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Biomedical subjects

C R Cooke

Publications and source records attributed to C R Cooke.

At least 37 records · Page 2Linked to original sources
PubMed1991

Reversible changes in osmoregulation of vasopressin release due to impaired water excretion.

Studies of renal water handling and the effects of altered hydration and posture on the osmoregulation of vasopressin release were performed on a chronically hyponatremic patient with complete cervical spinal cord transection at the C-5 level. Acute oral water loading studies showed marked reduction in free water clearance and urine diluting ability, despite appropriate suppression of plasma vasopressin concentrations. Orthostatic reductions in arterial blood pressure during head-up tilting and following the assumption of sitting posture were also demonstrable, and may have contributed to, but could not fully account for, the defect in renal water excretion, which persisted in supine posture. Hypertonic sodium chloride infusion studies performed before fluid restriction showed that low preinfusion plasma osmolality was associated with a reduced osmotic threshold for vasopressin release, which was subsequently corrected by a period of fluid restriction that restored the patient's plasma osmolality to a normal level. This shift in osmotic threshold can be inferred from both linear regression and log-linear regression analysis of the data. These studies show that marked impairment of renal water excretion coupled with unrestricted water intake can result in altered osmoregulation of vasopressin release in association with persistent plasma hypo-osmolality, which can be corrected by fluid restriction.

Arginine Vasopressin↗
PubMed1990

Reversible nephrotic range proteinuria and renal failure in atheroembolic renal disease.

A case is described in which atheroembolic renal disease was associated with nephrotic range proteinuria, sub-acute renal failure, severe hypertension and microhematuria, in the absence of typical peripheral stigmata of atheroemboli. Nephrotic range proteinuria has not been previously reported in atheroembolic renal disease. With sustained aggressive treatment of hypertension there was diminution and eventual clearing of the proteinuria accompanied by marked improvement in renal function. The histopathology, the indications for renal biopsy, and possible causes of proteinuria are discussed.

Arteriosclerosis↗
PubMed1990

Altered sensitivity of osmotically stimulated vasopressin release in quadriplegic subjects.

Osmoregulation of vasopressin release was studied in 15 quadriplegic subjects (Quad) and 7 healthy control subjects (Con). Hypertonic NaCl (0.85 M) was infused intravenously (0.05 ml.kg-1.min-1) over 90 min in studies on supine subjects and in comparable studies on the same subjects erect (sitting). Erect posture in Quad, but not in Con, was accompanied by orthostatic reductions in arterial blood pressure and by significantly increased plasma aldosterone (P less than 0.001) and cortisol (P less than 0.001) concentrations and increased plasma renin activity (P less than 0.025). Changes in plasma arginine vasopressin concentration (PAVP) during hypertonic NaCl infusions were also greater in erect than in supine Quad (P less than 0.005), despite identical changes in plasma osmolality (Posm). Linear regression analysis of the PAVP/Posm relationship during hypertonic NaCl infusions showed highly significant correlations (P less than 0.0002) in both Quad and Con. Mean slope values for regression lines, however, were significantly higher in erect than in supine Quad (P less than 0.005) but did not differ in relation to posture in Con. Differences in posture were not associated with differences in abscissal intercepts in either Quad or Con. These studies show significant alterations in the sensitivity of osmotically stimulated vasopressin release related to differences in posture in Quad, characterized by enhanced sensitivity in erect posture due to nonosmotic stimuli not evident in Con.

Adult↗
PubMed1990

Nonosmotic stimuli alter osmoregulation in patients with spinal cord injury.

