Search PubMed⌕ Search

Biomedical subjects

L I Juncos

Publications and source records attributed to L I Juncos.

At least 19 recordsLinked to original sources
PubMed2005

The efficiency of potassium removal during bicarbonate hemodialysis.

Patients on chronic hemodialysis often portray high serum [K+]. Although dietary excesses are evident in many cases, in others, the cause of hyperkalemia cannot be identified. In such cases, hyperkalemia could result from decreased potassium removal during dialysis. This situation could occur if alkalinization of body fluids during dialysis would drive potassium into the cell, thus decreasing the potassium gradient across the dialysis membrane. In 35 chronic hemodialysis patients, we compared two dialysis sessions performed 7 days apart. Bicarbonate or acetate as dialysate buffers were randomly assigned for the first dialysis. The buffer was switched for the second dialysis. Serum [K+], [HCO3-], and pH were measured in samples drawn before dialysis; 60, 120, 180, and 240 min into dialysis; and 60 and 90 min after dialysis. The potassium removed was measured in the dialysate. During the first 2 hr, serum [K+] decreased equally with both types of dialysates but declined more during the last 2 hr with bicarbonate dialysis. After dialysis, the serum [K+] rebounded higher with bicarbonate bringing the serum [K+] up to par with acetate. The lower serum [K+] through the second half of bicarbonate dialysis did not impair potassium removal (295.9 +/- 9.6 mmol with bicarbonate and 299.0 +/- 14.4 mmol with acetate). The measured serum K+ concentrations correlated with serum [HCO3-] and blood pH during bicarbonate dialysis but not during acetate dialysis. Alkalinization induced by bicarbonate administration may cause redistribution of K during bicarbonate dialysis but this does not impair its removal. The more marked lowering of potassium during bicarbonate dialysis occurs late in dialysis, when exchange is negligible because of a low gradient.

Adult↗
PubMed2001

Hyperkalemia, renal failure, and converting-enzyme inhibition: an overrated connection.

Hyperkalemia is widely viewed as a common complication of ACE inhibition in azotemic patients. These renal failure patients are the patients who benefit most from ACE inhibition. Because we could not confirm this notion after a retrospective evaluation of 236 azotemic patients, we studied 2 models of renal mass reduction. In the first, we did a 5/6 nephrectomy (Nx) on rats and studied them 2 weeks after surgery (before chronic renal changes had developed). A second group was studied 16 weeks after Nx, once chronic renal failure was established. Rats in both models were treated with quinapril in drinking water. After baseline evaluation, we challenged them either by a high-K(+) diet or by blocking aldosterone receptors. We found that although quinapril blocked the K(+)-induced increase in aldosterone, serum K(+) levels and K(+) balance were maintained before and during high K(+) intake or during simultaneous spironolactone administration. We conclude that in hemodynamically stable rats with reduced renal mass and renal dysfunction, the administration of an ACE inhibitor does not cause severe hyperkalemia.

Adolescent↗
PubMed2000

Renal tubular acidosis and vasculitis associated with IgE deposits in the kidney and small vessels.

We report a woman with a history of allergies, polyuria, polydipsia, proteinuria, renal loss of electrolytes, renal tubular acidosis, nephrocalcinosis, and palpable purpura. A proximal defect was excluded by a normal bicarbonate reabsorption curve, and a distal tubular defect was shown because urine pH did not decrease to less than 6.4 despite ammonium chloride-induced systemic acidosis. Moreover, furosemide failed to improve urinary acidification. Urine-to-blood PCO(2) gradient was less than 14 mm Hg, although the urine bicarbonate level reached values as high as 89 mEq/L. Combining bicarbonate and neutral phosphate infusions increased the urine-to-blood PCO(2) gradient to only 20 mm Hg. These subnormal PCO(2) gradient values point to proton-pump dysfunction in the collecting tubule. Histological evidence of tubulointerstitial disease accompanied the tubular defects. The striking histological feature was the presence of immunoglobulin E (IgE) deposits in glomeruli, tubuli, and vessels. Concurrent with these findings, she had high serum IgE titers and CD23 levels. IgE antibodies from her serum were reactive against human renal tubuli, with binding to two regions that matched two different proteins present in cortex and medulla. One of these proteins corresponded to carbonic anhydrase II (31 kd); the second, to an unidentified protein that seems attached to cell membranes. We suggest that these IgE antibodies could have had a pathogenic role in this patient's glomerular, tubular, and small-vessel disease.

