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Biomedical subjects

S P Kelleher

Publications and source records attributed to S P Kelleher.

12 recordsLinked to original sources
PubMed2001

Gout, bradycardia, and hypercholesterolemia after renal transplantation.

Approximately 17,000 solid organ transplantations are done annually in the United States. Increasingly, care of these patients will be provided by primary care physicians. In this report, we illustrate the complexity of common medical problems in a patient who had cellulitis and who had had a cadaveric renal transplantation 10 years earlier. Immunosuppressive therapy was cyclosporine (100 mg twice a day) and prednisone (10 mg once a day). The patient's hospital course was complicated by acute gout and symptomatic bradycardia. In both instances, usual treatment--full-dose indomethacin for gout and withholding verapamil for bradycardia--could have had significant interaction with the cyclosporine. At the time of discharge, a therapeutic plan for long-term management of hypercholesterolemia included possible drug interactions with cyclosporine. The potential for drug toxicity in the transplant patient necessitates careful monitoring of immunosuppressive drug levels. Ongoing communication with the transplant center is also needed.

Bradycardia↗
PubMed1988

Eosinophiluria.

Hansel's stain is a simple technique that can easily be performed in a clinical or office setting. It allows for improved detection of the eosinophiluria when compared with conventional Wright's stain. The mechanism underlying the superiority of the Hansel's stain remains to be elucidated. Eosinophiluria demonstrated by Hansel's stain appears to be a sensitive marker for drug-induced acute interstitial nephritis and probably allows differentiation from acute tubular necrosis. However, the spectrum of eosinophiluria also includes acute glomerulonephritis, rapidly progressive glomerulonephritis, prostatitis, and urinary tract obstruction. Therefore, the finding of eosinophiluria on Hansel's stain clearly cannot be considered diagnostic of acute interstitial nephritis. In the absence of renal biopsy or other clinical clues to suggest the diagnosis, eosinophiluria should not be used as the sole criterion for the diagnosis of acute interstitial nephritis or a a justification for empiric steroid therapy.

Drug Hypersensitivity↗
PubMed1987

Severe metabolic alkalosis complicating regional citrate hemodialysis.

Regional citrate hemodialysis has been effectively used as an alternative to heparin anticoagulation during dialysis of patients at increased risk for bleeding. Few complications have been noted; however, we report the occurrence of severe metabolic alkalosis in two patients requiring high infusion rates of citrate during hemodialysis while being mechanically ventilated. Careful monitoring of acid-base status is mandatory in this setting, and reduction of citrate dose may be advisable.

Aged↗
PubMed1987

Effect of hemorrhagic reduction in blood pressure on recovery from acute renal failure.

The effect of hemorrhagic reduction in systemic blood pressure (SBP) to 90 mm Hg for four hours on autoregulation of renal blood flow (RBF), renal function, and renal histology was examined in control rats, one week norepinephrine-induced acute renal failure (NE-ARF) rats with intact renal nerves, and one week NE-ARF rats with prior renal denervation. The results showed that in control rats, hemorrhagic SBP reduction to 90 mm Hg had no effect on autoregulation of RBF (autoregulatory index = 0.09 +/- 0.02), creatinine clearance, or renal histology. However, in one week NE-ARF rats with intact renal nerves, hemorrhagic reduction in SBP to 90 mm Hg was associated with marked impairment of autoregulation of RBF (autoregulatory index = 3.49 +/- 0.25), further reduction in creatinine clearance from 0.59 +/- 0.08 ml/min to 0.36 +/- 0.14 ml/min, and histologic evidence of recurrent ischemic injury. Renal denervation prior to SBP reduction improved autoregulation of RBF (autoregulatory index = 0.30 +/- 0.09), prevented the further reduction in creatinine clearance, and significantly ameliorated the deleterious effect on renal histology seen in innervated NE-ARF rats. These results suggest the potential importance of the loss of autoregulation of RBF on the course of NE-ARF, and further support the pathogenetic role of renal nerves in the loss of autoregulation.