Studies on two quadriplegic patients who developed severe hyponatremia during episodes of acute respiratory distress were performed to determine whether differences in osmoregulation of vasopressin release could be identified in these patients compared to other quadriplegic subjects previously studied in a similar manner. Both patients were clinically stable and normonatremic, with no signs or symptoms of respiratory distress, when the studies were performed. However, both exhibited evidence of hemodynamic instability in the sitting posture. Linear regression analysis of the plasma vasopressin/plasma osmolality (Pavp:Posm) relationship during infusions of 0.85 M sodium chloride showed no significant differences in either the slope (sensitivity) or abscissal intercept (osmotic threshold) of this relationship compared to that of other quadriplegic subjects when the patients were supine. In contrast, when the patients were studied in the sitting posture there was a marked shift in the relationship of Pavp:Posm indicative of increased sensitivity and reduced osmotic threshold for vasopressin release. The slopes of the Pavp:Posm relationships were 0.249 and 0.178 for the two patients, respectively, compared to 0.092 +/- 0.03 ( +/- SD) for previously studied quadriplegic subjects. Oral water-loading studies performed on one patient revealed marked impairment of urine-diluting ability and free water clearance in the sitting posture compared with observations in similar studies performed when the patient was supine. Impairment of renal water excretion could not be attributed to an effect of vasopressin, which was reduced to unquantifiable levels by water loading. These studies have shown that hemodynamic stress related to autonomic dysfunction in quadriplegic patients may result in marked alteration of osmoregulation of vasopressin release in more severely affected individuals. Such altered osmoregulation, which may also be associated with vasopressin-independent impairment of renal water excretion in the sitting posture, may be a predisposing factor in the development of hyponatremia, especially in the presence of other potent nonosmotic stimuli.

Aged↗
PubMed1986

De novo diabetic nephropathy with functional impairment in a renal allograft.

Recurrence of diabetic nephropathy in the allograft of diabetics with end-stage renal disease who undergo renal transplantation has been reported. We report a case of a patient who underwent cadaveric renal transplantation for end-stage renal disease secondary to chronic glomerulonephritis 13 years ago. He developed steroid-induced, insulin-dependent diabetes mellitus 9 months after transplantation and florid nephrotic syndrome with progressive functional impairment due to biopsy-proven diabetic nephropathy 11 years later. This is, to our knowledge, the first report of de novo diabetic nephropathy in a renal allograft of a patient who was not a diabetic at the time of transplantation. It is suggested that histopathologic changes of diabetes mellitus cannot only recur in a renal allograft, but also can develop de novo and lead to functional impairment and ultimately affect graft survival. In view of increasing patient and graft survival in transplanted diabetic and non-diabetic patients, it is reasonable to anticipate an increased incidence of this complication.

Biopsy↗
PubMed1986

Chronic continuous PTH infusion results in hypertension in normal subjects.

The factors responsible for the frequent occurrence of hypertension in patients with primary hyperparathyroidism have not been elucidated. Suggested mediators have included hypercalcemia, renal insufficiency, and increased plasma renin activity. However, experimental results have not been reported in any species that test the hypothesis that sustained hypertension in this clinical syndrome is due to consequences of parathyroid hormone (PTH) excess versus unrelated factors (e.g., primary hypersecretion of other hormones, NaCl sensitivity, genetic factors). Moreover, no systematic evaluation of the renin or adrenal cortical responses to chronic PTH excess has been reported in any species. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous b-(1-34) PTH infusion in normal human subjects (n = 4). PTH infusion resulted in persistent hypercalcemia and hypertension, reversible during a 4-8-day recovery period. Transient but significant increases in urinary tetrahydroaldosterone excretion and plasma cortisol concentration were observed as hypercalcemia and hypertension developed. No significant changes in plasma potassium concentration or plasma renin activity were observed, suggesting that hypercalcemia-induced transient hypersecretion of ACTH was responsible for both cortisol and aldosterone responses. The present results suggest that hypertension associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and requires neither the long-term consequences/complications of the clinical disorder (e.g., severe nephrocalcinosis, renal insufficiency) nor primary hypersecretion of additional hormones. These results are consistent with the hypothesis that hypercalcemia alone or in combination with at least permissive levels of PTH can generate short-term, but persistent (12 days) hypertension in human subjects and thus may be the initiating mechanism for hypertension in clinical primary hyperparathyroidism.

Adult↗
PubMed1984

Effect of extracellular fluid volume depletion on renal regulation of acid-base and potassium equilibrium during prolonged mineral acid administration.