Acidosis, Renal Tubular↗
PubMed1999

Abnormal renal vasodilation to an amino acid infusion in congestive heart failure: normalization by enalapril.

In congestive heart failure (CHF), the neurohormonal mechanisms that cause renal vasoconstriction, particularly those depending on the renin-angiotensin system, could interfere with renal vasodilating mechanisms. To elucidate this issue, we studied the kidney response to an amino acid infusion (known to cause renal vasodilation in healthy individuals) in eight patients with CHF. We found that the amino acid infusion (0.7 mL/kg/h of a 10% solution) elicited no renal hemodynamic response, in marked contrast to healthy subjects. We next hypothesized that the renin-angiotensin system (known to be activated in heart failure) has a role in the lack of response to the amino acid infusion. To test this hypothesis, we repeated the study after two 5-mg doses of enalapril, an inhibitor of the angiotensin-converting enzyme, administered 12 hours apart. After enalapril treatment, the amino acid infusion caused a 45% increase in mean renal blood flow (RBF) from 383 +/- 55 to 557 +/- 51 mL/min at the fifth hour (P < 0.05). This normalization of the renal response to the amino acid infusion occurred without changes in cardiac output or in systemic vascular resistance. Hence, the renal fraction of the cardiac output increased during the amino acid infusion. The recovery of the renal vascular response was not accompanied by an increase in glomerular filtration rate (GFR; filtration fraction decreased), suggesting a predominant efferent arteriole dilatation. Our study shows that, in heart failure, the kidney loses its ability to increase RBF in response to an amino acid load. This lack of renal vascular response can be restored by inhibiting the renin-angiotensin system and is unrelated to changes in systemic hemodynamics.

Aged↗
PubMed1997

Abnormal endothelium-dependent responses in early radiation nephropathy.

While arterial hypertension and renal dysfunction are well recognized complications of renal irradiation, the mechanisms that trigger the development of these complications are unknown. Recently, it was reported that the endothelium is a major target in radiation injury. Because dysfunction of the endothelial cells may lead or contribute to the development of hypertension and renal dysfunction in radiation nephropathy, we tested the hypothesis that endothelium-dependent vasodilation is impaired in radiated kidneys prior to the onset of hypertension. To test this hypothesis, we used Long-Evans rats that had undergone left nephrectomy (3 weeks earlier) and irradiation (3000 r's) to the right kidney 8 days earlier (mean blood pressures in the irradiated rats were not different than in the controls). We then measured the changes in renal blood flow (RBF) induced by endothelium-dependent (acetylcholine and bradykinin) and -independent (nitroprusside, norepinephrine, and angiotensin II) vasoactive agents. We found that the increases in RBF induced by the endothelium-dependent but not independent vasodilators were markedly impaired in the irradiated kidneys. Blocking nitric oxide synthesis with nitro L-arginine methyl ester in sham rats mimicked the blunted responsiveness of the irradiated rats, whereas indomethacin (an inhibitor of prostaglandin synthesis) had no effect on either sham or irradiated rats. Finally, the RBF responses to the endothelium-independent vasoconstrictors, norepinephrine and angiotensin II, were not altered in the irradiated kidneys. These results suggest that renal irradiation causes endothelial dysfunction (prior to the onset of hypertension) but spares the vascular smooth muscle cells.

Acetylcholine↗
PubMed1995

Right-sided bacterial endocarditis due to Flavobacterium odoratum in a patient on chronic hemodialysis.

Bacterial endocarditis, particularly involving the left side, has been shown to occur in patients in regular hemodialysis. We report a case of right-sided endocarditis characterized by a very torpid evolution. Although the diagnosis was suspected early in the course, confirmation was obtained 2 months after the onset. Flavobacterium odoratum was identified in the fourth month of evolution and only after multiple blood cultures had been obtained. We believe the very low infectivity of F. odoratum and its very slow growth in culture media prevented an early diagnosis.