Acute Kidney Injury↗
PubMed1986

Eosinophiluria--a new method of detection and definition of the clinical spectrum.

Eosinophiluria is considered a useful marker of drug-induced acute interstitial nephritis. However, recognition of eosinophiluria by Wright's staining is technically difficult, and the spectrum of disorders causing eosinophiluria is not completely defined. We have adapted Hansel's stain for the examination of urinary sediment. Whereas there was a variable uptake of Wright's stain by eosinophils in the urine, such eosinophils were readily recognized with Hansel's stain by the presence of bright red granules. The prevalence of eosinophiluria in acute interstitial nephritis was 10 of 11 patients, in acute tubular necrosis none of 30, in acute pyelonephritis none of 10, in acute cystitis 1 of 15, in postinfectious glomerulonephritis 1 of 6, in rapidly progressive glomerulonephritis 4 of 10, and in acute prostatitis 6 of 10. Eosinophiluria in acute interstitial nephritis was demonstrated by Hansel's stain in 10 of 11 patients but by Wright's stain in only 2 of 11 patients. We conclude that Hansel's stain substantially improves the recognition of eosinophiluria as compared with Wright's stain. Eosinophiluria is useful in distinguishing acute interstitial nephritis from acute tubular necrosis. The clinical spectrum of eosinophiluria also includes rapidly progressive glomerulonephritis, acute prostatitis, and occasionally, acute cystitis or postinfectious glomerulonephritis.

Acute Disease↗
PubMed1986

Reduced or absent serum anion gap as a marker of severe lithium carbonate intoxication.

Two patients with life-threatening lithium carbonate intoxication (serum levels, greater than 4 mEq/L [greater than 4 mmol/L]) presented with a reduced or absent serum anion gap. In both subjects, hemodialysis simultaneously removed the excess lithium ion and normalized the anion gap. Conversely, the anion gap was normal in subjects with therapeutic serum lithium ion levels. Severe lithium carbonate intoxication should be added to the category of illnesses (multiple myeloma, bromide intoxication) causing a marked reduction in the anion gap. In the comatose patient, a reduced anion gap may serve as an important clinical clue to the presence of this drug intoxication.

Acid-Base Equilibrium↗
PubMed1986

The role of intensive dialysis in acute renal failure.

The efficacy of vigorous dialysis in the management of acute renal failure remains controversial. In order to examine the beneficial role of vigorous dialysis, a prospective study was carried out in 34 patients paired by acute renal failure etiology and treated with sufficient dialysis to maintain predialysis blood urea nitrogen and serum creatinine below either 60 and 5 mg/dl (intensive) or 100 and 9 mg/dl, respectively (non-intensive). Serum creatinine was at least 8 mg/dl in all patients prior to random assignment to intensive or non-intensive dialysis. Mean predialysis blood urea nitrogen and serum creatinine, respectively, were 60 +/- 23 and 5.3 +/- 1.5 mg/dl in the intensively dialyzed group and 101 +/- 18 and 9.1 +/- 1.4 mg/dl in the non-intensively dialyzed group (both p less than .001). Predialysis serum bicarbonate and blood pH were lower and serum phosphate higher in the non-intensively dialyzed patients. Daily weight changes, increases in blood urea nitrogen, protein and calorie intakes were similar. While hemorrhagic episodes tended to be more frequent in non-intensively dialyzed patients, overall complication rates were not different between the two groups. Mortality rates, which were 58.8% in the intensive and 47.1% in the non-intensive groups, also were not different. On the other hand, urine output prior to dialysis did influence survival. It is concluded that, within the limits of the study, there is no advantage to intensive dialysis in the management of acute renal failure.

Acute Kidney Injury↗
PubMed1985

Acute pyelonephritis as a cause of late transplant dysfunction.