Previous studies of the renal and systemic acid-base response to prolonged administration of mineral acids in dogs have suggested that during the steady state of acidosis, the level at which plasma bicarbonate concentration is regulated by the kidney is dependent on the degree of augmentation of "distal delivery" of sodium imposed by the increased filtered load of administered mineral acid anion with filtered sodium, and on the degree of augmentation of "distal avidity" for sodium reabsorption imposed by ECF volume ( ECFV ) contraction secondary to renal sodium losses accompanying the administered mineral acid anion. This formulation, however, fails to predict the level at which plasma bicarbonate concentration would be regulated under conditions of preexisting ECFV depletion, which would simultaneously limit distal delivery of sodium salts and yet increase distal avidity for sodium reabsorption. Our studies assessed the renal and systemic acid-base responses to prolonged daily administration of 5.0 mEq/kg of H+ as HCl (groups 1 and 2) or H2SO4 (groups 3 and 4) in dogs with normal ECFV (groups 1 and 3) vs. preexisting ECFV depletion (groups 2 and 4) induced by administration of ethacrynic acid. In response to HCl administration, dogs with depleted ECFV developed more severe acidosis than ECFV -replete dogs (delta[HCO-3,]p, -5.0 +/- 0.6 mEq/L, group 2 vs. -2.7 +/- 0.5 mEq/L, group 1, p less than 0.02). The exacerbated metabolic acidosis in group 2 persisted in the steady state, even though the steady-state net systemic acid load was not greater than in group 1. No exacerbation of acidosis was observed in H2SO4-fed dogs with depleted ECFV . In response to either HCl or H2SO4, persistent hypokalemia caused by increased renal potassium clearance occurred in ECFV -replete dogs but not in ECFV -depleted dogs. Our results indicate that preexisting ECFV depletion results in impaired renal hydrogen ion secretion during prolonged HCl feeding, but not during H2SO4 feeding. These results suggest that during prolonged HCl loading under conditions of preexisting ECFV depletion, hypovolemia-mediated restriction of the normal augmentation of distal delivery of sodium salts overrides the effects of enhanced distal cation secretory capacity that attends hypovolemia-mediated augmentation of distal avidity for sodium reabsorption.

Acid-Base Equilibrium↗
PubMed1983

Hormonal responses to acute volume changes in anephric subjects.

The response of plasma aldosterone and cortisol concentrations to acute volume depletion was studied in 18 chronically anephric subjects and four recently nephrectomized subjects. Volume-depleting hemodialysis and hemodialysis without volume depletion produced insignificant changes in plasma aldosterone concentrations in chronically anephric subjects. Failure of volume depletion to increase plasma aldosterone concentrations in these subjects could not be attributed to reductions in plasma potassium concentrations and was in marked contrast to the effect on plasma cortisol concentrations, which increased significantly during volume depletion. Changes in plasma cortisol concentrations exhibited a negative correlation with changes in diastolic blood pressure (r = -0.712, P less than 0.001) and were shown to correspond to similar changes in plasma ACTH concentrations. Comparable increases in plasma cortisol and ACTH concentrations were also demonstrated in the studies on recently nephrectomized subjects, who, in contrast to chronically anephric subjects, exhibited increases in plasma aldosterone concentrations which were concordant with the changes in plasma cortisol and ACTH concentrations. These findings suggest that plasma aldosterone concentrations are regulated by a volume-sensitive mechanism in recently nephrectomized subjects but not in chronically anephric subjects. We interpret these data as evidence of aldosterone responsiveness to ACTH that persists for a limited time only after removal of the stimulus provided by the renin-angiotensin system. Volume-related changes in plasma cortisol and ACTH concentrations occur in the absence of stimulation by a functioning renin-angiotensin system.

Adolescent↗
PubMed1979

Plasma levels and hepatic extraction of renin and aldosterone in alcoholic liver disease.

Arterial plasma levels and hepatic extraction of renin and aldosterone (ALDO) were measured in 24 patients with alcoholic liver disease and in 14 normal subjects being evaluated as prospective kidney donors. Patients with liver disease had higher plasma concentrations and lower fractional hepatic extractions of both renin and ALDO than the normal subjects. The quantity of renin extracted by the liver was highly correlated with plasma renin in both normal subjects and patients. Plasma ALDO concentration was positively correlated with plasma renin (p less than 0.001) but not with serum sodium, potassium or albumin concentration, inferior vena cava pressure, corrected hepatic venous wedge pressure, plasma volume or sulfobromophthalein storage or transport. Sixteen patients were restudied after one month. Six had received 40 mg/day of prednisolone, and the remaining 10 had received a placebo. Neither group had a change in plasma volume, corrected hepatic venous wedge pressure, plasma concentration or hepatic extraction of renin or ALDO. Serum albumin concentration increased and inferior vena cava pressure decreased with prednisolone therapy. These studies document high plasma levels and impaired hepatic extraction of renin and ALDO in patients with liver disease that are not corrected by short-term prednisolone therapy.