Endocarditis, Bacterial↗
PubMed1993

Long-term enalapril and hydrochlorothiazide in radiation nephritis.

Radiation of the kidney often leads to renal failure. The contribution of arterial hypertension to the development of this complication is unclear. The aim of this study was to determine the renal effects of antihypertensive therapy in 1- and 2-kidney rat models of radiation nephritis. Five groups of Long Evans rats had X-irradiation of the left kidney. In groups 1 and 2, the right kidney was left undisturbed (2-kidney model). The rats in group 3, 4 and 5 underwent right nephrectomy 21 days before radiation (1-kidney model). Groups 1 and 3 received no drug treatment and served as controls for each model. Groups 2 and 4 had enalapril 50 mg/l in drinking water and group 5 hydrochlorothiazide (HCT) 200 mg/l, also in drinking water. Blood pressure increased significantly in both control groups and remained normal throughout the study in all treated groups. At the end of the study, mean urinary protein excretion was lower in the two enalapril-treated groups but not in HCT-treated animals. Groups 1 and 2 (2-kidney models) showed similar increments in plasma creatinine (PCreat), and, in both groups, the creatinine clearance (CCreat) dropped to the same extent. Among nephrectomized animals (1-kidney model), PCreat was lower and CCreat higher in the enalapril-treated group. Consistent with these findings, glomerular sclerosis was less severe in both enalapril-treated groups. We conclude that, in radiation nephritis, lowering blood pressure with enalapril exerts a beneficial effect on renal function and structure, whereas a similar reduction in blood pressure induced by HCT does not.

Animals↗
PubMed1992

The effect of upright tilt on nifedipine-induced natriuresis.

Calcium channel blockers are antihypertensive agents with diuretic actions. Yet edema occurs in some patients receiving long-term treatment with these drugs. As with other vasodilators, stimulation for fluid retention could result from systemic vasodilation. We speculated that the upright posture could enhance sodium retention. To test this hypothesis, we studied the effect of upright tilt in 10 patients before and after the oral administration of 20 mg nifedipine. Before nifedipine upright tilt caused a 41% drop in the sodium excretion rate, from 0.27 +/- 0.04 to 0.16 +/- 0.03 meq/min (p less than 0.05). Fractional sodium excretion decreased by 46%, from 2.4 +/- 0.5 to 1.3 +/- 0.3% (p less than 0.01). Urinary volume and renal plasma flow also decreased (p less than 0.05). Plasma renin activity (PRA) rose by 46% (p less than 0.005). With the patients in the supine posture nifedipine increased the sodium excretion rate to 0.49 +/- 0.09 meq/min (p less than 0.05). Fractional sodium excretion was 3.1 +/- 0.6 meq/min (p = 0.2). The natriuresis took place despite a fall in mean blood pressure and a significant rise in PRA (up 115% from prenifedipine supine values, p less than 0.005). Renal plasma flow also increased (p less than 0.01). The upright tilt caused a reversal of the nifedipine-induced natriuresis. The sodium excretion rate dropped to 0.23 +/- 0.05 meq/min and fractional sodium excretion to 1.3 +/- 0.2% (both not different from control). This drop in natriuresis occurred while mean blood pressure was at its lowest and PRA was 254% above the initial levels (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Patient compliance and angiotensin converting enzyme inhibitors in hypertension.

Patient compliance is crucial to successful medical treatment. Many factors contribute to compliance, including age, sex, other sociodemographic factors, finances, intelligence, complexity of therapeutic regimen, and patient-physician rapport. Compliance is especially critical in medical conditions requiring prolonged therapy, such as hypertension. Historically, compliance among hypertensive patients has been alarmingly poor, with a 50% drop-off after 1 year and fewer than 20% still in therapy after 5 years. The use of enalapril, the long-acting angiotensin converting enzyme (ACE) inhibitor that allows for a once-daily regimen, has improved treatment success and compliance. This probably is due to the efficacy of the drug, coupled with a low incidence of side effects.

Adult↗
PubMed1979

Obstruction of the inferior vena cava complicating hemodialysis in polycystic kidney disease.