In a renal transplant recipient, acute pyelonephritis of the allograft developed in association with acute deterioration of renal function. No other cause of renal dysfunction was delineated, and the serum creatinine level promptly returned to baseline with antimicrobial therapy. Acute pyelonephritis is an important cause of late transplant dysfunction, and prompt diagnosis and treatment result in complete recovery of renal function.

Acute Kidney Injury↗
PubMed1984

Nephron heterogeneity in ischemic acute renal failure.

To uncover the reasons for reported internephron heterogeneity in acute renal failure (ARF) serial micropuncture experiments in norepinephrine-induced ARF and sham-infused control rats were carried out to investigate this phenomenon. Proximal tubular pressures (PT) were scattered at 24, 48, and 72 hr in ARF rats ranging from 4 to 42 mm Hg, but the majority were greater than the mean control values (10 +/- 1 mm Hg). One week ARF PT were less variable than on previous days (5 to 17 mm Hg). The decreased variability was the result of a reduced number of PT values that were greater than controls. When single nephron filtration rates (SNGFR) were measured with spontaneous flow collections without maintaining the existent tubular pressures, results were widely scattered on each day. When SNGFR were measured at the existent PT, individual determinations were tightly clustered on each experimental day, clearly different from controls (all P less than 0.001), and correlated closely with predicted values from whole kidney inulin clearance (all P less than 0.001). Thus, existent internephron SNGFR was uniform in ARF rats and apparent heterogeneity, in large part, was attributable to an artifact of the tubular fluid collection technique. Despite the uniformity of SNGFR, values of PT ranging below as well as above controls, suggested that a mechanism in addition to tubular obstruction was operative in reducing SNGFR. Recoveries of microperfused 14C-inulin were similar to controls excluding significant backleak of tubular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1984

Sympathetic nervous system in the loss of autoregulation in acute renal failure.

The responsiveness of the renal vascular system was investigated in uninephrectomized Sprague-Dawley rats in which acute renal failure had been induced by norepinephrine. The animals were studied at 1' and 3 wk after norepinephrine infusion. Uninephrectomized littermates served as controls. Compared with controls, there was an absence of renal blood flow autoregulation in 1-wk acute renal failure that returned in part by 3 wk. In 1-wk rats there was a marked increase, rather than decrease, in renovascular resistance as renal perfusion pressure was decreased. The renal vasculature was significantly less responsive in 1-wk rats than in control or 3-wk animals when acetylcholine, angiotensin II, or norepinephrine was infused into the renal artery at minimal vasoactive doses (all P less than 0.01). Paradoxically, renal vasoconstriction in response to renal nerve stimulation was greater in 1-wk than in 3-wk and control rats (P less than 0.01) and was not inhibited by renal artery infusion of phenoxybenzamine. Renal denervation significantly improved renal blood flow autoregulation in 1-wk animals (P less than 0.001) and completely abolished the increase in renovascular resistance as renal perfusion pressure was lowered. No effects of renal denervation on renal blood flow autoregulation were seen in control and 3-wk rats. It is concluded that renovascular responses to neurohumoral stimuli are aberrant in acute renal failure. The loss of renal blood flow autoregulation is related to an increased renovascular resistance that is due to increased activity of non-alpha-adrenergic mechanisms of the autonomic nervous system.

Acetylcholine↗
PubMed1984

Intranasal deamino-8-D-arginine vasopressin shortens the bleeding time in uremia.

Clinical bleeding in uremia is a frequent problem and seems to correlate with a prolonged bleeding time. The vasopressin analog deamino-8-D-arginine vasopressin has been shown to shorten the bleeding time and to decrease clinical bleeding when administered intravenously to uremic patients. In the present study we administered the readily available intranasal deamino-8-D-arginine vasopressin to 2 uremic patients and demonstrated a decreased bleeding time and improvement in clinical bleeding.

Administration, Intranasal↗