Adult↗
PubMed1979

Effect of acute metabolic acidemia on renal electrolyte transport in man.

The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p less than 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 +/- 16 mueq/min (mean +/- SEM) to 310 +/- 49 mueq/min (p less than 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O/(CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV. UKV fell acutely from 91 +/- 13 to 45 +/- 5 mueq/min (p less than 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 +/- 15 to 143 +/- 18 microgram/min and fractional excretion of calcium increased from 0.55 +/- 0.13 to 1.24 +/- 0.21% (p less than 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 +/- 0.05 to 4.30 +/- 0.03 mg/dl (p less than 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independetn of changes in parathyroid hormone (as reflected by urinary cAMP).

Acidosis↗
PubMed1979

Dissociation of the diurnal variation of aldosterone and cortisol in anephric subjects.

Diurnal variation of plasma aldosterone and cortisol concentration in man was studied in 13 anephric subjects and 7 normal subjects. All subjects were ambulatory and active throughout the study except during an 8-hour sleep period. Six anephric subjects received Kayexalate (sodium polystyrene sulfonate) during the studies to prevent potassium accumulation and increase in plasma potassium concentration. Diurnal variation of plasma aldosterone concentration with peak and nadir concentrations at 12:00 noon and 12:00 midnight respectively was demonstrated in the studies on normal subjects. Changes in plasma aldosterone concentration were not significantly correlated with changes in plasma concentration but were highly correlated with changes in PRA (P less than 0.001). There was a highly significant correlation between plasma aldosterone and potassium concentration in the anephric subjects studied without Kayexalate administration (P less than 0.001). In the anephric subjects who received Kayexalate, plasma aldosterone and potassium concentration remained stable, and no correlation could be demonstrated. No diurnal variation of plasma aldosterone concentration could be demonstrated in either group of anephric subjects, whereas plasma cortisol concentration varied as in the studies on normal subjects. Conclusion. Diurnal variation of plasma aldosterone concentration is dependent on continued stimulation by the renin-angiotensin system. Loss of this stimulation has no demonstrable effect on the diurnal variation of plasma cortisol concentration.

Adult↗
PubMed1979

Acute renal failure after ruptured abdominal aortic aneurysm: an improved clinical prognosis.

Eleven cases of renal failure associated with resection of ruptured abdominal aortic aneurysm and requiring hemodialysis are reported. Previously described series have emphasized the extremely high mortality rate in such patients. In our clinical experience, however, 8 of 11 consecutively treated patients with this clinical problem survived and recovered adequate renal function. We believe that these favorable results can be largely explained by the low incidence of pulmonary infection in our patients as opposed to the frequent occurrence of pulmonary sepsis in other reported series. The reduction in the incidence of pulmonary infection can probably be attributed to the early discontinuance of artificial ventilation after prompt removal of pulmonary edema fluid by intensive hemodialysis ultrafiltration. These survival figures demonstrate that, with appropriate intensive management, full recovery is possible in the majority of patients with acute renal failure complicating ruptured aortic abdominal aneurysm. Our experience serves as a stimulus to render full intensive care support to such patients.

Acute Kidney Injury↗
PubMed1979

The syndrome of inappropriate antidiuretic hormone secretion (SIADH): pathophysiologic mechanisms in solute and volume regulation.