Two patients with polycystic kidney disease and renal failure developed profound hypotension within 30 minutes after starting hemodialysis. After ruling out all recognized causes of hypotension during early dialysis, we found that their vena cavas were obstructed by compression of the vessels against the spinal column by the greatly enlarged polycystic kidneys. Immediately after bilateral nephrectomy, the patients had dialysis, with removal of large amounts of fluid without causing hypotension. We speculate that compression of the vena cava by massively enlarged polycystic kidneys may significantly contribute to the renal insufficiency by greatly increasing renal venous pressure.

Humans↗
PubMed1979

Intravascular clotting preceding crescent formation in a patient with Wegner's granulomatosis and rapidly progressive glomerulonephritis.

Rapidly progressive glomerulonephritis is thought to be a proliferative reaction common to a number of disorders. Animal experiments implicate clotting or a product of it as its cause. In the human, the presence of fibrin in crescents, as well as the response to heparinization in some cases, support the role of coagulation in the genesis of extracapillary cell proliferation. We describe the clinical and histologic course in a patient with Wegener's granulomatosis who presented with a picture of intracapillary clotting which evolved into rapidly progressive glomerulonephritis. The patient had a remarkable return of renal function.

Adult↗
PubMed1978

New method for obtaining uncontaminated urine from women.

Midstream sampling and colony counts have greatly improved precision in diagnosing urinary tract infections. In women, however, contamination by vaginal flora and cells still poses a diagnostic problem. We have devised an instrument for helping collect uncontaminated urine from women and have tested it in three sets of observations. Approximately 96% of 200 women were able to use the device successfully after minimal instruction. Bacterial colony counts and quantitative estimation of vaginal epithelial cells were performed on urine collected by 18 female volunteers using conventional clean-catch technics and on urine collected by the same 18 women using the Clean Streamer. The average bacterial colony count in conventionally collected urine was 8,100/ml while in Clean Streamer collected urine it was 1,722/ml. The average number of vaginal epithelial cells in conventionally collected urine was 22.4/ml while in Clean Streamer collected urine it was 14.1/ml. The difference in both comparisons is statistically significant (P = .01). We believe that use of the Clean Streamer greatly facilitates the ability of a woman to collect a urine sample uncontaminated by vaginal secretions and flora.

Bacteriuria↗
PubMed1977

Renins and prostaglandins in segmental renal artery aneurysm associated with accelerated hypertension.

A patient with hypertension of sudden onset and with segmental renal ischemia due to an aneurysm in a renal artery branch underwent a nephrectomy which apparently cured his arterial hypertension. The nephrectomy specimen was studied to determine the activity of the juxtaglomerular cells and the concentration of prostaglandins in both ischemic and normal renal tissue. As compared with the normal tissue, the ischemic cortex had an increased number of heavily granulated juxtaglomerular cells. Interstitial fibrosis in the ischemic segment was associated with considerably lower tissue concentration of both prostaglandins A2 and E2 when compared with surrounding normal medulla. These findings appear to correlate well with present theories that consider renal ischemia to be associated with decreased production or response of prostaglandins that normally would counteract the effects of angiotensin.

Adult↗
PubMed1977

Prognostic value of angiography in management of severe acute renal transplant rejection.

Angiograms of 34 kidney transplant patients with progressive decrease in renal function after multiple doses of intravenous methylprednisolone (MP) were evaluated retrospectively in regard to the prognostic value of angiography. The following parameters were included in evaluation: prolonged arterial washout time, large vessel vasculitis, presence of arteriovenous shunting, poor cortical perfusion as evidenced by non-filling of cortical vessels, poor definition of cortico-medullary junction, and a poor nephrogram. When 1 to 3 of these abnormalities existed in angiogram, 67% of living related donor transplants (LRD) recovered under continued MP-therapy. With 4-6 angiographic abnormalities the recovery rate was reduced to 30%. The overall recovery rate for LRD transplants was 44%. Cadaveric transplants (CAD) had a statistically significant poorer prognosis as evidenced by only 8% recovery rate under continued MP-therapy.

Acute Disease↗