from control rats at all levels of pressure above 100 mm Hg. The most striking differences in all functional parameters were noted in kidneys from rats with malignant HBP. Kidneys from both hypertensive and control rats failed to show changes in vascular resistance in response to Saralasin. We conclude that the nonclipped kidney in GHR exhibits a blunted natriuresis in response to elevated perfusion pressure which occurs in the absence of angiotensin II (AII) and renin substrate. This diminished pressure natriuresis may be caused partly by the lower GFR and by reduced pressure transmission due to greater renal vascular resistance and thus may be partially responsible for the maintenance of the hypertensive state.

Animals↗
PubMed1982

Lower gastrointestinal tract dysfunction in patients receiving long-term hemodialysis.

Severe bowel dysfunction developed in 25 of 945 patients receiving long-term hemodialysis during a ten-year period. Colonic perforation occurred in 12 patients, six of whom died due to peritonitis. In seven instances, the perforation occurred spontaneously. Ten other individuals exhibited prolonged, severe adynamic ileus that progressed to colonic pseudo-obstruction in eight patients. Medical decompression (eight patients) and surgical bowel decompression (two patients) resulted in recovery in nine. Aluminum hydroxide gel, which was taken regularly by all patients, was associated with notable chronic constipation prior to the occurrence of bowel perforation or protracted adynamic ileus in 78% of these individuals.

Adult↗
PubMed1981

Treatment of secondary hyperparathyroidism in patients with chronic renal failure by total parathyroidectomy and parathyroid autograft.

Sixty-one patients with chronic renal failure and secondary hyperparathyroidism underwent total parathyroidectomy and parathyroid autograft. Symptoms relieved by parathyroidectomy included bone pain, pruritus, soft tissue calcification, muscle weakness and healing of fractures. Serum parathormone levels measured before and after operation in 48 patients returned to normal in all but two patients. Serum alkaline phosphatase levels also returned toward normal after operation, except in one patient with a retained parathyroid gland. Complete radiographic studies before and after operation were available in 30 of 61 patients. Twenty-three of 24 patients with osteitis fibrosa had evidence of healing, and in one patient no change occurred. Osteosclerosis noticed in 23 patients improved slightly in eight patients, did not change in 14 and became worse in one. Pathologic examinations revealed 45 patients to have diffuse hyperplasia and 16 nodular hyperplasia. There were two early postoperative deaths, in the first 30 days, and 16 late postoperative deaths, from four months to four years afterward. In no case did the operation contribute to death. Some patients required the administration of supplemental calcium after operation, but in no instance did profound hypocalcemia occur. No patient developed recurrent hyperparathyroidism.

Adolescent↗
PubMed1980

Urinary acidification in a patient with glucose-6-phosphate dehydrogenase deficiency. A reevaluation of the role of the hexose monophosphate shunt in renal acid secretion.

The relationship between renal metabolism and urinary acidification is poorly understood. During the past decade evidence has accrued to suggest that the hexose monophosphate (HMP) shunt might serve in the process of urinary acidification by providing reducing equivalents for a redox-coupled membrane-bound proton pump that could transport protons into the tubular lumen. The major support for this hypothesis has come from the finding that HMP shunt activity increases with acute and chronic metabolic acidosis. In the present study, we examine the urinary acidification capacity of a young man with severe erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and with unmeasurable G-6-PD activity in renal cortical tissue. We found that despite unmeasurable G-6-PD activity in renal tissue, the patient was capable of generating a maximally acid urine and increasing total acid secretion. Our findings suggest that the HMP shunt may not be necessary for the urinary acidification process.

Adolescent↗
PubMed1980

The effect of insulin and of anti-insulin serum on handling of sodium by the isolated, perfused kidney of the streptozotocin-diabetic rat.

We studied the effects of insulin and of anti-insulin serum (AIS) on sodium excretion in isolated diabetic and normal, fed, rat kidneys perfused at a constant pressure of 100 mm Hg with Krebs-Ringer bicarbonate buffer containing 7.5% bovine serum albumin and 5 mM glucose and gassed with 95% O2 and 5% CO2. The addition of insulin produced antinatriuresis in kidneys from diabetic rats but not in those from normal rats. Moreover, before the addition of insulin, the baseline rate of sodium excretion was greater in the diabetic rat kidney than in the normal rat kidney, while no differences in glomerular filtration rate (GFR) were observed. The addition of AIS (enough to bind 1.4 mU of insulin per milliliter of perfusate) produced a brisk natriuresis in kidneys from normal rats, and this natriuresis could be reversed by the addition of saturating amounts of insulin. By contrast, the addition of normal guinea pig serum to the perfusate of normal kidneys or AIS to the perfusate of diabetic kidneys was unassociated with natriuresis. We conclude that (a) insulin promoted antinatriuresis in diabetic but not in normal rat kidneys, (b) AIS promoted natriuresis in normal kidneys, and (c) this natriuresis was a specific effect of AIS and was reversed by the addition of insulin. Our data support the view that insulin-induced antinatriuresis depends on endogenous levels of circulating insulin and on the availability of insulin-binding sites in the kidney.

Animals↗
PubMed1980

Mycobacteriosis in patients with chronic renal failure.

Active mycobacterial disease developed in nine of 885 patients undergoing long-term maintenance dialysis during an 8 1/2-year period. An additional eight patients, who had chronic renal failure but did not require long-term dialysis, contracted active mycobacterial infection during the same interval. Fifty-six percent of the dialyzed group had predominantly extrapulmonary disease and 33% were infected with mycobacteria other than Mycobacterium tuberculosis. Tuberculin sensitivity was present infrequently and examination of sputum and other fluids for acid-fast bacilli was usually unrewarding. The presence of mycobacteria was demonstrated most reliably by tissue biopsy and culture. Failure to diagnose mycobacteriosis resulted in the death of three patients, while the remaining patients responded satisfactorily to drug therapy.

Adult↗