1. Studies on eight patients were performed to clarify the mechanism(s) of altered sodium metabolism and volume regulation in SIADH. The mechanism controlling water excretion was also studied to determine whether there is evidence that altered osmoregulation may be the basis for inappropriate ADH secretion in some patients. 2. These studies show that cumulative sodium balance and aldosterone secretion rates in patients with SIADH are negatively correlated with water intake. There is also a negative correlation between aldosterone secretion and urinary sodium excretion. In the absence of normal urine diluting ability, this increased excretion of sodium becomes a mechanism that allows an increased quantity of water to be excreted despite the persistence of an ADH effect on the renal tubules. 3. Within the range of hyponatremia observed in our studies, changes in serum sodium concentration were accounted for by changes in solute and water balance. One patient, who was potassium deficient during the studies, retained large quantities of sodium and potassium that could not be accounted for by an increase in either serum osmolality or body weight. These observations suggest that intracellular osmotically active solute is either lost or "inactivated" in some manner as intracellular potassium is replenished. 4. Marked impairment of urine diluting ability was demonstrated in all patients. However, two patients with SIADH associated with pulmonary tuberculosis exhibited graded responses to water loading, which suggests that ADH secretion may have been suppressed as serum osmolality was progressively reduced. Whether this can be attributed to a basic alteration or "re-setting" or osmoreceptor function, or is merely an indication that greater than normal reductions of serum osmolality are required to inhibit potent nonosmotic stimuli, remains to be determined.

Adult↗
PubMed1979

Impaired renal tubular potassium secretion in sickle cell disease.

We examined renal tubular function in six patients with sickle cell hemoglobin. All had normal inulin and para-aminohippurate clearances and impaired urinary concentrating and acidifying abilities. After intravenous potassium chloride administration, maximum excretion of potassium (U,V) was significantly lower in sickle cell patients than in control subjects, and the percentage of potassium load excreted in 5 h was markedly reduced. Urinary potassium excretion after sodium sulfate infusion was also markedly reduced in sickle cell patients compared to control subjects. After 40 mg of oral furosemide, U,V was also diminished in sickle cell patients. Plasma aldosterone response to ACTH and intravenous potassium was similar to that of control subjects. Plasma renin activity increased normally after volume contraction. We conclude that sickle cell patients have a defect in their ability to excrete an acute potassium load that cannot be attributed to abnormal renin or aldosterone secretion. Overall potassium homeostasis is maintained by extrarenal mechanisms during acute potassium loading.

Aldosterone↗
PubMed1979

Focal glomerulosclerosis and erythrocytosis.

A 22-year-old black male presented with erythrocytosis and proteinuria. The erythrocytosis was characterized by increased red cell mass, normal arterial oxygen saturation, and normal hemoglobin electrophoresis and oxygen affinity. There was no splenomegaly, and the white blood cell count, platelet count, serum uric acid concentration, serum B12 levels and leukocyte alkaline phosphatase activity were normal. Tumors of the liver, lung, kidney and cerebellum, which have been associated with erythrocytosis, were not found. The only associated disease was biopsy proven focal glomerulosclerosis. Renal vein thrombosis was excluded by renal venography and arteriography. This case illustrates the rarely reported association of the nephrotic syndrome and erythrocytosis. Other nephrogenic causes of erythrocytosis are mentioned, including renal cysts, tumors, renal artery stenosis and transplantation. The role of the kidney in erythropoietin production and possible mechanisms of nephrogenic erythrocytosis are discussed.

Adult↗
PubMed1978

Renal function in patients with multiple myeloma.

Renal tubular and glomerular functions were evaluated in 35 consecutive patients with multiple myeloma and were correlated with changes in renal histopathology and myeloma protein patterns. All nine patients without Bence Jones proteinuria had CCr greater than 50 ml/min. In contrast 16/26 patients with Bence Jones proteinuria had CCr less than 50 ml/min and the magnitude of the Bence Jones proteinuria correlated well with the degree of renal insufficiency. Frequent abnormalities in renal tubular acidifying and concentrating ability were observed only in patients with Bence Jones proteinuria and occurred in the absence of significant reductions of glomerular filtration rate. Severely deranged renal histology was seen only in patients with Bence Jones proteinuria and consisted primarily of tubular atrophy and degeneration; glomeruli appeared normal. These data suggest that Bence Jones proteins exert a direct nephrotoxic effect at the tubular level with resultant tubular dysfunction and tubular atrophy. Glomerular filtration rate remains relatively preserved despite the significant abnormalities of tubular function. Although obstructing tubular casts were observed only in patients with severely impaired glomerular filtration rate, many patients with similarly impaired renal function had no evidence of such casts. Instead, tubular atrophy and degeneration correlated best with renal dysfunction.

Adult↗